Neuroimaging of the aging brain: introduction to the special issue of neuropsychology review.
Neuroimaging of the aging brain: introduction to the special issue of neuropsychology review.
复制标题
衰老大脑的神经影像学：神经心理学评论特刊简介。
DOI：
10.1007/s11065-014-9269-2
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发表时间：
2014
影响因子：
5.8
通讯作者：
Fama,Rosemary
中科院分区：
文献类型：
--
作者：
Lockhart,Samuel;DeCarli,Charles;Fama,Rosemary
Everyone knows what cognitive aging is, to borrow from William James’ famous definition of attention (James 1890). Cognitive aging is a gradual, late-life decline in cognitive performance, experienced to a degree by most individuals fortunate to reach old age (Grady 2008). Decades of scientific research have shown that there exist age-correlated deficits both in basic cognitive processes (such as speed of processing) and in higher-order cognitive functions, particularly episodic memory (ability to recall events) and cognitive control (ability to control our behaviors). Cognitive aging research also indicates that while some functions decline, others remain relatively intact and may even improve with age (such as semantic knowledge (Grady and Craik 2000; Park and Reuter-Lorenz 2009; Salthouse 2004, 2009)). Still, relatively subtle declines in cognitive performance—for example, in memory and executive functions—are frequently observed in rigorous studies of older adults without clinical conditions. This phenomenon of age-associated cognitive declines, unrelated to detectable clinical processes and distinct from Mild Cognitive Impairment (MCI), is often termed “normal” or “healthy cognitive aging,” and these elders are considered “cognitively normal” or “cognitively healthy older adults.” Even such mild cognitive declines, however, can affect functionally relevant clinical outcomes related to older age including increasing the rate of hospitalization (Wilson et al. 2014) and predicting poorer medication adherence (Hayes et al. 2009).Brain structural morphology differs with age (DeCarli et al. 2005; Fjell et al. 2013; Head et al. 2008; Raz et al. 1998; Raz et al. 1997, 2005) and accompanies age-related differences in cognition. These differences are regionally specific with the most consistent and notable age-related differences in frontal lobar and medial temporal regions (Buckner 2004; DeCarli et al. 2005; Fjell et al. 2014; Head et al. 2008; Raz et al. 1998). Newer and more technologically sophisticated imaging tools have also identified relevant age-related differences in white matter microstructure which may either underpin gray-matter atrophy differences or accompany such differences (Andrews-Hanna et al. 2007; O’Sullivan et al. 2001; Sullivan et al. 2001; Sullivan and Pfefferbaum 2006, 2007). The notion of agerelated dysfunction of specific brain systems has led to the development of a host of theories aimed at integrating these two apparently related processes. The frontal theory of aging, which is consistent with the known age-related differences in frontal gray matter, is one early example (West 1996). Another theory (Salthouse 1988, 1996, 2000; Salthouse and Lichty 1985) invoked the notion of slowed or degraded signal processing, which is finding greater supportive evidence through the study of white matter microstructure. Of course these are only two of the many theories. As our knowledge of cognitive processes expands, more refined hypotheses such as that of separate and dissociable memory processes related to familiarity and recall as discussed in papers by Schoemaker and colleagues and Koen and Yonelinas in this issue (Schoemaker et al. 2014 and Koen and Yonelinas 2014) are being developed. Novel hypotheses incorporate individual differences in cognitive aging through forms of reserve capacity as discussed in this issue by Reuter-Lorenz and Park (Reuter-Lorenz and Park 2014). These relatively recent hypotheses also have recognized discrete anatomical underpinnings that may be further understood by imaging and physiological techniques on the scientific horizon.
