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normal aging from disease in the medial temporal lobe by distinguishing between cell loss in speci c regions (see Small), but novel techniques are required Mueller and colleagues have utilized quantitative volumetric MRI techniques to examine a cohort of 46 nondemented elderly individuals They found small, constant rates of loss of brain volume with aging Moreover, the rates of volume loss in the last decades of life were no greater than in the immediately preceding decades suggesting that large changes in brain volume in the elderly are attributable to the dementing diseases common to this age period Serial MRIs of elderly persons have been found by Rusinick and colleagues to predict which individuals will develop disproportionate atrophy and dementia In particular, hippocampal atrophy increases at the rate of less than 2 percent per year in healthy elderly people, in comparison to 4 to 8 percent a year in early Alzheimer disease This longitudinal method of study is more sensitive than cross-sectional populations studies Among lumbosacral anterior horn cells, sensory ganglion cells, and putaminal and Purkinje cells, neuronal loss amounts to at most 25 percent between youth and old age Not all neuronal groups are equally susceptible For example, the locus ceruleus and substantia nigra, as already commented, lose about 35 percent of their neurons, whereas the vestibular nuclei and inferior olives maintain a fairly constant number of cells throughout life A very subtle loss, decade by decade, of the major systems of nerve cells and myelinated bers of the spinal cord has been demonstrated by Morrison This accelerates after the age of 60 (Tomlinson and Irving) As described above, in normal aging, there is a gradual decline in memory and in some cognitive functions In light of the studies just summarized, it is no longer considered that these changes can be ascribed simply to neuronal loss Rather, they are probably due at least in part to alterations in synaptic connectivity within critical cortical structures Scheibel and coworkers have described a loss of neuronal dendrites in the aging brain, particularly the horizontal dendrites of the third and fth layers of the neocortex However, the Golgi method, which was used in these studies, is dif cult to interpret because of artifacts The morphometric studies of Buell and Coleman have shown that the surviving neurons actually exhibit expanded dendritic trees, suggesting that even aging neurons have the capacity to react to cell loss by developing new synapses Overall, the evidence suggests shrinkage of cells With advancing age, there is an increasing tendency for neuritic (amyloid and neuro lbrillary) plaques to appear in the brains of nondemented individuals At rst the plaques appear in the hippocampus and parahippocampus, but later they become more widespread These are loose aggregates of amorphous argentophilic material containing amyloid They occur in increasing numbers with advancing age; by the end of the ninth decade of life, few brains are without them However, as shown by Tomlinson and colleagues, relatively fewer plaques are present in the brains of mentally intact old people, in contrast to the large numbers in those with Alzheimer disease Even more impressive is the correlation of neuro brillary tangles and Alzheimer disease Very few such tangles are found in the brains of mentally sound individuals, and such as are found are essentially con ned to the hippocampus and adjacent entorhinal cortex By contrast, neuro brillary tangles are far more abundant and diffusely distributed in patients with Alzheimer disease The view is often expressed that neuritic plaques and Alzhei-.

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