X-Message-Number: 28320
Date: Thu, 17 Aug 2006 14:34:29 -0700 (PDT)
From: Doug Skrecky <>
Subject: curry probably prevents Alzheimer's

[Age related memory impairment is all too common. I've see it in
relatives, and even at least one coworker. Nobody wants to mention the
"A" word (Alzheimer's), but I'm sure many of these people will be
diagnosed with it within a decade, and die shortly thereafter. I've been
impressed with the multiple benefits of a high ORAC diet. (Oxygen radical
absorbance capacity) Although free radicals might not be an important
feature of human aging, increases in inflammation, and protein aggregates
such as amyloid are. A high ORAC diet can also act against these. In
particular, adding turmeric to ones diet looks likely to help
at least delay memory decrements. Tumeric is a spice found in curry and
mustard, which provides the yellow pigment curcumin. Curcumin scavenges
beta amyloid, and can help to reduce inflammation. It appears that a
little curcumin can go a long way. Curcumin supplements are also
available. (Also please check out blueberry as well.)]

Am J Epidemiol. 2006 Jul 26; [Epub ahead of print]
Curry Consumption and Cognitive Function in the Elderly.
  Curcumin, from the curry spice, tumeric, has been shown to possess
potent antioxidant and antiinflammatory properties and to reduce
beta-amyloid and plaque burden in experimental studies, but epidemiologic
evidence is lacking. The authors investigated the association between
usual curry consumption level and cognitive function in elderly Asians. In
a population-based cohort (n = 1,010) of nondemented elderly Asian
subjects aged 60-93 years in 2003, the authors compared Mini-Mental State
Examination (MMSE) scores for three categories of regular curry
consumption, taking into account known sociodemographic, health, and
behavioral correlates of MMSE performance. Those who consumed curry
"occasionally" and "often or very often" had significantly better MMSE
scores than did subjects who "never or rarely" consumed curry. The
authors reported tentative evidence of better cognitive performance from
curry consumption in nondemented elderly Asians, which should be
confirmed in future studies.

Neurobiol Aging. 2005 Dec;26 Suppl 1:133-6. Epub 2005 Nov 2.
Prevention of Alzheimer's disease: Omega-3 fatty acid and phenolic
anti-oxidant interventions.
  Alzheimer's disease (AD) and cardiovascular disease (CVD) are syndromes
of aging that share analogous lesions and risk factors, involving
lipoproteins, oxidative damage and inflammation. Unlike in CVD, in AD,
sensitive biomarkers are unknown, and high-risk groups are
understudied. To identify potential prevention strategies in AD, we have
focused on pre-clinical models (transgenic and amyloid infusion models),
testing dietary/lifestyle factors strongly implicated in reducing risk in
epidemiological studies. Initially, we reported the impact of
non-steroidal anti-inflammatory drugs (NSAIDs), notably ibuprofen, which
reduced amyloid accumulation, but suppressed few inflammatory markers and
without reducing oxidative damage. Safety concerns with chronic NSAIDs
led to a screen of alternative NSAIDs and identification of the phenolic
anti-inflammatory/anti-oxidant compound curcumin, the yellow pigment in
turmeric that we found targeted multiple AD pathogenic cascades. The
dietary omega-3 fatty acid, docosahexaenoic acid (DHA), also limited
amyloid, oxidative damage and synaptic and cognitive deficits in a
transgenic mouse model. Both DHA and curcumin have favorable
safety profiles, epidemiology and efficacy, and may exert general
anti-aging benefits (anti-cancer and cardioprotective.).

Curr Alzheimer Res. 2005 Apr;2(2):131-6.
A potential role of the curry spice curcumin in Alzheimer's disease.
  There is substantial in-vitro data indicating that curcumin has
antioxidant, anti-inflammatory, and anti-amyloid activity. In addition,
studies in animal models of Alzheimer's disease (AD) indicate a direct
effect of curcumin in decreasing the amyloid pathology of AD. As the
widespread use of curcumin as a food additive and relatively small
short-term studies in humans suggest safety, curcumin is a promising
agent in the treatment and/or prevention of AD. Nonetheless, important
information regarding curcumin bioavailability, safety and tolerability,
particularly in an elderly population is lacking. We are therefore
performing a study of curcumin in patients with AD to gather this
information in addition to data on the effect of curcumin on biomarkers
of AD pathology.

J Biol Chem. 2005 Feb 18;280(7):5892-901. Epub 2004 Dec 7.
Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds
plaques, and reduces amyloid in vivo.
  Alzheimer's disease (AD) involves amyloid beta (Abeta) accumulation,
oxidative damage, and inflammation, and risk is reduced with increased
antioxidant and anti-inflammatory consumption. The phenolic yellow curry
pigment curcumin has potent anti-inflammatory and antioxidant activities
and can suppress oxidative damage, inflammation, cognitive deficits, and
amyloid accumulation. Since the molecular structure of curcumin suggested
potential Abeta binding, we investigated whether its efficacy in AD
models could be explained by effects on Abeta aggregation. Under
aggregating conditions in vitro, curcumin inhibited aggregation (IC(50) =
0.8 microM) as well as disaggregated fibrillar Abeta40 (IC(50) = 1
microM), indicating favorable stoichiometry for inhibition. Curcumin was
a better Abeta40 aggregation inhibitor than ibuprofen and naproxen, and
prevented Abeta42 oligomer formation and toxicity between 0.1 and 1.0
microM. Under EM, curcumin decreased dose dependently Abeta fibril
formation beginning with 0.125 microM. The effects of curcumin did not
depend on Abeta sequence but on fibril-related conformation. AD and
Tg2576 mice brain sections incubated with curcumin revealed
preferential labeling of amyloid plaques. In vivo studies showed that
curcumin injected peripherally into aged Tg mice crossed the blood-brain
barrier and bound plaques. When fed to aged Tg2576 mice with advanced
amyloid accumulation, curcumin labeled plaques and reduced amyloid levels
and plaque burden. Hence, curcumin directly binds small beta-amyloid
species to block aggregation and fibril formation in vitro and in
vivo. These data suggest that low dose curcumin effectively disaggregates
Abeta as well as prevents fibril and oligomer formation, supporting the
rationale for curcumin use in clinical trials preventing or treating AD.

J Neurosci. 2001 Nov 1;21(21):8370-7.
The curry spice curcumin reduces oxidative damage and amyloid pathology
in an Alzheimer transgenic mouse.
  Inflammation in Alzheimer's disease (AD) patients is characterized by
increased cytokines and activated microglia. Epidemiological studies
suggest reduced AD risk associates with long-term use of nonsteroidal
anti-inflammatory drugs (NSAIDs). Whereas chronic ibuprofen suppressed
inflammation and plaque-related pathology in an Alzheimer transgenic APPSw
mouse model (Tg2576), excessive use of NSAIDs targeting cyclooxygenase I
can cause gastrointestinal, liver, and renal toxicity. One alternative
NSAID is curcumin, derived from the curry spice turmeric. Curcumin has an
extensive history as a food additive and herbal medicine in India and is
also a potent polyphenolic antioxidant. To evaluate whether it could
affect Alzheimer-like pathology in the APPSw mice, we tested a low (160
ppm) and a high dose of dietary curcumin (5000 ppm) on inflammation,
oxidative damage, and plaque pathology. Low and high doses of curcumin
significantly lowered oxidized proteins and interleukin-1beta, a
proinflammatory cytokine elevated in the brains of these mice. With
low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP
was reduced, and insoluble beta-amyloid (Abeta), soluble
Abeta, and plaque burden were significantly decreased by 43-50%. However,
levels of amyloid precursor (APP) in the membrane fraction were not
reduced. Microgliosis was also suppressed in neuronal layers but not
adjacent to plaques. In view of its efficacy and apparent low toxicity,
this Indian spice component shows promise for the prevention of
Alzheimer's disease.

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