CryoNet #32234 - #32236
CryoNet <[email protected]>
| Newsgroups | gmane.culture.science.cryogenics |
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CryoNet - Sat 19 Dec 2009
#32234: Re: CryoNet #32226 - #32233 [Freeposity]
#32235: Bidoun magazine article about FM-2030 [Mark Plus]
#32236: evidence based OTC treatment of Alzheimer's disease I [oberon]
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Message #32234
References: <[email protected]>
Date: Fri, 18 Dec 2009 12:16:32 -0600
Subject: Re: CryoNet #32226 - #32233
From: Freeposity <[email protected]>
On Fri, Dec 18, 2009 at 4:00 AM, CryoNet <[email protected]> wrote:
>
> Message #32226
> From: David Stodolsky <[email protected]>
> Subject: Re: Grim story on cryonics
>
> This misses the point of the article. The question being addressed is
> whether religion is a neurological built-in or a function of social
> conditions. If it is the second, then it is a psychological process,
> not an evolved brain function.
>
It could be that this is a false dichotomy. It could be a combination
of the two or even those two plus additional factors.
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Message #32235
From: Mark Plus <[email protected]>
Subject: Bidoun magazine article about FM-2030
Date: Fri, 18 Dec 2009 19:14:57 -0800
It includes photographs and FM's sketch of a telemedically monitored body, none of which I've seen before.
The Future Takes Forever: Becoming FM-2030
By Benjamin Tiven
http://bidoun.com/bdn/magazine/19-noise/the-future-takes-forever-becoming-fm-2030-by-benjamin-tiven/
Mark Plus
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Hotmail: Trusted email with powerful SPAM protection.
http://clk.atdmt.com/GBL/go/177141665/direct/01/
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Message #32236
Date: Fri, 18 Dec 2009 23:29:00 -0800 (PST)
From: [email protected]
Subject: evidence based OTC treatment of Alzheimer's disease I
[Clinical trials with over-the-counter supplements have concentrated either on items which suppress inflammation, or on antioxidants which scavenge oxygen derived free radicals. Most of these items have proved to be worthless in the treatment of Alzheimer's disease. Similarly most drugs used to treat Alzheimer's disease do little to slow the deterioration, but instead offer a mild temporary symptom relief. However, evidence has been accumulating that the primary driver of Alzheimer's disease is a nitrogen derived free radical called peroxynitrite, which may mediate both amyloid and tau accumulation as well as their toxicity. Excellent results have been obtained with peroxynitrite scavengers, with reversals of Alzheimer's disease in human clinical trials being repeatedly demonstrated. IMHO,
the only thing which may be preventing the abolition of Alzheimer's disease is the mental inertia of scientists, as well as the bureaucrats who fund them. Unfortunately, most bureaucrats keep throwing money into repeatedly testing discredited interventions, while ignoring successful ones. Common sense is anything but...]
[Abolition of amyloid induced memory deficits by rosmarinic acid is due to peroxynitrite scavenging.]
Behav Brain Res. 2007 Jun 18;180(2):139-45. Epub 2007 Mar 12.
A natural scavenger of peroxynitrites, rosmarinic acid, protects against impairment of memory induced by Abeta(25-35).
Alkam T, Nitta A, Mizoguchi H, Itoh A, Nabeshima T. Department of Neuropsychopharmacology & Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
Peroxynitrite (ONOO(-))-mediated damage is regarded to be responsible for the cognitive dysfunction induced by amyloid beta protein (Abeta) in Alzheimer's disease (AD). In the present study, we examined the protective effects of rosmarinic acid (RA), a natural scavenger of ONOO(-), on the memory impairment in a mouse model induced by acute i.c.v. injection of Abeta(25-35). Mice daily received i.p. several doses of RA after the injection of Abeta(25-35). RA prevented the memory impairments induced by Abeta(25-35) in the Y maze test and novel object recognition task. RA, at the effective lowest dose (0.25mg/kg), prevented Abeta(25-35)-induced nitration of proteins, an indirect indicator of ONOO(-) damage, in the hippocampus. At this dose, RA also prevented nitration of proteins and impai
rment of recognition memory induced by ONOO(-)-i.c.v.-injection. Co-injection of the non-memory-impairing dose of ONOO(-) with Abeta(25-35) blocked the protective effects of RA (0.25mg/kg). These results demonstrated that the memory protective effects of RA in the neurotoxicity of Abeta(25-35) is due to its scavenging of ONOO(-), and that daily consumption of RA may protect against memory impairments observed in AD.
PMID: 17420060
[Peroxynitrite is linked to the accumulation of tau filaments.]
Am J Pathol. 2003 Sep;163(3):1021-31.
Nitration of tau protein is linked to neurodegeneration in tauopathies.
Horiguchi T, Uryu K, Giasson BI, Ischiropoulos H, LightFoot R, Bellmann C, Richter-Landsberg C, Lee VM, Trojanowski JQ. Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-4283, USA.
Erratum in: Am J Pathol. 2003 Dec;163(6):2645.
Oxidative and nitrative injury is implicated in the pathogenesis of Alzheimer's disease (AD) and Down syndrome (DS), but no direct evidence links this type of injury to the formation of neurofibrillary tau lesions. To address this, we generated a monoclonal antibody (mAb), n847, which recognizes nitrated tau and alpha-synuclein. n847 detected nitrated tau in the insoluble fraction of AD, corticobasal degeneration (CBD), and Pick's disease (PiD) brains by Western blots. Immunohistochemistry (IHC) showed that n847 labeled neurons in the hippocampus and neocortex of AD and DS brains. Double-label immunofluorescence with n847 and an anti-tau antibody revealed partial co-localization of tau and n847 positive tangles, while n847 immunofluorescence and Thioflavin-S double-staining showed that
a subset of n847-labeled neurons were Thioflavin-S-positive. In addition, immuno-electron microscopy revealed that tau-positive filaments in tangle-bearing neurons were also labeled by n847 and IHC of other tauopathies showed that some of glial and neuronal tau pathologies in CBD, progressive supranuclear palsy, PiD, and frontotemporal dementia with parkinsonism linked to chromosome 17 also were n847-positive. Finally, nitrated and Thioflavin-S-positive tau aggregates were generated in a oligodendrocytic cell line after treatment with peroxynitrite. Taken together, these findings imply that nitrative injury is directly linked to the formation of filamentous tau inclusions.
PMID: 12937143
Free text>
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1868254/pdf/3770.pdf
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