AS RECENTLY as 1900, tuberculosis, influenza, and pneumonia were the leading causes of death in our country (1). For the most part, however, these infectious diseases, as well as those of poor hygiene or undernutrition, no longer plague us. Instead, we succumb most frequently to heart disease and cancer, diseases of slow degeneration (1). Most of all, unlike so many in the generations before us, we are in a position to age. Regardless of what else occurs, we age, we become more constrained by the discrepancy between what we were and what we have become, and each step becomes harder. The goal in the study of aging is not to halt the process, because we can no more be cured of aging than of birth. The goal, instead, is to slow and soften the sharpest edges of the biological unraveling that constitutes aging. Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stress to...

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis*

Over the past 5 yr, we have examined some of the sharpest edges of the pathology of aging. We have studied the capacity of aged organisms to respond appropriately to stress and the capacity of stre...

The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis

Glucocorticoid toxicity in the hippocampus: in vitro demonstration.

Nosologically, Alzheimer disease may not be considered to be a single disorder in spite of a common clinical phenotype. Only a small proportion of about 5% to 10% of all Alzheimer cases is due to genetic mutations (type I) whereas the great majority of patients was found to be sporadic in origin. It may be assumed that susceptibility genes along with lifestyle risk factors contribute to the causation of the age-related sporadic Alzheimer disease (type II). In this context, the desensitization of the neuronal insulin receptor similar to not-insulin dependent diabetes mellitus may be of pivotal significance. This abnormality along with a reduction in brain insulin concentration is assumed to induce a cascade-like process of disturbances including cellular glucose, acetylcholine, cholesterol, and ATP associated with abnormalities in membrane pathology and the formation of both amyloidogenic derivatives and hyperphosphorylated tau protein. Sporadic Alzheimer disease may, thus, be considered to be the brain type of diabetes mellitus II. Experimental evidence is provided and discussed.

The brain insulin signal transduction system and sporadic (type II) Alzheimer disease: an update.

Abnormal cortisol response in alzheimer's disease linked to hippocampal atrophy

Fifteen seconds after intracarotid injection of either 14C-glucose or tritiated water in adrenalectomized rats, the net uptake of the respective tracer by 18 brain regions and by the anterior pituitary was measured. Corticosterone added to the injection solution (1 or 100 micrograms ml-1; 0.2 ml per animal) caused a dose-dependent decrease of net uptake of 14C-glucose in twelve regions. Compared to the net uptake of tritiated water which was used as a measure of relative blood flow, it suggests that this effect, at least partially, is due to a decreased blood-brain barrier permeability to 14C-glucose. Furthermore, the regional net uptake of 14C-glucose was estimated in rats with different endogenous corticosterone levels but injected with an identical solution in each case. Statistically significant differences could be observed between adrenalectomized and restrained animals in three brain regions.

Regional net uptake of 14C-glucose by rat brain under the influence of corticosterone.

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Regional net uptake of 14C-glucose by rat brain under the influence of corticosterone.