A gazillion things are neuroprotective. No point advocating one over the
other, in the end it will come to the metabolism of the individual in
question. Moreover, most of these natural compounds have their downsides,
something frequently overlooked because of the prevalence of the
"naturalistic fallacy". Cortisol precludes protectives responses via
inhibiting the p65 component of NFkb, increases beta amyloid production,
damages arterial walls via downstream effects, and does the hippocampus much
damage. The most universal protection against AD is a happy life and leafy
So I'm all for Ren and Stimpy: Happy Happy Joy Joy.
"Ian Goddard" <igoddard at erols.mom> wrote in message
news:bieh9vsbqhuk129k5eh46806bbc39a927o at 4ax.com...
> "James Michael Howard" <jmhoward at arkansas.net> wrote:
>> >DHEA is known to produce "neuroprotective" effects on the brain. In
> >copyrighted the hypothesis that low DHEA may result in AD in vulnerable
> >people. (My principal hypothesis is that DHEA evolved to optimize
> >replication and transcription of DNA, so I decided that reduced DHEA
> >adversely affect neuronal tissues, tissues which I believe to be
> >sensitive to levels of DHEA.) If one assumes that declining DHEA results
> >lack of support of neuron function, then "disease" processes may accrue.
> >(Neuronal maintenance declines to the point of neuronal dysfunction.) If
> >this disease process advances to a point where normal neuron functions
> >not able to repair the damage, then the stimulus of supplemental DHEA
> >probably not increase repair. The key to studying DHEA is a large study
> >involving a large number of people taking DHEA before the average onset
> >AD pathology. The study you cite fails in the same way gasoline fails to
> >help cars which have already failed.
> >> http://www.eurekalert.org/pub_releases/2003-04/aaon-dss033103.php>>> IAN: A likely flaw in that study is the relatively low dose used,
> 100 mg. I've seen much higher doses in non-Alzheimer's studies.
> The Life Extension Foundation says for DHEA, "the usual dose
> is ... 40-100 mg in males." It seems reasonable that in extreme
> cases such as dementia larger doses might be required. I think
> the study should have examined much higher doses than 100 mg.
>> Note also that at three months, 100 mg produced a benefit although
> "the benefit narrowly missed statistical significance." Mr Howard's
> DHEA-Alzheimer's hypothesis is not without indications in research
> such as the following selections, which are just a few among many:
>>> Brain Res Mol Brain Res 1999 Mar 20;66(1-2):35-41
>> Dehydroepiandrosterone (DHEA) protects hippocampal cells from
> oxidative stress-induced damage.
>> Bastianetto S, Ramassamy C, Poirier J, Quirion R.
>> Department of Psychiatry, Douglas Hospital Research Centre, McGill
> University, 6875 LaSalle Boulevard, Verdun, Quebec, Canada.
>> It has been postulated that decreases in plasma levels of
> dehydroepiandrosterone (DHEA) may contribute to the development of
> some age-related disorders. Along with neuroprotective and memory
> enhancing effects, DHEA has been shown to display antioxidant
> properties. Moreover, oxidative stress is known to cause lipid
> peroxidation and degenerative changes in the hippocampus, an area
> involved in memory processes and especially afflicted in Alzheimer's
> disease (AD). Accordingly, we investigated the antioxidant effects of
> DHEA in models of oxidative stress using rat primary hippocampal cells
> and human hippocampal tissue from AD patients and age-matched
> controls. A pre-treatment of rat primary mixed hippocampal cell
> cultures with DHEA (10-100 microM) protected against the toxicity
> induced by H2O2 and sodium nitroprusside. Moreover, DHEA (10-100
> microM) was also able to prevent H2O2/FeSO4-stimulated lipid oxidation
> in both control and AD hippocampal tissues. Taken together, these data
> suggest that DHEA may be useful in treating age-related central
> nervous system diseases based on its protective effects in the
> hippocampus. Copyright 1999 Elsevier Science B.V.
>> PMID: 10095075 [PubMed - indexed for MEDLINE]
>>> Neuropsychobiology 2000;42(2):51-7
>> Hippocampal perfusion and pituitary-adrenal axis in Alzheimer's
>> Murialdo G, Nobili F, Rollero A, Gianelli MV, Copello F, Rodriguez G,
> Polleri A.
>> Department of Endocrinological and Metabolic Sciences, Epidemiology
> Service, University of Genova, Italy. disem at unige.it>> The hippocampus is involved in Alzheimer's disease (AD) and regulates
> the hypothalamus-pituitary-adrenal axis (HPAA). Enhanced cortisol
> secretion has been reported in AD. Increased cortisol levels affect
> hippocampal neuron survival and potentiate beta-amyloid toxicity.
> Conversely, dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are
> believed to antagonize noxious glucocorticoid effects and exert a
> neuroprotective activity. The present study was aimed at investigating
> possible correlations between hippocampus perfusion - evaluated by
> SPECT - and HPAA function in AD. Fourteen patients with AD and 12
> healthy age-matched controls were studied by (99m)Tc-HMPAO
> high-resolution brain SPECT. Plasma adrenocorticotropin, cortisol, and
> DHEAS levels were determined at 2.00, 8.00, 14.00, 20.00 h in all
> subjects and their mean values were computed. Cortisol/DHEAS ratios
> (C/Dr) were also calculated. Bilateral impairment of SPECT hippocampal
> perfusion was observed in AD patients as compared to controls. Mean
> cortisol levels were significantly increased and DHEAS titers were
> lowered in patients with AD, as compared with controls. C/Dr was also
> significantly higher in patients. Using a stepwise procedure for
> dependent SPECT variables, the variance of hippocampal perfusional
> data was accounted for by mean basal DHEAS levels. Moreover,
> hippocampal SPECT data correlated directly with mean DHEAS levels, and
> inversely with C/Dr. These data show a relationship between
> hippocampal perfusion and HPAA function in AD. Decreased DHEAS, rather
> than enhanced cortisol levels, appears to be correlated with changes
> of hippocampal perfusion in dementia. Copyright 2000 S. Karger AG,
>> Publication Types:
> Clinical Trial
>> PMID: 10940758 [PubMed - indexed for MEDLINE]
>>>http://IanGoddard.net/journal.htm>> "To lengthen thy life, lessen thy meals." Benjamin Franklin
>> Ongoing CR monkey study update: "In the monkeys...those on
> reduced feeding since the study started are dying at a rate
> that is about half that of the monkeys receiving a full food
> ration." Associated Press: Eating less may extend human life.
> August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=->