About 40% of the intoxications after drug administration occur in the elderly. A significant proportion of the disease states in elderly patients is related to adverse reactions to prescribed drugs. Declining renal function, a reduction in both renal blood flow and glomerular filtration rate, is a major contributor to drug toxicity in the elderly. Therefore, a review (based on newer papers from Medline) of age-dependent changes of the kidneys and their consequences for drug therapy in geriatric patients is presented. Renal changes that occur with aging are: a decrease of renal weight, a thickening of the intrarenal vascular intima, sclerogenous changes of the glomeruli, and infiltration of chronic inflammatory cells and fibrosis in the stroma. Altered renal tubular function, including impaired handling of water, sodium, acid, and glucose, is also frequently present in old age. Impaired ‘endocrinologic’ functioning manifested by changes of the renin-angiotensin system, vitamin D metabolism, and antidiuretic hormone responsiveness has been reported. The aging kidney is constantly exposed to the effects of a variety of potential toxic processes, i.e., drugs and chronic illnesses including hypertension, diabetes, and atherosclerotic disease. Renal changes that occur with aging also consist of impairment in the ability to concentrate urine and to conserve sodium and water. These physiological changes increase the risks of volume depletion and prerenal type of acute renal failure. A frequent cause of acute renal failure in the elderly is drug-induced nephropathy. Nonsteroidal anti-inflammatory drugs, antibiotics, and diuretics are most often involved. Due to the age-dependent decline of renal function, the pharmacokinetics of many drugs are altered in elderly patients. Therefore, the most important renal function to monitor with aging is the creatinine clearance. Changes in pharmacokinetics of many drugs and most decisions on drug dosage can be based on this information alone, as tubular functions of the kidney decrease at rates paralleling the age-dependent decrease in glomerular filtration rate (which is approximately measured by the creatinine clearance). As a conclusion, age-dependent changes of renal function are not only responsible for changes in pharmacokinetics and pharmacodynamics. In many cases, the kidneys are the target organ of adverse drug reactions too.

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cells were rapidly incorporated into the glial scar, but these neuroepithelial-like cells did not make a significant contribution to neurogenesis in the infarcted cortex in young or aged animals. The response of plasticity-associated proteins like MAP1B, was delayed in aged rats. Tissue recovery was further delayed by an age-related increase in the amount of the neurotoxic C-terminal fragment of the ␤ -amyloid precursor protein (A-␤ ) at 2 weeks poststroke. Conclusion: The available evidence indicates that the aged brain has the capability to mount a cytoproliferative response to injury, but the timing of the cellular and genetic response to cerebral insult is dysregulated in aged animals, thereby further compromising functional recovery. Elucidating the molecular basis for this phenomenon in the aging brain could yield novel approaches to neurorestoration in the elderly.

Event-related P300 potentials are closely reflecting cognitive functions such as stimulus evaluation time (P300 latency) and task relevance (P300 amplitude). Hence, both their potential clinical application for detecting slight cognitive disturbances and an increasing interest in the aging of cognitive human brain functions resulted in a growing number of studies on age-related P300 changes. Although there are converging lines of evidence that aging results in prolongations of P300 latencies, reductions of P300 amplitudes and a more equipotential P300 scalp distribution, the amount of these changes and the best fit for the P300-age interactions, respectively, remain still controversial. In general, these P300 alterations obviously reflect only minor cognitive changes during normal aging. For their clinical application, however, it is necessary to obtain an age-matched normative database. Furthermore, the increased P300 variability in the elderly has to be reduced – as far as possible – by appropriate simple P300 paradigms which should be preferentially applied in longitudinal analyses to differentiate normal from pathological aging of cognitive functions. Finally, additional cross-correlational analyses between the P300 and morphological as well as neurobiochemical data are needed. By these means, our knowledge about age-related changes of cognitive brain functions should be considerably enlarged.