Abstract
During aging, some individuals are resilient to the decline of cognitive functions whereas others are vulnerable. These inter‐individual differences in memory abilities have been associated with differences in the rate of hippocampal neurogenesis measured in elderlies. Whether the maintenance of the functionality of neurons generated throughout adult life is linked to resilience to cognitive aging remains completely unexplored. Using the immediate early gene Zif268, we analyzed the activation of dentate granule neurons born in adult (3‐month‐old), middle‐aged (12‐month‐old), or senescent (18‐month‐old) rats (n = 96) in response to learning when animals reached 21 months of age. The activation of neurons born during the developmental period was also examined. We show that adult‐born neurons can survive up to 19 months and that neurons generated 4, 10, or 19 months before learning, but not developmentally born neurons, are activated in senescent rats with good learning abilities. In contrast, aged rats with bad learning abilities do not exhibit activity‐dependent regulation of newborn cells, whatever their birthdate. In conclusion, we propose that resilience to cognitive aging is associated with responsiveness of neurons born during adult life. These data add to our current knowledge by showing that the aging of memory abilities stems not only from the number but also from the responsiveness of adult‐born neurons.
Highlights
The rapidly growing elderly population and the increasing occurrence of cognitive disorders make the maintenance of “successful” aging a problem of increasing priority in public health [Batles and Batles 1993]
Memory deficits have been associated to the exhaustion of cell genesis: rats with preserved spatial memory produced after learning a higher number of new neurons in comparison with animals with memory impairments
An alteration of adult hippocampal neurogenesis (ANg) has been proposed to be involved in the appearance of spatial relational memory deficits [Abrous et al 2005;Drapeau and Abrous 2008;Klempin and Kempermann 2007]. Supporting this view, we showed that successful aging –i.e. preserved memory functions- is associated with the maintenance of a relatively high neurogenesis level measured after learning whereas pathological (“unsuccessful”) aging –i.e. memory deficits- is linked to exhaustion of neurogenesis [Drapeau et al 2003]
Summary
The rapidly growing elderly population and the increasing occurrence of cognitive disorders make the maintenance of “successful” (or ‘healthy’ or ‘optimal’) aging a problem of increasing priority in public health [Batles and Batles 1993]. Neuropathological events featuring early stages of Alzheimer's disease (AD) and of mild cognitive impairment (MCI) appear in the hippocampus, a key structure in spatial and episodic memory learning and memory. The newly born cells develop into granule neurons that are integrated into functional circuits and play a crucial role in complex forms of learning and memory i.e; pattern separation and relational memory [Aimone et al 2014;Koehl and Abrous 2011]. Both the addition and the elimination of new neurons in young adult rodent before, during or after learning are important for learning, remembering and forgetting [Dupret et al 2007;Trouche et al 2009;Akers et al 2014]
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