Decline-induced plastic changes of brain and behaviour in aging
During the last two decades we have witnessed an important body of empirical reports from several longitudinal studies of cognitive aging, such as the Betula study (Nilsson et al., 1997). Thanks to this work, we can now describe the hallmarks of cognitive aging. At the group level, we ﬁnd accelerating mean negative changes in ﬂuid abilities such as working memory, reasoning, episodic memory, and spatial orientation (e.g., Rönnlund & Nilsson, 2006; Rönnlund, Nyberg, Bäckman, & Nilsson, 2005; Schaie, 1996). These changes are in full view roughly around the age of 65. Diﬀerent individuals, of course, show substantially diﬀerent levels of performance, and, more importantly, between-person diﬀerences in change appear in old age (DeFrias, Lövdén, Lindenberger, & Nilsson, 2007). Together, these ﬁndings draw a chart of the cognitive aging terrain that is depicted in Figure 10.1. During younger adulthood, groups of individuals display normal distribution of individual diﬀerences, and individuals travel in parallel. In older age, groups of individuals display mean decline, and individuals starts to display diﬀerences among each other in the amount of change in performance. The age at which a functional impairment threshold (e.g., dementia or impairment in everyday functioning; thick black line) is reached is determined by the individual’s level of performance when entering adulthood (compare Persons 2 and 3) as well as the individual’s amount of change in old age (compare Persons 1 and 2). Prominent potential candidates of brain correlates of these behavioural changes include marked decrements in grey matter volume of, for example, the prefrontal cortex and the hippocampus (Raz et al., 2005), deteriorating white matter integrity that follows an anterior to posterior gradient (Sullivan & Pfeﬀerbaum, 2006), declines in receptor density and concentration of neurotransmitters (e.g., dopamine; Bäckman, Nyberg, Lindenberger, Li, & Farde, 2006; Bäckman & Nyberg, chapter 11, this volume), and negative cerebrovascular alterations (Farkas & Luiten, 2001).