A randomized clinical trial of low-dose cannabis extract in Alzheimer's disease
Rafael de Morais Cury https://orcid.org/0000-0001-6745-5390, Taynara da Silva https://orcid.org/0000-0002-3915-4109, […], and Francisney Pinto Nascimento https://orcid.org/0000-0002-6657-4045francisney.nascimento@unila.edu.br+10View all authors and affiliations Volume 108, Issue 4 https://doi.org/10.1177/13872877251389608
Abstract
Background Preclinical and clinical evidence suggest that low-dose cannabinoids could ameliorate Alzheimer's disease (AD) signs and symptoms. We designed this trial to evaluate the safety and efficacy of low-dose THC-CBD balanced cannabinoid extract in the treatment of patients with AD-associated dementia.
Objective The objective of this phase 2 trial was to evaluate the safety and efficacy of a balanced THC-CBD cannabinoid extract for symptomatic patients with AD. Methods A Phase 2, randomized, double-blind, placebo-controlled, clinical trial including patients between 60 and 80 years-old diagnosed with AD-associated dementia. For 26 weeks, participants orally received either placebo or THC-CBD extract (0.350 mg/THC and 0.245 mg/CBD), daily.
Results At week 26, Mini-Mental State Exam total score was significantly higher in cannabis- when compared to placebo-treated patients, which was assessed using the mixed model analysis. No significant difference was detected between placebo and cannabis groups in terms of secondary outcomes and adverse events incidence.
Conclusions To this date, this is the longest clinical trial evaluating cannabinoids effects on AD patients. We initially demonstrate that low-dose THC-CBD potentially can be an effective and safe therapeutic option for AD-related dementia. Nonetheless, larger and longer trials are necessary to confirm this finding and establish cannabinoid administration as therapy for AD dementia.
Trial Registration The Brazilian Registry of Clinical Trials (ReBEC) registration #U1111-1258-2058 - REBEC (ensaiosclinicos.gov.br).
Cannabinoid extract in microdoses ameliorates mnemonic and nonmnemonic Alzheimer’s disease symptoms: a case report Case report
Open access Published: 12 July 2022 Volume 16, article number 277, (2022) Cite this article You have full access to this open access article Download PDF Journal of Medical Case Reports Aims and scope Submit manuscript Cannabinoid extract in microdoses ameliorates mnemonic and nonmnemonic Alzheimer’s disease symptoms: a case report Download PDF Ana Carolina Ruver-Martins, Maíra Assunção Bicca, Fabiano Soares de Araujo, Beatriz Helena Lameiro de Noronha Sales Maia, Fabrício Alano Pamplona, Elton Gomes da Silva & Francisney Pinto Nascimento 11k Accesses 18 Citations 133 Altmetric 13 Mentions Explore all metrics
Abstract
Background Cannabinoid-based therapy has been shown to be promising and is emerging as crucial for the treatment of cognitive deficits, mental illnesses, and many diseases considered incurable. There is a need to find an appropriate therapy for Alzheimer’s disease, and cannabinoid-based therapy appears to be a feasible possibility.
Case presentation This report addresses the beneficial effect of cannabinoids in microdoses on improving memory and brain functions of a patient with mild-stage Alzheimer’s disease. The patient is a 75-year-old white man presenting with main symptoms of memory deficit, spatial and temporal disorientation, and limited daily activity. The experimental therapeutic intervention was carried out for 22 months with microdoses of a cannabis extract containing cannabinoids. Clinical evaluations using Mini-Mental State Examination and Alzheimer’s Disease Assessment Scale-Cognitive Subscale were performed.
Conclusions Here we provide original evidence that cannabinoid microdosing could be effective as an Alzheimer’s disease treatment while preventing major side effects. This is an important step toward dissociating cannabinoids’ health-improving effects from potential narcotic-related limitations.
ALZHEIMER’S TREATMENT SEE UPDATED SCIENCE 2016
Public Release: 28-Jun-2016 Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells
Salk Institute
IMAGE: Preliminary lab studies by Salk Professor David Schubert suggest that the molecule THC reduces beta amyloid proteins in human neurons. view more
Credit: Salk Institute
LA JOLLA -- Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer's disease.
While these exploratory studies were conducted in neurons grown in the laboratory, they may offer insight into the role of inflammation in Alzheimer's disease and could provide clues to developing novel therapeutics for the disorder.
"Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer's, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells," says Salk Professor David Schubert, the senior author of the paper.
Alzheimer's disease is a progressive brain disorder that leads to memory loss and can seriously impair a person's ability to carry out daily tasks. It affects more than five million Americans according to the National Institutes of Health, and is a leading cause of death. It is also the most common cause of dementia and its incidence is expected to triple during the next 50 years.
It has long been known that amyloid beta accumulates within the nerve cells of the aging brain well before the appearance of Alzheimer's disease symptoms and plaques. Amyloid beta is a major component of the plaque deposits that are a hallmark of the disease. But the precise role of amyloid beta and the plaques it forms in the disease process remains unclear.
In a manuscript published in June 2016's Aging and Mechanisms of Disease, Salk team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer's disease.
The researchers found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. They demonstrated that exposing the cells to THC reduced amyloid beta protein levels and eliminated the inflammatory response from the nerve cells caused by the protein, thereby allowing the nerve cells to survive.
"Inflammation within the brain is a major component of the damage associated with Alzheimer's disease, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves," says Antonio Currais, a postdoctoral researcher in Schubert's laboratory and first author of the paper. "When we were able to identify the molecular basis of the inflammatory response to amyloid beta, it became clear that THC-like compounds that the nerve cells make themselves may be involved in protecting the cells from dying."
Brain cells have switches known as receptors that can be activated by endocannabinoids, a class of lipid molecules made by the body that are used for intercellular signaling in the brain. The psychoactive effects of marijuana are caused by THC, a molecule similar in activity to endocannabinoids that can activate the same receptors. Physical activity results in the production of endocannabinoids and some studies have shown that exercise may slow the progression of Alzheimer's disease.
Schubert emphasized that his team's findings were conducted in exploratory laboratory models, and that the use of THC-like compounds as a therapy would need to be tested in clinical trials.
In separate but related research, his lab found an Alzheimer's drug candidate called J147 that also removes amyloid beta from nerve cells and reduces the inflammatory response in both nerve cells and the brain. It was the study of J147 that led the scientists to discover that endocannabinoids are involved in the removal of amyloid beta and the reduction of inflammation.
###
Other authors on the paper include Oswald Quehenberger and Aaron Armando at the University of California, San Diego; and Pamela Maher and Daniel Daughtery at the Salk Institute.
The study was supported by the National Institutes of Health, The Burns Foundation and The Bundy Foundation.
About Salk Institute:
Every cure has a starting point. The Salk Institute embodies Jonas Salk's mission to dare to make dreams into reality. Its internationally renowned and award-winning scientists explore the very foundations of life, seeking new understandings in neuroscience, genetics, immunology and more. The Institute is an independent nonprofit organization and architectural landmark: small by choice, intimate by nature and fearless in the face of any challenge. Be it cancer or Alzheimer's, aging or diabetes, Salk is where cures begin. Learn more at: salk.edu.
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
*** National Cancer Institute at the National Institutes of Health ***
Cannabis and Cannabinoids (PDQ®), Cancer Antitumor Effects, Prion prevention, Pain management, muscle relaxer, and Palliative Medicine
Cannabis and Cannabinoids (PDQ®)
Laboratory/Animal/Preclinical Studies
Antitumor Effects Appetite Stimulation Analgesia
Laboratory/Animal/Preclinical Studies
Antitumor Effects
Appetite Stimulation
Analgesia
Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Antitumor Effects One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9-12] One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents.[13] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[14]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[15] Both agents reduced the viability of hepatocellular carcinoma cells in vitro and demonstrated antitumor effects in hepatocellular carcinoma subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma [16] and breast cancer.[17]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.[18]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[19] In the experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation.
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[20] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[21,22]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[23] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[24-27]
Appetite Stimulation Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[28] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[29]
Analgesia Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[30] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[31,32]
Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[33-35] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[36]
References
snip...
J Neurosci. 2007 Sep 5;27(36):9537-44.
Nonpsychoactive cannabidiol prevents prion accumulation and protects neurons against ***prion*** toxicity.
*** Our results suggest that CBD may protect neurons against the multiple molecular and cellular factors involved in the different steps of the neurodegenerative process, which takes place during prion infection. When combined with its ability to target the brain and its lack of toxic side effects, CBD may represent a promising new anti-prion drug.
Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy
Brenda E. Porter x Brenda E. Porter Search for articles by this author , Catherine Jacobson x Catherine Jacobson Search for articles by this author Correspondence Corresponding author. email Received: May 24, 2013; Received in revised form: July 23, 2013; Accepted: August 30, 2013; DOI: http://dx.doi.org/10.1016/j.yebeh.2013.08.037 Abstract Full Text Images/Data References Related Articles To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect.
Abstract
Severe childhood epilepsies are characterized by frequent seizures, neurodevelopmental delays, and impaired quality of life. In these treatment-resistant epilepsies, families often seek alternative treatments. This survey explored the use of cannabidiol-enriched cannabis in children with treatment-resistant epilepsy. The survey was presented to parents belonging to a Facebook group dedicated to sharing information about the use of cannabidiol-enriched cannabis to treat their child's seizures. Nineteen responses met the following inclusion criteria for the study: a diagnosis of epilepsy and current use of cannabidiol-enriched cannabis. Thirteen children had Dravet syndrome, four had Doose syndrome, and one each had Lennox–Gastaut syndrome and idiopathic epilepsy. The average number of antiepileptic drugs (AEDs) tried before using cannabidiol-enriched cannabis was 12. Sixteen (84%) of the 19 parents reported a reduction in their child's seizure frequency while taking cannabidiol-enriched cannabis. Of these, two (11%) reported complete seizure freedom, eight (42%) reported a greater than 80% reduction in seizure frequency, and six (32%) reported a 25–60% seizure reduction. Other beneficial effects included increased alertness, better mood, and improved sleep. Side effects included drowsiness and fatigue. Our survey shows that parents are using cannabidiol-enriched cannabis as a treatment for their children with treatment-resistant epilepsy. Because of the increasing number of states that allow access to medical cannabis, its use will likely be a growing concern for the epilepsy community. Safety and tolerability data for cannabidiol-enriched cannabis use among children are not available. Objective measurements of a standardized preparation of pure cannabidiol are needed to determine whether it is safe, well tolerated, and efficacious at controlling seizures in this pediatric population with difficult-to-treat seizures.
Original Contribution| January 11, 2012 Association Between Marijuana Exposure and Pulmonary Function Over 20 Years
Conclusion Occasional and low cumulative marijuana use was not associated with adverse effects on pulmonary function.
Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1
Cannabinoids inhibit cancer cell invasion via increasing tissue inhibitor of matrix metalloproteinases-1 (TIMP-1).
Cannabis in Palliative Medicine: Improving Care and Reducing Opioid-Related Morbidity
Published online before print March 28, 2011, J HOSP PALLIAT CARE August 2011 vol. 28 no. 5 297-303
Published online ahead of print August 30, 2010 CMAJ 10.1503/cmaj.091414
Smoked cannabis for chronic neuropathic pain: a randomized controlled trial
Conclusion
Our results support the claim that smoked cannabis reduces pain, improves mood and helps sleep. We believe that our trial provides a methodological approach that may be considered for further research. Clinical studies using inhaled delivery systems, such as vaporizers,32,33 are needed.
Cases J. 2009; 2: 7487.
Published online 2009 May 18
Standardized natural product cannabis in pain management and observations at a Canadian compassion society: a case report
The roughly 4000 members of the Green Cross Society find similar benefit from standardized natural product cannabis medicine. To follow, will be publication of the Society's demographic data regarding use for various conditions such as arthritis, fybromyalgia, HIV/AIDS, and chronic pain, to name a few. A breakdown of the illnesses, what strains (cannabinoid profiles) is most effective, and at what dosages will be published at a later time.
Effect of D9-tetrahydrocannabinol, a cannabinoid receptor agonist, on the triggering of transient lower oesophageal sphincter relaxations in dogs and humans
These findings confirm previous findings in dogs and indicate that CB receptors are also involved in the triggering of TLESRs in humans.
Drugs: 9 July 2010 - Volume 70 - Issue 10 - pp 1245-1254
Pharmacological Management of Pain in Patients with Multiple Sclerosis
Cannabinoids have been among the few treatments studied in well designed, randomized, placebo-controlled trials for central neuropathic pain. In the largest of these trials, which included 630 subjects, a 15-week comparison between Δ9-tetrahydrocannabinol and placebo was performed. More patients receiving active treatment perceived an improvement in pain than those receiving placebo, although approximately 20% of subjects reported worsening of pain while on active treatment.
Cannabinoids control spasticity and tremor in a multiple sclerosis model
The exacerbation of these signs after antagonism of the CB1 and CB2 receptors, notably the CB1 receptor, using SR141716A and SR144528 (ref. 8) indicate that the endogenous cannabinoid system may be tonically active in the control of tremor and spasticity. This provides a rationale for patients' indications of the therapeutic potential of cannabis in the control of the symptoms of multiple sclerosis2, and provides a means of evaluating more selective cannabinoids in the future.
Thursday, June 30, 2016
Cannabinoids remove plaque-forming Alzheimer's proteins from brain cells
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
***> Singeltary Reply
Published: 09 September 2015
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Singeltary Comment at very bottom of this Nature publishing;
re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
where have we all heard this before? it's been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country's) with the BSE mad cow TSE Prion debacle.
That 'anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients ?
who got pooled extracts injected from thousands of cadavers ? were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find 'alarming' is pathetic.
Sounds like the journalists had it right in the first place: 'Alzheimer's may be a transmissible infection' in The Independent to 'You can catch Alzheimer's' in The Daily Mirror or 'Alzheimer's bombshell' in The Daily Express
if not for the journalist, the layperson would not know about these important findings.
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer's, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to wait?
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
in my opinion, it's one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it's bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer's of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer's and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://www.nature.com/articles/nature15369
Singeltary Comment at very bottom of this Nature publishing, takes a while to load...terry
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
The only tenable public line will be that "more research is required’’ <<<
possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Singeltary 2001
Subject: CJD or Alzheimer's or the same ???
Date: Sun, 29 Apr 2001 12:45:28 -0700
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Bovine Spongiform Encephalopathy
Greetings List,
thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.
just my opinion...snip…end
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
http://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
''on the possible transmissibility of Alzheimer's''
9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly
(1) concerning a farmer with CJD who had BSE animals,
(2) on the possible transmissibility of Alzheimer's and
(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.
MRC
BSE101/1 013:
Medical Research Council 20 Park Crescent. London W1N 4AL
teteonone 071-636 5422 telex 24897 (Medresco London) fax 071-436 6179
23 October 1992
IN STRICT CONFIDENCE
Dear Ken,
Transmission of Alzheimer type plaques to primates
I am sending you for information the attached paper prepared by Dr Ridley on the results of a part of a large series of experiments on the transmissibility of various neurodegenerative diseases.
You will see that there will not be any public disclosure of these results until January (at the meeting of the British Neuropathological Society) however I thought you would wish to know about them at this stage. We are preparing a public statement to put the findings into proper context for use either in January or if there are any earlier leaks. We would be happy to discuss drafts with DH if that would be helpful.
If you or your colleagues would like to have further discussion of the findings with the scientists involved and perhaps the Neurosciences Board expert(s) then please let me know and I ensure that arrangements are made.
Yours Sincerely,
Diana Dunstan Director of Research Management
Dr K C Calman Department of Health Richmond House 79 Whitehall London SWIA 2NS
cc: Professor M Peckham Dr H Pickles
92/10.23/1.1
IN STRICT CONFIDENCE
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
IN CONFIDENCE
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
H F BAKER, R M RIDLEY, L W DUCHEN, T J CROW, C J BRUTON
As part of a larger series of experiments designed to assess the transmissibility of various neurodegenerative disease including the spongiform encephalopathies (eg Creutzfeldt-Jakob disease and BSE we injected several marmosets (Callithrix Jacchus) intracerebrally with brain homogenate from :
1) a 56 year old patient with severe Alzheimer's disease - B - amyloid plaques and conogophilic angiopathy (CAA) and neurofibrillary tangles; and
2) a 62 year old patient with Gerstmann-Straussler disease, a spongiform encephalopathy with PrP Plaques and, in this case, B-amyloid plaques and CAA.
These monkeys were killed more than 6 years after inoculation and their brains were found to contain moderate numbers of B-amyloid plaques and CAA but NO neurofibrillary tangles NO PrP. The brains of more than 12 monkeys killed at an older age did not contain these changes. B-amyloid was not found in the brains of monkeys injected with brain material which did not contain B-amyloid. These results suggest that B-amyloidosis is a transmissible process resembling the transmissibility of PrP amyloidosis in transmissible dementia and strengthens the parallels between Alzheimer's disease and Creutzfeldt-Jakob disease.
It should be stressed, however, that we are not claiming to have transmitted Alzheimer's disease because
1) the animals were behaving normally when killed and
2) no neurofibrillary tangles were seen.
We have argued previously that transmission of spongiform encephalopathy, particularly from the genetic cases (GSS and some CJD), does not imply that the donor cases themselves acquired the disease by infection. We would apply the same arguments in this case, particularly in view of the genetic basis of some cases of Alzheimer's disease and the extensive epidemiological data which does not link Alzheimer's disease to infection.
DISCLOSURE
This work is currently under preparation for publication BUT IN VIEW OF PUBLIC CONCERN OVER THE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (eg BSE) AND THE HIGH INCIDENCE OF ALZHEIMER'S DISEASE IN THE GENERAL POPULATION, IT IS IMPORTANT THAT THESE FINDINGS ARE NOT DISCUSSED OPENLY BEFORE FULL PUBLICATION.
Furthermore, BEFORE DISCLOSURE, IT IS IMPORTANT THAT INTERESTED PARTIES BE PROPERLY APPRAISED OF THE DATA AND THERE IMPLICATIONS.
Previous attempts to transmit Alzheimer's disease to rodents and large primates have been unsuccessful. It is our belief that post-mortem tissue from these animals still exists and we are anxious that research workers (in the USA) SHOULD NOT RE-EXAMINE this material until our data are published.
SAFETY
At this point we would like to stress again the lack of evidence relating Alzheimer's disease to exposure to brain tissue through neurosurgery or occupation. NEVERTHELESS it is appropriate that proper bodies should consider whether the results of our experiments have any implications for human health.
FURTHER EXPERIMENTS
The interpretation we have made that B-amyloidosis as a self-peretuating process has important implications for understanding the process of neurodegeneration, which are best studied at the level of protein chemistry. However, we can see arguments for some transmission experiments including:
1) serial passage of B-amyloidosis in order to strengthen the evidence of transmissibility;
2) transmission from other cases of Alzheimer's disease in order to establish the generality of this effect;
3) transmission to primates which are allowed to run their full course, ie to see whether the full syndrome of Alzheimer's disease develops including neurofibrillary tangle formation, astrocytosis, neuronal loss and concomitant cognitive decline. (We are already expert in the neuropsychological assessment of marmosets). It should be remembered that, at the present time, only the amyloidosis have been found to be transmissible such that Alzheimer's disease PER SE has not been transmitted;
4) comparison of transmission from cases which contain only CAA and those which contain only B-amyloid plaques. These two forms of amyloid differ very slightly and it is not known whether this difference is preserved on transmission;
5) establishment of the time course of the development of B-amyloidosis. The present experiment suggests that the time course is somewhere between 1-5 years;
6) transmission using larger quantities of purified preparations of B-amyloid. This may reduce the transmission time considerably;
7) transmission using animals of different initial ages to investigate the relationship between transmission time and chronological age, eg transmission into mature animals may decrease transmission time through an interaction between the pathological process and senescence;
8) manipulation of transmission time by treatments which may speed up plaque formation, eg by increasing the production of amyloid precursor protein, or which may slow down plaque formation and protect from disease progression.
The proposal is to inoculate about 25 marmosets in the first instance and to replace them in a 'rolling' experiment as they die or are killed according to the experimental design. The marmosets will be kept in the MRC Marmoset Colony in Cambridge. Additional facilities and personnel are not required over and above that awarded to Dr. Ridley in an MRC Programma Grant.
A preliminary report of our findings will be presented by Professor L W Duchan at the January 1993 meeting of the British Neuropathological Society.
Int J Exp Pathol. 1993 Oct; 74(5): 441–454. PMCID: PMC2002177
Evidence for the experimental transmission of cerebral beta-amyloidosis to primates.
H. F. Baker, R. M. Ridley, L. W. Duchen, T. J. Crow, and C. J. Bruton Author information ► Copyright and License information ► This article has been cited by other articles in PMC.
Abstract
The brains of three marmosets (Callithrix jacchus) injected intracerebrally 6-7 years earlier with brain tissue from a patient with early onset Alzheimer's disease were found to contain moderate numbers of amyloid plaques with associated argyrophilic dystrophic neurites and cerebral amyloid angiopathy but no neurofibrillary tangles. The plaques and vascular amyloid stained positively with antibodies to beta (A4)-protein. The brains of three age-matched control marmosets from the same colony did not show these neuropathological features. The brain of one of two marmosets injected with brain tissue from a patient with prion disease with concomitant beta-amyloid plaques and cerebral amyloid angiopathy also showed beta-amyloid plaques and angiopathy but no spongiform encephalopathy. An occasional plaque was found in the brains of two of four marmosets injected with brain tissue from three elderly patients with age-related pathology, two of whom had an additional diagnosis of possible prion disease. Neither plaques nor cerebral amyloid angiopathy were found in six other marmosets who were older than the injected animals, in 12 further marmosets who were slightly younger but who had been injected several years previously with brain tissue which did not contain beta-amyloid, or in 10 younger marmosets who had been subjected to various neurosurgical procedures. These results suggest that cerebral beta-amyloidosis may be induced by the introduction of exogenous amyloid beta-protein.
see substantial increase in Alzheimer's disease;
2012 Singeltary on CJD and Alzheimer’s and iatrogenic threat
Proposal ID: 29403
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both disease, and it’s variants, in many cases are merely names of the people that first discovered them. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer than the TSE prion disease. Symptoms are very similar, and pathology is very similar. I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
Conclusions
There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics let science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already. what’s the use of science progressing human life to the century mark, if your brain does not work?
http://aaic.scsubmissions.com/index.aspx
combined cannot exceed 350 Words
shortened to proper word count ;
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references ...end...tss
Hello Nicole,
by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.
please see old correspondence below...
From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission
Dear Terry,
The decline of proposal number 30756 is registered in the system. Thank you for your consideration.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
Alzheimer’s Association – National Office
225 North Michigan Avenue – Floor 17
Chicago, Illinois 60601
Office: 312-335-5897| Fax: 866-560-0650 | Email: nicole.sanders@alz.org
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net] Sent: Saturday, April 07, 2012 9:47 PM To: Nicole Sanders Subject: Re: re-submission
Greetings, Alzheimer’s Association and Ms Nicole Sanders,
Thank You for accepting my submission # 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? and the opportunity to present it, at the Alzheimer’s Association International Conference 2012 (AAIC), as a poster presentation. However, with great sadness, I must regretfully decline the invitation due to a medical reasons, and traveling to Canada, of which is not possible. ...
Thank You,
With Kindest Regards,
I am sincerely,
Terry S. Singeltary Sr.
xxx
Bacliff, Texas USA 77518
flounder9@verizon.net
From: Nicole Sanders
Sent: Saturday, April 07, 2012 8:20 PM
To: Terry S. Singeltary Sr.
Subject: RE: re-submission
Dear Terry,
*** Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
Alzheimer’s Association – National Office
225 North Michigan Avenue – Floor 17
Chicago, Illinois 60601
Office: 312-335-5897| Fax: 866-560-0650 | Email: nicole.sanders@alz.org
From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net] Sent: Tuesday, April 03, 2012 10:06 AM To: Nicole Sanders Subject: re-submission
Hi Ms Sanders Ma’am,
I am a bit confused as to the format this was accepted.
do I have to attend for this to be presented as a poster. I am disabled and cannot attend. I hope this is not the case.
Thanks !
kind regards,
terry
From: Nicole.sanders@alz.org
Sent: Tuesday, April 03, 2012 9:26 AM
To: flounder9@verizon.net
Subject: 2012 AAIC Oral Abstract Notification
Dear Terry S. Singeltary:
We regret to inform you that your abstract entitled, "Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?," has not been accepted for an oral presentation but I am pleased to inform you that your abstract submission has been accepted for a poster presentation at the Alzheimer’s Association International Conference(AAIC) 2012 in Vancouver, British Columbia, Canada, July 14-19, 2012.
Please refer to the presentation format below and confirm your intent to present by Friday, April 6, 2012 by selecting “Confirm” or “Decline” within this message. Once you have made your selection, you will be unable to makes changes. Please contact Nicole Sanders mailto:nicole.sanders@alz.org for assistance. If you do not reply by Friday April 6, your abstract will be removed from the program.
Click Here to Accept http://www.softconference.com/Subs/icad/2012/ICAD_Accept_Decline_Poster.asp?FacID=129919&PID=70543&Status=1
Click Here to Decline http://www.softconference.com/Subs/icad/2012/ICAD_Accept_Decline_Poster.asp?FacID=129919&PID=70543&Status=2
Session/Presentation Details Poster Date:Jul 17, 2012 *Please use the Proposal Number in all correspondence regarding your presentation.
Presentation Format Poster presentations are numbered and grouped by overall topic category. 500 posters will be displayed each day in the Exhibit Hall.
=======================================================
From: Nicole Sanders Sent: Friday, May 04, 2012 6:10 PM To: flounder9@verizon.net Subject: Urgent Request- Response Required- AAIC 2012 Poster Presentation
Dear Terry Singeltary:
The Scientific Program Committee, has accepted your proposal for a poster presentation at the Alzheimer’s Association International Conference in Vancouver, British Columbia, Canada, July 14 - 19, 2012. However we have not received your response.
Please refer to the presentation format below and confirm your intent to present by Wednesday, May 9, 2012 by responding to this e-mail. If we do not receive a response by May 9 your presentation will be removed from the program.
Session/Presentation Detail Proposal Number*: 29403
Presentation Title: Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? Session Type: Poster Session Title: 2012 Tuesday Posters Session Date and Time: Tuesday, July 17 1 – 3 p.m. Presentation Number: P3-151
*Please use Proposal Number in all correspondence regarding your presentation.
Presentation Format The Oral Presentation is a 90-minute session, grouped by overall category topic, which will begin with introductions by the session chair. There will be seven concurrent oral presentation sessions with six speakers per session. Each speaker will have approximately 12 minutes for presentation, followed by a three-minute questions-and-answer period. The session location can be found in the on-site program book and or on the conference web site beginning in June.
Best Regards,
Nicole
Nicole Sanders Senior Specialist, Membership & Conference Programming Alzheimer's Association nicole.sanders@alz.org
end...tss
MONDAY, SEPTEMBER 11, 2023
Professor John Collinge on tackling prion diseases
“The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide.”
There is accumulating evidence also for iatrogenic AD. Understanding prion biology, and in particular how propagation of prions leads to neurodegeneration, is therefore of central research importance in medicine.
Iatrogenic TSE Prion
Terry S. Singeltary Sr.
A randomized clinical trial of low-dose cannabis extract in Alzheimer's disease
December 18, 2025
