Alzheimer’s disease is a brain disorder named after German physician
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
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.
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%
 of the nursing home residents and in only 6%  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
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.