www.perpetualcommotion.com
"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The
Children of Hurin
- The Distillery -
(In other words, "I found it interesting, but
haven't had the time to research and catagorize it yet.")
(Source: Medscape) - Poor dental health has been linked to
an increased risk for dementia, new research shows.
In a study of more than 4000 elderly adults in Japan,
those who had few teeth and who did not use dentures or
who did not visit a dentist regularly had a significantly
higher risk for dementia onset than the participants who
practiced better dental health practices...
http://r20.rs6.net/tn.jsp?e=001NJkHqF6BqziZqEtbJhoHGVUsG1vnQuEzFeCQiPaoA32MSt-J_NlLnAvqEFKoZ6a8x-rVR4m4ExcKivyITNg67fxSZCwvjPuetl_qm1oSoZv6VHBJHEVcqWr3lmaatDK5TeHzLUCHx2I=
A Combination of Green
Tea Extract and l-Theanine Improves Memory and Attention
in Subjects with Mild Cognitive Impairment: A
Double-Blind Placebo-Controlled Study
Journal of Medicinal Food
Published in Volume: 14 Issue 4: March 28, 2011
Abstract
A combination of green tea extract and l-theanine
(LGNC-07) has been reported to have beneficial effects on
cognition in animal studies.
http://online.liebertpub.com/doi/abs/10.1089/jmf.2009.1374
http://www.alzconnected.org/discussion.aspx?g=posts&t=2147487244
...at amazon.com and elsewhere it's easy to buy capsules
of green tea extract + L-theanine, though I don't know how
their potency compares to what was successful in the above
study. And I don't yet know possible side-effects...
Also note that L-Theanine should not be confused with
L-Threonate
(LG Household and Health Care Ltd.)
http://www.nutraingredients-usa.com/Research/Green-tea-extract-shows-memory-boosting-activity-Study
...when he gave his relative glucuronolactone powder in combination
with theanine she
became more alert and her behavior improved (the theanine
by itself was not particularly effective). A
metabolite of glucuronolactone--glucaric acid--is found in
apple juice (although the sugar in the juice may be
somewhat of a problem). Apple juice like green tea has been
suggested as a way to delay the onset of Alzheimer's
disease and as a possible treatment for Alzheimer's
disease especially during its early stages.
http://www.eurekalert.org/pub_releases/2009-01/ip-nsp012209.php
http://www.ncbi.nlm.nih.gov/pubmed/20338990
It turns out that the same toxin (peroxynitrite) that
probably causes damage to the brain in Alzheimer's disease
also damages the brain as a result of a stroke.
http://www.jneurosci.org/content/19/14/5910.short
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865248/
Various essential oils protect the brain in four ways:
they limit the formation of peroxynitrites, they lower
levels of peroxynitrites, they inhibit
peroxynitrite-mediated damage, and they partially reverse
the damage done by peroxynitrites. In essence, they
limit the damage done to the brain by stroke and
Alzheimer's disease.
See also"aromatherapy in the treatment of Alzheimer's
disease" http://www.alzconnected.org/discussion.aspx?g=posts&t=2147484055
The following article is from The Vitamin D Council:
http://blog.vitamindcouncil.org/2012/04/23/dietary-vitamin-d-intake-and-sun-exposure-linked-to-lower-risk-of-alzheimers-in-france/
Dietary vitamin D intake
and sun exposure linked to lower risk of Alzheimer’s in
France
Posted on April 23, 2012 by Dr. William Grant
A paper published ahead of print on April 13 found that
consumption of vitamin D-rich foods and midday sun
exposure were associated with significantly reduced risk
of developing Alzheimer’s disease [Annweiler et al.,
2012]. The study was an add-on to the Epidemiology of
Osteoporosis (EPIDOS) Toulouse cohort study at 43.6º
N.
Annweiler C, et al. Higher vitamin D dietary intake
is associated with lower risk of Alzheimer’s disease: A
7-year follow-up. J Gerontol A Biol Sci Med Sci. 2012 Apr
13.
This cohort included women over the age of 75 years at
time of enrollment and was designed to study risk factors
for hip fractures over a four-year period. Women who had
taken vitamin D supplements in the 18 months prior to
enrollment were excluded. Dietary factors and midday sun
exposure habits were examined at time of enrollment. The
mean dietary vitamin D intake was 334±172 IU/day.
The presence of Alzheimer’s disease and other dementias
was assessed seven years after enrollment.
Those in the highest fifth of vitamin D intake had
one-quarter the incidence rate of Alzheimer’s disease as
the other four fifths [odds ratio (OR) = 0.23 (95%
confidence interval (CI), 0.08-0.69)]. In addition, those
in the highest fifth of sun exposure had half the
incidence rate of Alzheimer’s disease [OR = 0.45 (95% CI,
0.24-0.85)]. Neither dietary vitamin D intake nor sun
exposure was significantly associated with risk of other
dementia.
As mentioned in the paper, there is a considerable body of
literature reporting that fish consumption is associated
with reduced risk of Alzheimer’s disease, with the usual
reason given that fish is an important dietary source of
omega-3 fatty acids. This finding was likely first
reported in an ecological study in 1997 [Grant, 1997].
Thus, it is not clear from the present study how much of
the reduced risk of Alzheimer’s disease was due to omega-3
fatty acids and how much to vitamin D.
However, the finding regarding sun exposure at midday
strongly supports the role of vitamin D in reducing risk.
Casual sun exposure in England for those aged 45 years is
sufficient to increase serum 25-hydroxyvitamin D
concentrations by 38 nmol/l (15 ng/ml) [Hyppönen and
Power, 2007]. This increase is equivalent to about
1500-2000 IU/day [Garland, 2011]. However, for those over
the age of 75 years, vitamin D production rates would be
less, perhaps one-half as much [MacLaughlin and Holick,
1985].
Thus, this study provides good evidence that fish
consumption and midday sun exposure reduce the risk of
Alzheimer’s disease, with vitamin D being the likely
agent. The neuroprotective actions of vitamin D are
discussed in the paper by Annweiler et al.
References
Annweiler C, Rolland Y, Schott AM, Blain H, Vellas B,
Herrmann FR, Beauchet O. Higher vitamin D dietary intake
is associated with lower risk of Alzheimer’s disease: A
7-year follow-up. J Gerontol A Biol Sci Med Sci. 2012 Apr
13. [Epub ahead of print]
Garland CF, French CB, Baggerly LL, Heaney RP. Vitamin D
supplement doses and serum 25-hydroxyvitamin D in the
range associated with cancer prevention. Anticancer Res
2011:31: 617-22.
Grant WB. Dietary links to Alzheimer’s disease. Alz Dis
Rev 1997;2:42-55. (http://www.sunarc.org/JAD97.pdf)
Hyppönen E, Power C. Hypovitaminosis D in British
adults at age 45 y: nationwide cohort study of dietary and
lifestyle predictors. Am J Clin Nutr. 2007
Mar;85(3):860-8.
MacLaughlin J, Holick MF. Aging decreases the capacity of
human skin to produce vitamin D3. J Clin Invest. 1985
Oct;76(4):1536-8.
Study Dusts Sugar
Coating Off Little-Known Regulation in Cells
ScienceDaily (Apr. 16, 2012) — In Alzheimer's disease,
brain neurons become clogged with tangled proteins.
Scientists suspect these tangles arise partly due to
malfunctions in a little-known regulatory system within
cells. Now, researchers have dramatically increased what
they know about this particular regulatory system in mice.
Such information will help scientists better understand
Alzheimer's and other diseases in humans and could
eventually provide new targets for therapies... The
O-GlcNAc system likely adds another layer of control to
the proteins that serve as a brain cell's widgets and
gears -- control that might be muddled in Alzheimer's
brains known to have problems
in sugar metabolism...
http://www.sciencedaily.com/releases/2012/04/120416154048.htm
Epo-D About a year ago in the Alzheimer's Research Forum
reported:
"In a study performed on three-month-old mice with
tauopathy, one of these compounds, epothilone D, when
given at the relatively low dose of 1 mg/kg body weight
for three months, decreased axon degeneration and improved
cognition in treated animals (see Brunden et al., 2010). [
NEED LINK ]
This month, in the Journal of Neuroscience, Brunden and
his colleagues report positive results in older tauopathy
mice using 1/30th to 1/100th of the dose used with cancer
patients. Here is the website for the original press
release http://www.uphs.upenn.edu/news/News_Releases/2012/03/alzheimer/
This drug is now in human trials with Alzheimer's patients
that ends in 2014.
Methylene Blue/2nd gen Rember. TauRx.com's website states:
"…the clinical tolerability profile of LMTX, one of
TauRx's second generation TAIs, is currently being
investigated clinically in trials conducted under an open
US IND. TauRx is now preparing to advance LMTX into
pivotal international phase 3 trials in mild and moderate
AD and related neurodegenerative diseases." [ NEED TO FIND
LINK ]
In the meantime, two OTC low toxicity agents with
established neuroprotective and neuro-repair properties
merit review: bio-available curcumin (Longvida) and a new
product that comes from research done at the Salk
Institute, fisetin
(Swanson). Both are strong anti-oxidants and
anti-inflammatories that protect and help neurons repair
damage from tauopathy.
San Francisco: Tau—Time
to Shine as Therapeutic Target?
17 May 2011. At the “Tau and Tauopathies: Pathogenic
Mechanisms” workshop held 28-30 March 2011 at the
Gladstone Institute of Neurological Disease (GIND) in San
Francisco... The researchers found that tau pathology
correlated with increased serum IL-1β in the transgenic
mice, and wondered whether blocking signals through this
inflammatory cytokine could possibly help... epothilone
D—a brain-penetrant, microtubule-stabilizing compound that
slowed axon degeneration and improved cognition...
hyperphosphorylated tau... “If you express c-Abl in the
forebrain, you get tau phosphorylation, cell death, and
gliosis accompanying the cell loss,”... The results are
reminiscent of the cognitive recovery seen in
tangle-bearing Tg4510 mice after tau transgene inhibition
with doxycycline (ARF related news story on Santacruz et
al., 2005), Cole wrote in an e-mail to ARF. The data
“support tau oligomers as a target and curcumin as a
pleiotropic drug capable of targeting pure tauopathy with
late intervention,” he noted. Investigators at Jaslok
Hospital and Research Centre in Mumbai, India, are
recruiting AD patients for a Phase 2 trial of a highly
absorbed, lipophilic curcumin formulation. Manufactured as
a food supplement called LongVida by Verdure Sciences...
eight-week treatment with the autophagy-promoting compound
trehalose cleared tau aggregates and improved behavior in
tauopathy mouse models with primarily motor...
http://www.alzforum.org/new/detail.asp?id=2792
This excerpt is from a 2010 case description (LaBuzetta,
et.al. 2010):
"Signs and symptoms of hyperammonemia are usually
neurological in nature and range from mild cognitive and
psychomotor changes to impaired intellectual functioning,
personality changes, altered levels of consciousness, and
neuromuscular dysfunction. At high enough concentrations,
coma or death can be observed."
New findings contradict
dominant theory in Alzheimer’s disease
28 October 2011
For decades the amyloid hypothesis has dominated the
research field in Alzheimer’s disease. The theory
describes how an increase in secreted beta-amyloid
peptides leads to the formation of plaques, toxic clusters
of damaged proteins between cells, which eventually result
in neurodegeneration. Scientists at Lund University,
Sweden, have now presented a study that turns this premise
on its head. The research group’s data offers an opposite
hypothesis, suggesting that it is in fact the neurons’
inability to secrete beta-amyloid that is at the heart of
pathogenesis in Alzheimer’s disease...
http://www.lunduniversity.lu.se/o.o.i.s?id=24890&news_item=5718
Clearance of beta
amyloid accumulation within neurons stops memory decline
the UCI research team is the first to identify that early
beta amyloid accumulation within neurons is the trigger
for the onset of memory decline in Alzheimer's.
"This finding has important and useful implications for
the pharmaceutical industry in terms of developing drugs
that can target beta amyloid as soon as it accumulates
within the neurons," said Frank LaFerla, principal
investigator of the research project, associate professor
of neurobiology and behavior, and co-director of the UCI
Institute for Brain Aging and Dementia. "Once the plaques
and tangles form, it is too late."
http://www.news-medical.net/news/2005/03/06/8174.aspx
Impaired β-Amyloid
Secretion in Alzheimer's Disease Pathogenesis
Davide Tampellini, Nawreen Rahman, Michael T. Lin,
Estibaliz Capetillo-Zarate1, and Gunnar K. Gouras
Abstract
A central question in Alzheimer's disease (AD) research is
what role β-amyloid peptide (Aβ) plays in synaptic
dysfunction. Synaptic activity increases Aβ secretion,
potentially inhibiting synapses, but also decreases
intraneuronal Aβ, protecting synapses. We now show that
levels of secreted Aβ fall with time in culture in neurons
of AD-transgenic mice, but not wild-type mice. Moreover,
the ability of synaptic activity to elevate secreted Aβ
and reduce intraneuronal Aβ becomes impaired in
AD-transgenic but not wild-type neurons with time in
culture. We demonstrate that synaptic activity promotes an
increase in the Aβ-degrading protease neprilysin at the
cell surface and a concomitant increase in colocalization
with Aβ42. Remarkably, AD-transgenic but not wild-type
neurons show reduced levels of neprilysin with time in
culture. This impaired ability to secrete Aβ and reduce
intraneuronal Aβ has important implications for the
pathogenesis and treatment of AD.
http://www.jneurosci.org/content/31/43/15384.abstract
Human Cytomegalovirus Essential hypertension:
Virus can cause high
blood pressure
2011/08/15
BEIJING: High blood pressure could be caused by a common
virus, according to a study carried out by a team of
Chinese doctors which has possible implications for
millions of people around the world.
The human cytomegalovirus (HCMV) infects most adults but
is repressed by the body’s immune system and rarely causes
any symptoms.
But a team from Beijing Chaoyang Hospital’s cardiology
centre has found the first evidence of a link between HCMV
and essential hypertension, according to a report
published on the website of the US medical journal
Circulation.
http://www.nst.com.my/nst/articles/Viruscancausehighbloodpressure/Article/
Virus can cause high
blood pressure: Chinese study
Agence France-Presse
Posted at 08/15/2011
http://www.abs-cbnnews.com/lifestyle/08/15/11/virus-can-cause-high-blood-pressure-chinese-study
Virus can cause high
blood pressure: Chinese study
Relaxnews – Wed, Aug 17, 2011
http://news.yahoo.com/virus-cause-high-blood-pressure-chinese-study-153649965.html
Virus can cause high
blood pressure: Chinese study
AFP NewsBy Philip Lim | AFP News – Mon, Aug 15, 2011
http://my.news.yahoo.com/virus-cause-high-blood-pressure-chinese-study-095735139.html
Treatment With Vitamin C
Dissolves Toxic Protein Aggregates in Alzheimer's
Disease
ScienceDaily (Aug. 18, 2011)
— Researchers at Lund University have discovered a
new function for vitamin C. Treatment with vitamin C can
dissolve the toxic protein aggregates that build up in the
brain in Alzheimer's disease...
http://www.sciencedaily.com/releases/2011/08/110818101645.htm
What form of vitamin C? How much? Is it
practical for someone to take orally?
Fish Oil's Impact On
Cognition and Brain Structure Identified in New Study
ScienceDaily (Aug. 17, 2011)
— Researchers at Rhode Island Hospital's Alzheimer's
Disease and Memory Disorders Center have found positive
associations between fish oil supplements and cognitive
functioning as well as differences in brain structure
between users and non-users of fish oil supplements. The
findings suggest possible benefits of fish oil supplements
on brain health and aging...
http://www.sciencedaily.com/releases/2011/08/110817120220.htm
Exercise May Help
Prevent Brain Damage Caused by Alzheimer's Disease
ScienceDaily (Aug. 15, 2011)
— Regular exercise could help prevent brain damage
associated with neurodegenerative diseases like
Alzheimer's, according to research published this month in
Elsevier's journal Brain, Behavior, and Immunity...
http://www.sciencedaily.com/news/mind_brain/alzheimer%27s/
Moderate Drinking May
Protect Against Alzheimer's and Cognitive Impairment,
Study Suggests
ScienceDaily (Aug. 15, 2011)
— Moderate social drinking may significantly reduce
the risk of dementia and cognitive impairment, suggests an
analysis of 143 studies by Loyola University Chicago
Stritch School of Medicine researchers...
http://www.sciencedaily.com/releases/2011/08/110816112134.htm
Red wine and resveratrol?
Alzheimer's disease - a
neurospirochetosis. Analysis of the evidence following
Koch's and Hill's criteria.
Judith Miklossy
Correspondence: Judith Miklossy judithmiklossy@bluewin.ch
Journal of Neuroinflammation 2011, 8:90
doi:10.1186/1742-2094-8-90
Published: 4 August 2011
Abstract (provisional)
It is established that chronic spirochetal infection can
cause slowly progressive dementia, brain atrophy and
amyloid deposition in late neurosyphilis.
Recently it has been suggested that various types of
spirochetes, in an analogous way to Treponema pallidum,
could cause dementia and may be involved in the
pathogenesis of Alzheimer's disease (AD).
Here, we review all data available in the literature on
the detection of spirochetes in AD and critically analyze
the association and causal relationship between
spirochetes and AD following established criteria of Koch
and Hill.
The results show a statistically significant association
between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95%
CI = 8-60, N = 247).
When neutral techniques recognizing all types of
spirochetes were used, or the highly prevalent periodontal
pathogen Treponemas were analyzed, spirochetes were
observed in the brain in more than 90% of AD cases.
Borrelia burgdorferi was detected in the brain in 25.3% of
AD cases analyzed and was 13 times more frequent in AD
compared to controls.
Periodontal pathogen Treponemas (T. pectinovorum, T.
amylovorum, T. lecithinolyticum, T. maltophilum, T.
medium, T. socranskii) and Borrelia burgdorferi were
detected using species specific PCR and antibodies.
Importantly, co-infection with several spirochetes occurs
in AD.
The pathological and biological hallmarks of AD were
reproduced in vitro.
The analysis of reviewed data following Koch's and Hill's
postulates shows a probable causal relationship between
neurospirochetosis and AD.
Persisting inflammation and amyloid deposition initiated
and sustained by chronic spirochetal infection form
together with the various hypotheses suggested to play a
role in the pathogenesis of AD a comprehensive entity.
As suggested by Hill, once the probability of a causal
relationship is established prompt action is needed.
Support and attention should be given to this field of AD
research.
Spirochetal infection occurs years or decades before the
manifestation of dementia.
As adequate antibiotic and anti-inflammatory therapies are
available, as in syphilis, one might prevent and eradicate
dementia.
...
Conclusion
Various types of spirochetes, including B. burgdorferi,
and six periodontal pathogen spirochetes ((T. socranskii,
T. pectinovorum, T. denticola, T. medium, T. amylovorum
and T. maltophilum) were detected in the brains of AD
patients.
The pathological and biological hallmarks of AD, including
increased AβPP level, Aβ deposition and tau
phosphorylation were induced by spirochetes in vitro.
The statistical analysis showed a significant association
between spirochetes and AD. The strongly significant
association, the high risk factor and the analysis of data
following Koch’s and Hill’s criteria, are indicative of a
causal relationship between neurospirochetoses and AD.
Spirochetes are able to escape destruction by the host
immune reactions and establish chronic infection and
sustained inflammation.
In vivo studies with long exposure times will be necessary
to efficiently study the sequence of events and the
cellular mechanisms involved in spirochete induced AD-type
host reactions and Aβ-plaque, “tangle” and
“granulovacuolar” formation.
The characterization of all types of spirochetes and
co-infecting bacteria and viruses is needed, in order to
develop serological tests for the early detection of
infection.
The pathological process is thought to begin long before
the diagnosis of dementia is made therefore, an
appropriate targeted treatment should start early in order
to prevent dementia.
Persisting spirochetal infection and their persisting
toxic components can initiate and sustain chronic
inflammatory processes through the activation of the
innate and adaptive immune system involving various
signaling pathways.
In the affected brain the pathogens and their toxic
components can be observed, along with host immunological
responses.
The response itself is characteristic of chronic
inflammatory processes associated with the site of tissue
damage.
The outcome of infection is determined by the genetic
predisposition of the patient, by the virulence and
biology of the infecting agent
and by various environmental factors, such as exercise,
stress and nutrition.
The accumulated knowledge, the various views, and
hypotheses proposed to explain the pathogenesis of AD form
together a comprehensive entity when observed in the light
of a persisting chronic inflammation and amyloid
deposition initiated and sustained by chronic spirochetal
infection.
As suggested by Hill, once the probability of a causal
relationship is established prompt action is needed.
Similarly to syphilis, one may prevent and eradicate
dementia in AD.
The impact on healthcare costs and on the suffering of the
patients would be substantial.
http://www.jneuroinflammation.com/content/8/1/90/abstract
http://www.jneuroinflammation.com/content/pdf/1742-2094-8-90.pdf
J Neuroinflammation. 2011 Aug 4;8(1):90. [Epub ahead of
print]
Alzheimer's disease - a neurospirochetosis. Analysis of
the evidence following Koch's and Hill's criteria.
Miklossy J.
Abstract
ABSTRACT: It is established that chronic spirochetal
infection can cause slowly progressive dementia, brain
atrophy and amyloid deposition in late neurosyphilis.
Recently it has been suggested that various types of
spirochetes, in an analogous way to Treponema pallidum,
could cause dementia and may be involved in the
pathogenesis of Alzheimer's disease (AD). Here, we review
all data available in the literature on the detection of
spirochetes in AD and critically analyze the association
and causal relationship between spirochetes and AD
following established criteria of Koch and Hill. The
results show a statistically significant association
between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95%
CI = 8-60, N = 247). When neutral techniques recognizing
all types of spirochetes were used, or the highly
prevalent periodontal pathogen Treponemas were analyzed,
spirochetes were observed in the brain in more than 90% of
AD cases. Borrelia burgdorferi was detected in the brain
in 25.3% of AD cases analyzed and was 13 times more
frequent in AD compared to controls. Periodontal pathogen
Treponemas (T. pectinovorum, T. amylovorum, T.
lecithinolyticum, T. maltophilum, T. medium, T.
socranskii) and Borrelia burgdorferi were detected using
species specific PCR and antibodies. Importantly,
co-infection with several spirochetes occurs in AD. The
pathological and biological hallmarks of AD were
reproduced in vitro. The analysis of reviewed data
following Koch's and Hill's postulates shows a probable
causal relationship between neurospirochetosis and AD.
Persisting inflammation and amyloid deposition initiated
and sustained by chronic spirochetal infection form
together with the various hypotheses suggested to play a
role in the pathogenesis of AD a comprehensive entity. As
suggested by Hill, once the probability of a causal
relationship is established prompt action is needed.
Support and attention should be given to this field of AD
research. Spirochetal infection occurs years or decades
before the manifestation of dementia. As adequate
antibiotic and anti-inflammatory therapies are available,
as in syphilis, one might prevent and eradicate dementia.
PMID: 21816039 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21816039
Vitamin B12 status and rate
of brain volume loss in community-dwelling elderly
doi: 10.1212/01.wnl.0000325581.26991.f2 Neurology September 9,
2008 vol. 71 no. 11 826-832
Conclusion: Low vitamin B12 status should be further
investigated as a modifiable cause of brain atrophy and of
likely subsequent cognitive impairment in the elderly.
http://www.neurology.org/content/71/11/826.abstract
Vitamin B clue to dementia
Thursday September 9 2010
NHS News (UK)
“Vitamin B tablets could slow and even halt the devastating
march of Alzheimer's disease,” The Daily Telegraph reported.
According to the newspaper, large daily doses of vitamin B can
halve the rate of brain shrinkage, a process that can precede
Alzheimer’s disease and dementia.
http://www.nhs.uk/news/2010/09September/Pages/vitamin-B12-brain-shrink-dementia.aspx
AD and dental work
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/3194074997
Tau-mediated neurodegeneration
in Alzheimer’s disease and related disorders
Nature Reviews Neuroscience | AOP, published online 8 August
2007; doi:10.1038/nrn2194
http://neuro.pathology.pitt.edu/webstuff/Journal%20Club/tau%20review.pdf
SARASOTA - A blood-pressure drug found by the Roskamp
Institute to show promise for arresting Alzheimer's disease
has been approved for a five-year, $8.4 million Phase III
human trial in Europe.
A Phase III clinical trial, which comes after studies on
safety in human patients, is usually the last stop on a
drug's long journey to market. The few medicines available
for Alzheimer's merely address symptoms that result from
this progressive brain disease. Just a handful that target
suspected causes — like the Roskamp drug, Nilvadipine — have
made it as far as Phase III, required for approval by the
U.S. Food and Drug Administration.
http://www.heraldtribune.com/article/20110525/ARTICLE/110529725
http://www.rfdn.org/news_release_052511.html
April 23, 2010
Reduction of β-amyloid pathology by celastrol in a
transgenic mouse model of Alzheimer’s disease
Filed under: alzheimer — Tags: Alzheimers disease, amyloid,
Celastrol — admin @ 2:59 pm
Daniel Paris, Nowell J Ganey, Vincent Laporte, Nikunj S
Patel, David Beaulieu-Abdelahad, Corbin Bachmeier, Amelia
March, Ghania Ait-Ghezala and Michael J Mullan
The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL
34243, USA
Journal of Neuroinflammation 2010,
7:17doi:10.1186/1742-2094-7-17
Published: 8 March 2010
Abstract
Background
Aβ deposits represent a neuropathological hallmark of
Alzheimer’s disease (AD). Both soluble and insoluble Aβ
species are considered to be responsible for initiating the
pathological cascade that eventually leads to AD. Therefore,
the identification of therapeutic approaches that can lower
Aβ production or accumulation remains a priority. NFκB has
been shown to regulate BACE-1 expression level, the rate
limiting enzyme responsible for the production of Aβ. We
therefore explored whether the known NFκB inhibitor
celastrol could represent a suitable compound for decreasing
Aβ production and accumulation in vivo.
Methods
The effect of celastrol on amyloid precursor protein (APP)
processing, Aβ production and NFκB activation was
investigated by western blotting and ELISAs using a cell
line overexpressing APP. The impact of celastrol on brain Aβ
accumulation was tested in a transgenic mouse model of AD
overexpressing the human APP695sw mutation and the
presenilin-1 mutation M146L (Tg PS1/APPsw) by immunostaining
and ELISAs. An acute treatment with celastrol was
investigated by administering celastrol intraperitoneally at
a dosage of 1 mg/Kg in 35 week-old Tg PS1/APPsw for 4
consecutive days. In addition, a chronic treatment (32 days)
with celastrol was tested using a matrix-driven delivery
pellet system implanted subcutaneously in 5 month-old Tg
PS1/APPsw to ensure a continuous daily release of 2.5 mg/Kg
of celastrol.
Results
In vitro, celastrol dose dependently prevented NFκB
activation and inhibited BACE-1 expression. Celastrol
potently inhibited Aβ1-40 and Aβ1-42 production by reducing
the β-cleavage of APP, leading to decreased levels of
APP-CTFβ and APPsβ. In vivo, celastrol appeared to reduce
the levels of both soluble and insoluble Aβ1-38, Aβ1-40 and
Aβ1-42. In addition, a reduction in Aβ plaque burden and
microglial activation was observed in the brains of Tg
PS1/APPsw following a chronic administration of celastrol.
Conclusions
Overall our data suggest that celastrol is a potent Aβ
lowering compound that acts as an indirect BACE-1 inhibitor
possibly by regulating BACE-1 expression level via an NFκB
dependent mechanism. Additional work is required to
determine whether chronic administration of celastrol can be
safely achieved with cognitive benefits in a transgenic
mouse model of AD.
http://www.roskampinstitute.us/articles/archives/70
Has a Tobacco Company Stumbled on an Alzheimer’s Cure?
Nicotene-based compound at the heart of clinical studies
Mar 1, 2011, 10:33 am EDT | By Jeff
Reeves, Editor, InvestorPlace.com
Tobacco stock Star Scientific (NASDAQ: CIGX) is a company
that focuses on smokeless tobacco products. But if Star
Scientific has its way, the public could have a very
different perception of tobacco — namely, as the plant that
cured Alzheimer’s. That could mean big things for tobacco,
and even bigger things for Star Scientific stock.
http://www.investorplace.com/32191/star-scientific-tobacco-alzheimers-cure-treatment-anatabine-cigrx/
Roskamp Institute Obtains
IRB Approval for Multi-Site Human Clinical Trial with Rock
Creek Pharmaceutical RCP-006 Compound
on February 28, 2011
GLEN ALLEN, Va., Feb. 28, 2011 /PRNewswire via COMTEX/ –
http://www.starscientific.com/news/roskamp-institute-obtains-irb-approval-for-multi-site-human-clinical-trial-with-rock-creek-pharmaceutical-rcp-006-compound/
Role of Anatabine (RCP006
from Rock Creek Pharmaceuticals) as an anti-inflammatory
agent
http://www.rfdn.org/inflammaging.html
Orally administrated
cinnamon extract reduces β-amyloid oligomerization and
corrects cognitive impairment in Alzheimer's disease
animal models.
Frydman-Marom A, Levin A, Farfara D,
Benromano T, Scherzer-Attali R, Peled S, Vassar R, Segal D,
Gazit E, Frenkel D, Ovadia M.
Source
Department of Molecular Microbiology
and Biotechnology, Tel Aviv University, Tel Aviv, Israel.
PLoS One. 2011 Jan 28;6(1):e16564.
Abstract
An increasing body of evidence
indicates that accumulation of soluble oligomeric assemblies
of β-amyloid polypeptide (Aβ) play a key role in Alzheimer's
disease (AD) pathology. Specifically, 56 kDa oligomeric
species were shown to be correlated with impaired cognitive
function in AD model mice. Several reports have documented
the inhibition of Aβ plaque formation by compounds from
natural sources. Yet, evidence for the ability of common
edible elements to modulate Aβ oligomerization remains an
unmet challenge. Here we identify a natural substance, based
on cinnamon extract (CEppt), which markedly inhibits the
formation of toxic Aβ oligomers and prevents the toxicity of
Aβ on neuronal PC12 cells. When administered to an AD fly
model, CEppt rectified their reduced longevity, fully
recovered their locomotion defects and totally abolished
tetrameric species of Aβ in their brain. Furthermore, oral
administration of CEppt to an aggressive AD transgenic mice
model led to marked decrease in 56 kDa Aβ oligomers,
reduction of plaques and improvement in cognitive behavior.
Our results present a novel prophylactic approach for
inhibition of toxic oligomeric Aβ species formation in AD
through the utilization of a compound that is currently in
use in human diet.
PMID: 21305046 [PubMed] PMCID:
PMC3030596
http://www.ncbi.nlm.nih.gov/pubmed/21305046
Full article: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016564
Alzheimer's
Risk Gene Disrupts Brain's Wiring 50 Years Before Disease
Hits
ScienceDaily (May 16, 2011) — What if you were told you
carried a gene that increases your risk for Alzheimer's
disease? And what if you were told this gene starts to do
its damage not when you're old but when you're young?...
http://www.sciencedaily.com/releases/2011/05/110513091638.htm
Naturally
Occurring Plant Alkaloids Could Slow Down Alzheimer's
Disease, Study Suggests
ScienceDaily (May 27, 2011) — A family of naturally
occurring plant compounds could help prevent or delay memory
loss associated with Alzheimer's disease, according to a new
study by the Translational Genomics Research Institute
(TGen). Beta-carboline alkaloids could potentially be
used in therapeutic drugs to stop, or at least slow down,
the progressively debilitating effects of Alzheimer's,
according to the study published recently in the scientific
journal Public Library of Science (PLoS) One....
http://www.sciencedaily.com/releases/2011/05/110526131244.htm
Tobacco-Derived Compound
Prevents Memory Loss in Alzheimer's Disease Mice
ScienceDaily (Apr. 28, 2011) — Cotinine, a compound derived
from tobacco, reduced plaques associated with dementia and
prevented memory loss in a mouse model of Alzheimer's
disease, a study led by researchers at Bay Pines VA
Healthcare System and the University of South Florida
found... Some epidemiological studies showed that people who
smoke tend to have lower incidences of Parkinson's disease
and Alzheimer's disease. Studies have widely attributed this
apparently beneficial effect to nicotine, which has been
reported to improve memory and reduce Alzheimer's-like
plaques in mice. However, nicotine's harmful cardiovascular
effects and addictive properties make the compound a less
than ideal drug candidate for neurodegenerative diseases.
The Bay Pines VA/USF team decided to look at the effects of
cotinine, the major byproduct of nicotine metabolism, in
Alzheimer's disease mice. Cotinine is nontoxic and longer
lasting than nicotine. Furthermore, its safety has already
been demonstrated in human trials evaluating cotinine's
potential to relieve tobacco withdrawal symptoms...
http://www.sciencedaily.com/releases/2011/04/110427131824.htm
Here's the press release dated today
4-27-2011:
Tobacco-derived compound prevents memory loss in Alzheimer's
disease mice
Tampa, FL (For immediate release) -- Cotinine, a compound
derived from tobacco, reduced plaques associated with
dementia and prevented memory loss in a mouse model of
Alzheimer's disease, a study led by researchers at Bay Pines
VA Healthcare System and the University of South Florida
found.
The findings are reported online in the Journal of
Alzheimer's Disease in advance of print publication...
More here: http://www.eurekalert.org/pub_releases/2011-04/uosf-tcp042711.php
Roskamp Institute to Begin Human
Alzheimer's Clinical Trials With a Natural Compound in
Tobacco
Oct 7, 2010
http://www.rfdn.org/news_release_100710.html
Also look into "Anatabloc" from Star
Scientific.
DHA
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/6894066487?r=8564020497#8564020497
Celiac disease
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/9514085397
MRI
May Predict Which Adults Will Develop Alzheimer's
ScienceDaily (Apr. 6, 2011) — Using MRI, researchers may be
able to predict which adults with mild cognitive impairment
are more likely to progress to Alzheimer's disease,
according to the results of a study published online and in
the June issue of Radiology...
http://www.sciencedaily.com/releases/2011/04/110406085054.htm
Compound
Effectively Halts Progression of Multiple Sclerosis in
Animal Model
ScienceDaily (Apr. 17, 2011) — Scientists from the Florida
campus of The Scripps Research Institute have developed the
first of a new class of highly selective compounds that
effectively suppresses the severity of multiple sclerosis in
animal models. The new compound could provide new and
potentially more effective therapeutic approaches to
multiple sclerosis and other autoimmune diseases that affect
patients worldwide...
http://www.sciencedaily.com/releases/2011/04/110418093846.htm
Progression
of Smell Loss Offers Clues to the Treatment of Alzheimer's
Disease
ScienceDaily (Apr. 6, 2011) — Loss of smell is a
characteristic early symptom among people with Alzheimer's
disease, but the relationship between olfactory dysfunction
and the progression of the disease is still relatively
unknown... Removing one olfactory bulb lowered the amount of
Aβ found 6 months later on that side of the brain by more
than 50 percent, even in regions that receive no direct
olfactory bulb input. This supports a role for early-life
olfactory bulb output in the spread of Aβ throughout the
brain...
http://www.sciencedaily.com/releases/2011/04/110406192513.htm
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