Aging, Neuropsychology, and Cognition: A Journal on Normal and Dysfunctional Development

Changes in cognition with aging have been claimed to be due in large part to a decline in frontal lobe function. However, at our present state of knowledge, the emphasis on the frontal lobes to the exclusion of the rest of the frontal-striatal circuits of which they are a part is unwarranted. To argue this point, I consider another anatomical candidate within these circuits, the caudate. Evidence is presented that the caudate decreases in size with age as much as the frontal lobes and that damage to either the frontal lobes or the caudate is accompanied by declines in inhibitory processes, executive control, and cognitive speed similar to those seen in normal aging. Separating the unique contributions of the frontal lobes and the caudate to these circuits is difficult but should be the focus of future studies of the biological basis of cognitive aging. Changes in the frontal lobes have been claimed to be the neurological basis of many of the cognitive declines that occur in aging (Albert & Kaplan, 1980; Daigneault & Braun, 1993; Demspter, 1992; Mittenberg, Seidenberg, O’Leary, & DiGiulio, 1989; Moscovitch & Winocur, 1992; Shimamura, 1994; Shimamura & Jurica, 1994; West, 1996; Whelihan & Lesher, 1985), even in papers with no other neural claims (Craik & Jennings, 1992). I argue that the standard documented declines in cognitive aging cannot be attributed to declines in frontal lobe function to the exclusion of declines in the rest of the frontal-striatal circuit. To substantiate this argument, I focus on one structure in that circuit, the caudate (technically the head of the caudate), which also declines with age. I choose the caudate because the strongest support can be made for this structure; the most data are available for it. For the caudate I will show that when its functioning declines, cognitive changes occur that are similar to those attributed to frontal lobe damage. Thus, attributing changes in normal aging to frontal lobe decline as opposed to caudate decline, though widely held, is at best premature. Oddly enough, I could find only two earlier arguments for the role of the caudate in cognitive aging. In a book on subcortical dementias (i.e., dementias often involving caudate damage), Van Gorp and Mahler (1990) presented a chapter relating subcortical dementia to normal aging. More directly, Hicks and Birren (1970) proposed that the caudate has a central role in cognitive aging because damage to it causes cognitive slowing. Three major empirical observations consistently appear in the literature on cognitive aging: (a) decreases in the functioning of inhibitory mechanisms, (b) decreases in executive control or planning, and (c) cognitive slowing as measured by increases in response time. Other common categories, such as decreases in sensory function (Park, 1998), are not central to the arguments made here because they are usually not D ow nl oa de d by [ D uk e U ni ve rs ity M ed ic al C en te r] a t 0 9: 07 2 1 M ay 2 01 5