LONGECITY

Wolfberries or Goji berries, Lycium barbarum and
the related Lycium chinensis (Chinese lycii).

http://www.ncbi.nlm....t_uids=17710531

http://www.mangostee...eurobiology.pdf

http://healthydoses....ycium-barbarum/

http://www.zhion.com...goji_berry.html

More on wolfberries.

http://www.ncbi.nlm....t_uids=16139464

http://www.ncbi.nlm....t_uids=20157238


http://www.mangostee.../sdarticle1.pdf

http://www.mangostee.../sdarticle2.pdf

http://www.rubygoji....library-002.pdf

" ..... prevent or delay the onset of
age-related neurodegenerative diseases
such as Parkinson's and Alzheimer's
via the prophylactic daily administration
of 1 mg (-)-deprenyl. "

http://www.ncbi.nlm...._uids=20150659


Selegiline and donepezil.

http://www.ncbi.nlm....t_uids=18420288

Citicholine in ApoE4 carriers.

http://www.ncbi.nlm....t_uids=10669911


Alpha GPC.

http://www.ncbi.nlm....t_uids=12637119


Optimal dose of galantamine.

http://www.ncbi.nlm....t_uids=19358618

The antique NSAID, mefenamic acid (Ponstan).

" We found that mefenamic acid attenuates
the neurotoxicities induced by amyloid beta
peptide (Abeta)(1-42) ..... "

" In addition, mefenamic acid upregulates
expression of the antiapoptotic protein Bcl-X(L).

" .... demonstrates for the first time that
mefenamic acid improves learning
and memory impairment in an Abeta
(1-42)-infused Alzheimer's disease
rat model. "

http://molpharm.aspe...nt/69/1/76.long

Celery's 3-n-butylphthalide.


http://microscopy.fs...lphthalide.html

http://www.phthalides.com/

http://www.ncbi.nlm....t_uids=19726345

http://www.ncbi.nlm....t_uids=19726301

http://www.ncbi.nlm....t_uids=19737553

http://www.ncbi.nlm....t_uids=20554868

http://www.ncbi.nlm....t_uids=19214478

http://jpet.aspetjou.../321/3/902.full

Doxycycline and rifampicin, the TB drug.

http://www.ncbi.nlm....t_uids=14962152


Lyme and dementia.

http://www.ncbi.nlm....t_uids=16528463



Minocycline reduces the development of abnormal
tau species in models of Alzheimer’s disease.

http://www.fasebj.or...t/23/3/739.long


" .... doxycycline administration inhibits transgenic
APP expression by greater than 95% and reduces
Abeta production to levels found in nontransgenic mice. "

http://www.ncbi.nlm....t_uids=16279840



" ..... tetracyclines, tetracycline and doxycycline,
classical antibiotics, exhibit anti-amyloidogenic activity. "

" Tetracyclines not only inhibited the beta-
amyloid aggregates formation but also
disassembled the pre-formed fibrils. "

http://www.ncbi.nlm....t_uids=11163366


" The anti-amyloidogenic activity of tetracyclines
was tested in other forms of peripheral and
central amyloidosis, with interesting results. "

http://www.ncbi.nlm....t_uids=19200012


http://www.ncbi.nlm....t_uids=15046864

If herpes really causes Alzheimer's then this next study only seems logical.

Could lysine supplementation prevent Alzheimer's dementia? A novel hypothesis.
Rubey RN.

Retired, Red Lodge, Montana, USA.


Abstract
There is a growing body of evidence that implicates the herpes simplex type 1 virus (HSV-1) in the development of Alzheimer's dementia (AD). HSV-1 has been found to be present in the cerebrum of the great majority of older adults, and in many of the same areas of the brain that are affected by AD. When active, the virus may contribute to the formation of the neuro-fibrillary tangles and amyloid plaques characteristic of AD. Like AD, HSV-1 encephalitis may cause long term memory loss. HSV-1 replication is suppressed in lysine-rich/arginine - poor environments, and population studies suggest that diets high in lysine and low in arginine may be associated with lower rates of AD. There are no prospective studies of the efficacy of lysine supplementation to prevent or reduce the incidence of AD. Supplementation with adequate doses of lysine could prevent the development of AD.

PMID: 21127688 [PubMed - in process]

Full Study: http://www.ncbi.nlm....f/ndt-6-707.pdf

If herpes really causes Alzheimer's then this next study only seems logical.

Could lysine supplementation prevent Alzheimer's dementia? A novel hypothesis.
Rubey RN.

Retired, Red Lodge, Montana, USA.


Abstract
There is a growing body of evidence that implicates the herpes simplex type 1 virus (HSV-1) in the development of Alzheimer's dementia (AD). HSV-1 has been found to be present in the cerebrum of the great majority of older adults, and in many of the same areas of the brain that are affected by AD. When active, the virus may contribute to the formation of the neuro-fibrillary tangles and amyloid plaques characteristic of AD. Like AD, HSV-1 encephalitis may cause long term memory loss. HSV-1 replication is suppressed in lysine-rich/arginine - poor environments, and population studies suggest that diets high in lysine and low in arginine may be associated with lower rates of AD. There are no prospective studies of the efficacy of lysine supplementation to prevent or reduce the incidence of AD. Supplementation with adequate doses of lysine could prevent the development of AD.

PMID: 21127688 [PubMed - in process]

Full Study: http://www.ncbi.nlm....f/ndt-6-707.pdf

...given that 'most' people have HSV-1 ......

Mike,

The difference stands in Lysine status. It says that adequate Lysine in the diet can even be prophylactic. Anyways, that's the kinda thinking we need to solve problems like these.

C. pneumoniae and Alzheimer's.

http://www.chlamydia..._alzheimers.asp



C. pneumoniae and Alzheimer's.

http://www.chlamydia..._alzheimers.asp


Apple juice.


" ..... 21 institutionalized individuals with
moderate-to-severe AD consumed two 4-oz
glasses of apple juice daily for 1 month.

..... caregivers reported an approximate
27% improvement in behavioral and psychotic
symptoms associated with dementia as quantified
by the Neuropsychiatric Inventory, with the
largest changes in anxiety, agitation, and delusion. "

http://www.ncbi.nlm....t_uids=20338990

http://www.ncbi.nlm....=15004325
Edited by tham, 08 December 2010 - 04:57 PM.

More on Thomas Shea's studies on apple juice.

http://www.scienceda...90122100826.htm

http://www.ncbi.nlm....t_uids=17183144

http://www.ncbi.nlm....t_uids=19158432

http://www.ncbi.nlm....t_uids=16914839

http://www.ncbi.nlm....t_uids=14978604

Lysine.

http://www.ncbi.nlm....t_uids=21127688


Infectious agents - herpes viruses,
C. pneumoniae, etc, and dementia.

http://stroke.ahajou.../full/34/9/2126

http://www.ncbi.nlm....t_uids=12115887

http://www.ncbi.nlm....l=pubmed_docsum


" .... a very high proportion of the VaD patients,
93%, but not of age-matched normals, 34%,
harbor CMV DNA. "

http://www.ncbi.nlm....t_uids=11848687


http://www.ncbi.nlm....t_uids=19560105

http://www.ncbi.nlm....t_uids=20011709

http://www.ncbi.nlm....t_uids=15207442



Viruses and ApoeE4.

http://www.ncbi.nlm....cles/PMC2830997



" .... three of the most important diseases of
aging: shingles, Alzheimer's disease and
atherosclerotic cardiovascular disease. All of
these diseases have significant immunological
components in either their etiology and/or
progression, suggesting that appropriate
immune intervention could be used in their
prevention or treatment. "

http://www.ncbi.nlm....t_uids=19541533



The immune system in extreme longevity.

" A major force able to drive a chronic pro-
inflammatory state during aging may be
represented by persistent viral infections
by EBV and CMV. "

" In all subjects the absolute number of
CMV-positive CD8+ cells outnumbered that
of EBV-positive ones. "

" These data indicate that the chronic antigenic
stimulation induced by persistent viral infections
during aging bring about important modifications
among CD8+ subsets, which are particularly
evident in the presence of CMV persistence. "

http://www.ncbi.nlm....t_uids=17870272

Stop blaming plaques for Alzheimer’s

Age-related changes, like plaques and tangles, only lead to a slow natural decline in cognitive function; they don’t in themselves cause Alzheimer’s disease, according to a new hypothesis.

The Kampo formula Hochu Ekki-To,
TJ41, against CMV, as mentioned in
the CFS thread.

Chinese name Bu Zhong Yi Qi Wan.

http://www.ncbi.nlm....t_uids=10884593


Black seed oil fights CMV.

http://www.ncbi.nlm....t_uids=10884593

Just published Malaysian study on
the common spice, coriander.

Commonly added raw as a garnishing
in Chinese cooking. When I ordered some
fried rice this evening at the usual restaurant
where I take my dinner, I requested the cook
to add lots of it on top. Tends to have cause
diarrhea though, due to its detoxifying action,
even though coriander is supposed to treat
diarrhea.

http://www.ncbi.nlm....t_uids=20848667

http://www.bioportfo...es-In-Mice.html

Prophylactic Treatment with Paroxetine Ameliorates Behavioral Deficits and Retards the Development of Amyloid and Tau Pathologies in 3xTgAD Mice

paroxetine treatment reduced Aβ1−40 levels by more than 50%

Abstract
A history of depression is a risk factor for Alzheimer’s disease (AD), suggesting the possibility that antidepressants administered prophylactically might retard the disease process and preserve cognitive function. Here we report that pre-symptomatic treatment with the antidepressant paroxetine attenuates the disease process and improves cognitive performance in the 3xTgAD mouse model of AD. Five month-old male and female 3xTgAD and non-transgenic mice were administered either paroxetine or saline daily for 5 months. Open-field activity was tested in 7 month-old mice and performance in passive avoidance and Morris swim tasks were evaluated at 10 months. 3xTgAD mice exhibited reduced exploratory activity, increased transfer latency in the passive avoidance test and impaired performance in the Morris spatial navigation task compared to nontransgenic control mice. Paroxetine treatment ameliorated the spatial navigation deficit in 3xTgAD male and female mice, without affecting swim speed or distance traveled, suggesting a preservation of cognitive function. Levels of amyloid beta-peptide (Aβ) and numbers of Aβ immunoreactive neurons were significantly reduced in the hippocampus of male and female paroxetine-treated 3xTgAD mice compared to saline-treated 3xTgAD mice. Female 3xTgAD mice exhibited significantly less tau pathology in the hippocampus and amygdala compared to male 3xTgAD mice, and paroxetine lessened tau pathology in male 3xTgAD mice. The ability of a safe and effective antidepressant to suppress neuropathological changes and improve cognitive performance in a mouse model, suggests that such drugs administered prophylactically might retard the development of AD in humans.

full study is here My link
Edited by rashlan, 28 January 2011 - 05:08 PM.

Rapamycin promotes beta-amyloid production.

http://www.unboundme..._10_inhibition_

There have been some positive developments. See Polite Requests.
All requests accepted, pending blood test results. Magnesium also being tested.
See also Mum's Proposed Ketogenic Diet for Dementia. and Well, stone the (expletive deleted) crows!

It's about time we life extension enthusiasts banded together and opened our own nursing homes...
Edited by Destiny's Equation, 24 May 2011 - 09:50 PM.

Refining Intravenous IgG Pools for AD Immunotherapy

Abeta Epitope DNA and Peptide Vaccination: Bridging the 'Therapeutic Threshold' for Cognitive Aging and Alzheimer's Disease

Aß "Affibodies:" A Novel Route to Comprehensive Clearance?

More Evidence for Endogenous Anti-Abeta Antibodies -- Therapeutic Potential

Progress and New Cautions in an "Universal Amyloid Strategy"

Active Aß Immunization Reverses (Some) Neuritic Pathology

Optimizing Abeta Clearance with Catalytic Immunoglobulins

Progress in Targeting Tau Pathology

Abeta Clearance Removes Early Tau Pathology in Neuronal Processes

These are a bunch of articles written by MR regarding antibody strategies to the beta-amyloid and its possible promising future.

Here is a recent editorial on antibodies targeted to BACE: http://www.scientifi...hore-2011-05-25


I've been doing some Alzheimer's research for investment purposes and haven't found anything hopeful (besides these antibodies). Too bad.

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
http://www.sciencedi...953620511000045

Abstract
Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause.

Was recently at a talk of Hilal A. Lashuel where I realized the complexity of the problem. If I recollect well he emphasized the importance of understanding the process in getting to AD with all intermediate steps vs only trying to find an inhibitor of the aggregation. In other words we should look at the aggregation process in all its molecular biology levels of detail. An interesting abstract from one of the publications here (red is mine):

A century-old debate on protein aggregation and neurodegeneration enters the clinic

A century-old debate on protein aggregation and neurodegeneration enters the clinicThe correlation between neurodegenerative disease and protein aggregation in the brain has long been recognized, but a causal relationship has not been unequivocally established, in part because a discrete pathogenic aggregate has not been identified. The complexity of these diseases and the dynamic nature of protein aggregation mean that, despite progress towards understanding aggregation, its relationship to disease is difficult to determine in the laboratory. Nevertheless, drug candidates that inhibit aggregation are now being tested in the clinic. These have the potential to slow the progression of Alzheimer's disease, Parkinson's disease and related disorders and could, if administered presymptomatically, drastically reduce the incidence of these diseases. The clinical trials could also settle the century-old debate about causality.

http://www.nature.co...ature05290.html

See also here: http://lashuel-lab.epfl.ch/

Celastrol from the Chinese Thunder of God vine.

http://www.jneuroinf.../content/7/1/17


" Low doses of celastrol administered to rats significantly
improved their performance in memory, learning and
psychomotor activity tests. "


" Celastrol's ability to modulate the expression of
pro-inflammatory cytokines, MHC II, HO-1, iNOS,
NF-kappaB, Notch-1, AKT/mTOR, CXCR4,
TRAIL receptors DR4 and DR5, CHOP, JNK,
VEGF, adhesion molecules, proteasome activity,
topoisomerase II, potassium channels, and heat
shock response has been reported. "

http://www.ncbi.nlm....t_uids=21168266



Curcumin.

" Using clinically feasible dosing, brain levels of
NSAIDs appear too low to implicate a number
of pharmacological dose targets that have been
demonstrated in vitro. Ibuprofen did not suppress
microglial markers related to phagocytosis. The
putative anti-inflammatory omega-3 fatty acid
DHA had a profound impact on pathogenesis but
did not lower inflammation, while vitamin E was
surprisingly ineffective in reducing oxidative
damage or amyloid in the aged APPsw mouse.

In contrast, the unconventional NSAID/antioxidant
curcumin was effective, lowering oxidative damage,
cognitive deficits, synaptic marker loss, and
amyloid deposition. "

http://www.ncbi.nlm....t_uids=15681801

These studies on coriander were sent to me
earlier this year by Dr Vasudevan Mani, the
local researcher at the Pharmacology faculty
of the University Technology Mara in Malaysia
here, when I enquired about his abstracts here

http://www.longecity...ndpost&p=450624


http://pharmacy.uitm...?tmpl=component


Coriander is synonymous with Chinese parsley
and cilantro.

Whenever I eat at the usual Chinese restaurant
near my office these days, the cook automatically
sprinkles lots of this raw garnish (leaves, not the
seeds) on top of the rice, per my request.

http://www.uni-graz....l/Cori_sat.html

http://chinesefood.a.../a/cilantro.htm
Edited by tham, 29 June 2011 - 08:44 PM.

Coriander (aka ciliantro, Chinese parsley) and chelation.


" Administration of Chinese parsley also significantly
decreased lead deposition in the femur and severe
lead-induced injury in the kidneys. In addition, urinary
excretion of delta-aminolevulinic acid (ALA) which is
known to increase with lead intake was significantly
decreased after administration of Chinese parsley. "

http://www.ncbi.nlm....t_uids=11535365


" Cilantro tea: The Poor Man's Chelation Therapy. "

http://www.autismtre...sages/1434.html


" Cilantro: A Common Spice/Herb That Can Save Your Life "

http://www.mnwelldir...ox/cilantro.htm


http://www.ncbi.nlm....st_uids=8914687

http://www.ncbi.nlm....st_uids=1521537

http://www.ncbi.nlm....st_uids=8688573


" .... cilantro, by some still-unknown mechanism, opens
up cell membranes so mercury can be taken out. She
noted that cilantro also performs this function in the brain,
and she has seen years of depression lifted in several
patients who have had heavy-metal detoxification. "

http://www.chemtrail...TML/000068.html

http://www.oodora.co...f-cilantro.html

http://www.newmediae...e_your_life.htm

Another link to this study was given earlier,
but has since moved.

" Melissa officinalis, Salvia officinalis and
Yi-Gan San and BDW (Ba Wei Di Huang Wan).
Ginkgo biloba was identified in a meta-analysis
study. All five herbs are useful for cognitive
impairment of AD. M. officinalis and Yi-Gan San
are also useful in agitation, for they have
sedative effects. "

http://www.ncbi.nlm....les/PMC1697739/

Risperidone Versus Yokukansan (Yi Gan San) in
the Treatment of Severe Alzheimer’s Disease.

http://www.scirp.org...publishStatus=2


" Who Wants a Younger Brain? Herbal Yokukansan May Help. "

http://www.cureology...ottom-line.html


" Yi-Gan San: Safe,effective replacement for
antipsychotics used for AD patients. "

http://alzheimers.in...61/m/4384001397
Edited by tham, 14 August 2011 - 08:05 PM.

" YKS is likely to be a potent and novel therapeutic
agent to prevent and/or treat AD, and that this
may be attributed to UH (Uncaria hook, synonymous
with Uncaria rhynchophylla). "

http://www.ncbi.nlm....t_uids=21303686


http://www.raysaheli...om/uncaria.html


" Yokukansan is a versatile herbal remedy with a
variety of effects on various neurological states,
without reported adverse effects. "

http://www.ncbi.nlm....t_uids=20812276

More on the classical Bupleurum Formula,
Shi Quan Da Bu Wan / Juzen taiho-to.


" Activated macrophages derived from bone marrow
cross the blood-brain barrier, and then develop into
microglia, which phagocytose aggregated amyloid-beta
(Abeta) in senile plaques. "

" .... orally administered Juzen taiho-to increased the
number of CD11b-positive ramified microglia in the
mouse brain. "

" Thus, the activation of peripheral macrophages by JTT
might be a potential new therapeutic strategy for AD. "

http://iospress.meta...3/fulltext.html