| Literature DB >> 24653907 |
Abstract
Aging is one of the most evident biological processes, but its mechanisms are still poorly understood. Studies of cognitive aging suggest that age is associated with cognitive decline; however, there may be individual differences such that not all older adults will experience cognitive decline. That is, cognitive decline is not intrinsic to aging, but there is some heterogeneity. Many researchers have shown that speech recognition declines with increasing age. Some of the age-related decline in speech perception can be accounted for by peripheral sensory problems but cognitive aging can also be a contributing factor. The potential sources of reduced recognition for rapid speech in the aged are reduction in processing time and reduction of the acoustic information in the signal. However, other studies also indicated that speech perception does not decline with age. Cognitive abilities are inherently involved in speech processing. Two cognitive factors that decline with age may influence speech perception performance. The first factor is working memory capacity and the second factor concerns the rate of information processing, defined generally as the speed at which an individual can extract content and construct meaning from a rapid signal. Cognitive function shows the adaptive processes with age which are consistent with the view that the brain itself has potentially a life-long capacity for neural plasticity. Assessing the speech perception difficulty in older adults, cognitive function could be considered in the evaluation and management of speech perception problem.Entities:
Keywords: Aging; Cognition; Plasticity; Speech perception
Year: 2013 PMID: 24653907 PMCID: PMC3936542 DOI: 10.7874/kja.2013.17.2.54
Source DB: PubMed Journal: Korean J Audiol ISSN: 2092-9862
Fig. 1Potential mechanisms responsible for age-related decline in neurogenesis (Adapted from Benedetta A, et al. Aging 2012, according to the Creative Commons license). Proliferating and quiescent neural stem and progenitors cells (NSCs; left column) are indicated by the presence or lack of mitotic spindles, respectively. Proliferating NSCs divide to generate (arrows) additional NSCs or immature neurons (right column). During maturation, many neurons undergo apoptosis (crosses). A: Schematic representation of adult neurogenesis in the young hippocampus. B-E: Schematic representation of adult neurogenesis in the senescent hippocampus. A reduced number of neurons in the senescent hippocampus (B-E) can be explained by an increase in quiescence i.e. a lower proportion of proliferating NSCs (B), a change in NSCs fate i.e. an increase in differentiative at the expense of proliferative and/or gliogenic at the expense of neurogenic division (C), depletion of NSCs by cell death (D), or a higher proportion of newborn neurons undergoing apoptosis (E). Continuous or dashed arrows (A-D) indicate a constant number or decreases in the proportion of proliferating NSCs and neurons generated from the total pool of NSCs, respectively.
Fig. 2Brain regions involved in speech processing in older age (Adapted from Aydelott, et al. Trends in Amplification 2011, with permission from SAGE). Schematic highlights in the left cortical regions involved in speech perception. Antero-ventral (aSTS) and postero-dorsal (pSTS) auditory streams originate from the primary auditory cortices (AC), auditory belt/Heschl's gyrus. The postero-dorsal stream interfaces with the premotor areas and pivots around the inferior parietal cortex (IPC). Object information, such as mapping speech onto semantics, is decoded in the antero-ventral stream to the inferior frontal cortex (IFC; Brodmann's area 44, 45). In the postero-dorsal route, attention- or intention-related changes in the inferior parietal lobule (IPL; Brodmann's area 40) influence the selection of context-dependent action programs in prefrontal cortex and premotor cortex (PMC; Brodmann's area 6) areas. Both routes can be modulated by activity in the dorsolateral prefrontal cortices (PLPFC; Brodmann's area 9, 46). STS: superior temporal sulcus, IFC: inferior frontal cortex, IPL: inferior parietal lobule, DLPFC: dorsolateral prefrontal cortical.