Biological markers of age-related memory deficits - Treatment of senescent physiology

In humans, age-related memory impairments begin in mid-life and cognitive weakening continues with advancing age. An important aspect of defining memory decline is the distinction between dementia as a result of neurological diseases, such as Alzheimer's disease, and memory loss not specifically associated with disease. Within the population of elderly without dementia, there is considerable variability in memory. This variability is likely to be a result of the interaction of genetic make-up and environment, which influences several processes for cell maintenance and repair including oxidative damage and cholesterol metabolism, leading to disruption of Ca2+ homeostasis, and ultimately Ca2+-dependent processes that underlie memory. In humans, several methods have been employed to distinguish biological markers of aging that may predict cognitive decline. Memory deficits associated with normal aging and Alzheimer's disease have been linked to a decrease in the volume of brain structures, such as the hippocampus and to genetic markers, such as apolipoprotein E. In this regard, examination of CSF for biomarkers of disease can help in differentiating normal aging from Alzheimer's disease. Measures of oxidative stress and cholesterol in plasma correlate with memory deficits; research suggests that treatments that reduce oxidative stress or cholesterol through exercise, diet or the use of antioxidant vitamins may delay cognitive decline. Nevertheless, to date, very little treatment is available to reverse memory deficits in later life. In this regard it is important to identify individuals at risk for memory deficits in order to discriminate different mechanisms of brain aging and develop treatments. Considerable effort is driving research to develop accurate biological markers of brain aging. In turn, these markers will provide information on mechanisms of aging and cognitive decline and point to potential treatments. Accordingly, the effectiveness of treatment needs to be verified for both cognitive changes and biological markers that are specific for age-related memory deficits.