Jun 302010

As readers of this blog are probably aware, the prevailing theory of AD is that amyloid precursor protein is somehow aberrantly cleaved as it is secreted by neurons, and leads to the formation of beta-amyloid. Beta amyloid is a toxic “oligomer” or protein fragment that becomes improperly folded, and deposits into plaques. It is believed that the small oligomers of beta amyloid are more toxic than their larger aggregated counterparts (i.e.,amyloid fibrils), and in fact, […]

Jun 242010

Building on their previous discovery that people with Alzheimer’s have beta-amyloid deposits that appear as unusual cataracts in the lens of the eye, a team of researchers led by Dr. Lee Goldstein at Boston University School of Medicine, has discovered that beta-amyloid also accumulates in the eyes of people with Down syndrome. Down syndrome patients develop symptoms of Alzheimer’s Disease often by the age of 30 because they have an extra copy of a key […]

Jun 162010

Readers, A relationship between vascular risk factors and Alzheimer disease has been considered for over 20 years. In fact, it was widely accepted that “a hardening of the arteries” was to blame for senile dementias. There is also evidence that vascular diseases such as stroke, atherosclerosis, and hypertension are associated with an increased risk of dementia and AD, and that an abnormally elevated level of fibrinogen, the protein critical for blood clot formation, is correlated […]

Jun 082010

Increasing evidence indicates that there are reductions in testosterone and estrogen levels in older men and women. These hormonal reductions may be risk factors for cognitive impairment and the development of Alzheimer’s disease (AD). As testosterone levels decline as men age, there is an urge to treat this natural process with hormone replacement, just as it is done for many women undergoing menopause. The enzyme aromatase in the male brain converts some of the testosterone […]

Jun 022010

Readers, The Alzheimer’s Disease Neuroimaging Initiative (ADNI) continues to provide us with greater and more detailed information about AD. For quite some time, we have known that the ApoE4 genotype leads to an increased risk of developing sporadic AD. Patients with the ApoE4 gene (carriers) typically develop Alzheimer’s disease five to seven years earlier than those without the gene (non-carriers). One or more copies of the ApoE4 gene are present in 20 percent to 30 percent of the […]

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