An end to Alzheimer’s disease
We can prevent, effectively treat, and make an Alzheimer’s cure possible by
2025.
An end to Alzheimer’s disease
“If we’re the kind of nation that cares for its citizens and supports
families, respects our elders, and takes care of our neighbors, then we’ve got
work to do. And we need to do better when it comes to diseases like
Alzheimer’s.”
Hillary, December 22, 2015
Alzheimer’s disease is the sixth leading cause of death in the United
States. It’s the only cause of death in the top 10 that we can’t prevent, cure,
or even delay.
As the population of our country ages, the number of people suffering from
Alzheimer’s is expected to grow to nearly 15 million Americans—and could cost
more than $1 trillion per year—by 2050.
As president, Hillary will: Commit to preventing, effectively treating, and
making a cure possible for Alzheimer’s disease by 2025. Invest $2 billion per
year in research for Alzheimer’s and related disorders, the level leading
researchers have determined necessary to prevent and effectively treat
Alzheimer’s and make a cure possible by 2025. Make sure that funding is reliable
and consistent so researchers can work steadily toward effective treatment. Put
the best and brightest on the case. Hillary will appoint a top-flight team of
research and health experts to oversee this ambitious initiative.
Alzheimer’s disease affects a growing number of Americans and their
families. To support those families, Hillary will: Make it easier for families
and individuals with Alzheimer’s to get the care they need. Medicare should
cover comprehensive Alzheimer’s care-planning sessions and the cost of properly
documenting every diagnosis and care plan. Help protect loved ones who wander.
Hillary will work with Congress to reauthorize the Missing Alzheimer’s Disease
Patient Alert Program to help find individuals who are reported missing. Ensure
our seniors are aware and can take advantage of their Medicare benefits. Hillary
will direct the Social Security Administration to raise awareness about the
wellness visits, cognitive screenings, and other preventive benefits covered by
Medicare.
Hillary’s plan builds on her long record of working across the aisle on
behalf of patients and families dealing with Alzheimer’s disease: In the U.S.
Senate, she consistently pushed for greater funding for Alzheimer’s research,
including federally funded stem cell research. She also co-chaired the
Congressional Task Force on Alzheimer’s Disease and introduced legislation to
restore funding for the Alzheimer’s Association 24/7 Contact Center and for
Alzheimer’s disease demonstration grants.
Greetings Madam Secretary Clinton et al,
I WOULD KINDLY LIKE TO ANALYZE THIS STATEMENT MA’AM ;
>>> We can prevent, effectively treat, and make an Alzheimer’s
cure possible by 2025.
PREVENT
this must be on the forefront of research i.e. ‘iatrogenic’ transmission.
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform
Encephalopathy TSE Prion disease, that is the question ???
>>> 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 ?
http://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
SWISS MEDICAL WEEKLY
Alzheimer-type brain pathology may be transmitted by grafts of dura mater
26/01/2016 Singeltary comment ;
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;
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the
intra- and cross-species transmission of AA amyloidosis Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by
extracellular deposition of AA fibrils. AA fibrils are found in several tissues
from food animals with AA amyloidosis. For hygienic purposes, heating is widely
used to inactivate microbes in food, but it is uncertain whether heating is
sufficient to inactivate AA fibrils and prevent intra- or cross-species
transmission. We examined the effect of heating (at 60 °C or 100 °C) and
autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western
blot analysis, transmission electron microscopy (TEM), and mouse model
transmission experiments. TEM revealed that a mixture of AA fibrils and
amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at
135 °C produced large amorphous aggregates. AA fibrils retained antigen
specificity in Western blot analysis when heated at 100 °C or autoclaved at 121
°C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and
bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly
stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA
fibrils at 121 °C or 135 °C significantly decreased amyloid deposition.
Moreover, amyloid deposition in mice injected with murine AA fibrils was more
severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils
autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These
results suggest that AA fibrils are relatively heat stable and that similar to
prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA
fibrils. These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD
54.00
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Transmissible Spongiform Encephalopathy TSE PRION UPDATE
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND
SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Sunday, July 17, 2016
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL REPORT UPDATE JULY 17 2016
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
*** NIH awards $11 million to UTHealth researchers to study deadly CWD
prion diseases Claudio Soto, Ph.D. ***
Public Release: 29-Jun-2016
Tuesday, July 12, 2016
Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE,
TSE, Prion Zoonosis Science History
see history of NIH may destroy human brain collection
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
Sunday, July 24, 2016
Chronic Wasting Disease Prions in Elk Antler Velvet and Marketing of this
Product in Nutritional Supplements for Humans?
Research Project: TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES: THE ROLE OF
GENETICS, STRAIN VARIATION, AND ENVIRONMENTAL CONTAMINATION IN DISEASE CONTROL
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No.
APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS,
are working to further legalize the trading of Transmissible Spongiform
Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in
Korea Prion 2016 Tokyo ***
Thursday, June 9, 2016
Advisory Committee; Transmissible Spongiform Encephalopathies Advisory
Committee; Termination
TREATMENT
However, this is where Confucius is confused Ma’am, see my letter to
President Clinton and his response back in 1997 ;
THE WHITE HOUSE
WASHINGTON
July 3, 1997
Mr. Terry S. Singletary, Sr.
xxx
Bacliff, Texas 77518
Dear Terry:
Thank you for writing to me regarding the use of marijuana for medical
purposes. I appreciate knowing your views. My Administration has worked very
hard to ensure that Americans have access to safe and effective medicine.
My Administration strongly opposes the California and Arizona drug
legalization measures because they contradict our federal law and our national
drug control strategy. They disregard the medical and scientific process by
which our nation evaluates and approves safe and effective medicines. And, most
important, they send the wrong message to our children -- undermining the
efforts of parents, educators, elected leaders, and countless others who are
working to ensure a healthy, drug-free society.
However, in response to anecdotal claims about marijuana's medical
benefits, the Office of National Drug Control Policy is funding a comprehensive
research review by the National Academy of Science's Institute of Medicine. The
purpose of this study is to ensure that good science remains the basis of our
drug control policy.
As we work to protect the health of children and our nation, I appreciate
your interest in this issue.
Sincerely,
Bill Clinton
end
1-7-97
Mr. President,
Hello, I’m writing in concern with the issues around the use of Medical
Marijuana for people suffering from Aids, Cancer, Glaucoma, Chronic Pain, Muscle
Spasms, and Multiple Sclerosis, and also Spinal Cord Injury.
I’m very concerned about the stance you and your...my administration has
taken against this. Somebody needs to wake up and read the medical findings over
the past years. Look at how it has helped people. ...
snip...(I get a bit long winded here)...snip
But what has disturbed me the most, is what happened in California and
Arizona, how our appointed federal government bureaucrats and law enforcement
agencies openly and actively engaged in a campaign to undermine, subvert and
ultimately destroy the voters decision to enact laws of their choosing.
If this keeps happening, you will destroy the voters hope of ever changing
anything. You will destroy the Democratic process.
Come on Bill, we all know you inhaled and I still voted for you twice.
Change this Refer Madness. We don’t need the politicians writing
prescriptions...
P.S. just think of the jail space you could use for murderers and
rapist.
Very Sincere,
Terry S. Singeltary Sr.
END
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.
Marijuana and Epilepsy
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
CURE?
we will never cure anything if we can never see the forest for the trees
$$$
we must get corporate political science, god save the industry at all cost
mentality, out of sound scientific policy making.
NEEDLESS CONFLICT
http://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
2016
What say ye Ma’am ?
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net