X-Message-Number: 24173
Date: Mon, 31 May 2004 20:15:25 -0700 (PDT)
From: Doug Skrecky <>
Subject: could headstands reduce alzheimer risk?

(Headstands increase cerebral blood flow, which in turn may decrease
alzheimer's risk.)

Int Rev Neurobiol. 2001;48:167-217.
Alzheimer's disease: its diagnosis and pathogenesis.
 A hypothesis has been presented that links many of the identified and
putative risk factors for AD and suggests a mechanism for their action.
Crawford (1996, 1998) proposes an association between AD and cerebral
blood flow (CBF) by citing evidence that many of the factors that are
linked with an increased risk of AD also decrease CBF (e.g., old age,
depression, underactivity, head trauma). Similarly, it is suggested
factors that increase CBF are associated with a decreased risk of AD
(e.g., education, exercise, smoking, NSAIDs). Although the authors
acknowledge that reduced CBF is not sufficient to cause AD, the reported
positive and negative associations provide tantalizing evidence for a
common mode of action for many of the equivocal risk factors reported to
date. This hypothesis is also consistent with other data that links
microvascular damage and impaired blood flow (de la Torre, 1997, 2000) and
low education with increased cerebrovascular disease (Del Ser et al.,
1999). Gaining a better understanding of the interaction between AD and
vascular disease is of great importance. Not only will it provide
insights into the pathogenesis of AD, but it may also provide us with
a rare opportunity for the treatment and possible prevention of AD. A
great many risk factors for vascular disease have been identified and
intervention programs have successfully reduced the incidence of heart
disease and stroke. The potential exists to provide the same level of
success with AD.

J Sports Sci. 2003 Nov;21(11):943-51.
Use of NSE/PS2m-transgenic mice in the study of the protective effect of
exercise on Alzheimer's disease.
In its late stage, Alzheimer's disease results in progressive muscle
weakness in the arms and legs. The aim of this study was to determine
whether mice expressing the skeletal muscle-specific mutant PS2 gene (a
model of Alzheimer's disease) are a useful experimental system to study
the protective effect of exercise on A beta-42 reduction, improvement of
behavioural function and changes in metabolic parameters. With this aim
in mind, the transgenic mice were subjected to treadmill exercise for 3
months. The results showed that in transgenic mice, but not in normal
mice, treadmill exercise resulted in a reduction of A beta-42 deposits and
an improvement in behavioural function, thereby restoring normal
concentrations of total cholesterol, high-density lipoprotein
cholesterol, low-density lipoprotein cholesterol and triglyceride. Thus,
exercise may represent a practical therapeutic strategy for use with human
patients with Alzheimer's disease.

Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=24173