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Alzheimer's Disease and DHEA

 

Alzheimer’s disease is a brain disorder named after German physician Alois Alzheimer, who first described it in 1906. Patients with Alzheimer disease have higher levels of cortisol (the “stress” hormone) and imbalanced cortisol/DHEA ratios. In a group of severely afflicted Alzheimer's patients, Dehydroepiandrosterone sulfate (DHEA-S) levels were significantly lower.
 

How DHEA helps the body overcome Alzheimer’s Dementia

H.D Danenberg reported findings in 1996 that may help explain a key aspect of DHEA's anti-dementia neuroprotection.
Amyloid ß protein (Aß) is the major component of senile plagues, a distinct lesion in brain tissue of Alzheimer's dementia patients.

These toxic amyloid deposits, which gradually kill Alzheimer's dementia brain cells, are produced from amyloid precursor protein (APP) by a specific enzymatic pathway - the “amyloidogenic pathway.” DHEA treatment increases amyloid precursor protein processing via the nonamyloidogenic pathway and may prevent the gradual accumulation of toxic Aß proteins observed in the elderly.  The increase in amyloid precursor protein production in DHEA-treated cells is accompanied by increased secretion of the nonamyloidogenic (non-toxic protein forms).

These non-toxic isoforms demonstrate neuroprotective properties, and participate in neurite outgrowth. Thus, not only is increased production of amyloid precursor protein not ultimately harmful, it may be beneficial when followed by nonamyloidogenic processing. It is possible that the age-associated decline in DHEA levels may contribute to the pathological amyloid precursor protein processing and eventually to the development of Alzheimer's dementia." Thus, there is hope for protecting the structure and function of aging brains through long-term DHEA supplementation.
 

Clinical Studies

  • D.Rudman, K. Shetty and D. Mattson published a major study on DHEA and the elderly in 1990.  They compared DHEA-S levels in 50 independently-living community men, age 55 - 94 with DHEA-S levels in 61 nursing home men, age 57- 104.  DHEA was significantly lower in the nursing home men, who were generally more debilitated, than in the community men.  Plasma DHEA-S was subnormal (less than 30 mcg/dL) in 40% [25] of the nursing home residents and in only 6% [3] of the community subjects.  In the nursing home men plasma DHEA-S was inversely related to the presence of an organic brain syndrome, Alzheimer's dementia or multi-infarct dementia, and to the degree of dependence in activities of daily living.  Plasma DHEA-S was subnormal in 80% of the nursing home men who required total care. In total care patients with either Alzheimer's dementia or multi-infarct dementia the prevalence of low DHEA-S was 68% and 100% respectively.
     

  • B. Nasman and co-workers compared 45 Alzheimer's dementia and 41 multi-infarct dementia patients to an elderly control group. They state: "Patients with Alzheimer's dementia and multi-infarct dementia had significantly lower serum DHEA-S values than the control group.  The ratio of plasma cortisol to serum DHEA-S was higher in Alzheimer's dementia and multi-infarct dementia patients than in healthy controls.  DHEA has been suggested to act as an antiglucocortiticoid. A high cortisol/DHEA-S ratio in demented patients may thus damage hippocampal cells these mid-brain "memory cells" die off in organic dementia especially - as these neurons are preferentially sensitive to the toxic effects of cortico steroids.
     

  • Other studies have examined the role of vascular endothelial growth factor (VEGF) among Alzheimer's patients. VEGF has been shown to protect the brain, and scientists now believe that low VEGF levels may be connected to the progression of Alzheimer's disease. DHEA-S was shown to significantly increase the bioavailability of VEGF in the brain, leading the study authors to conclude that it could be a valuable treatment for Alzheimer's and aging.

 

 




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