Kempermann Gerd
German Center for Neurodegenerative Diseases (DZNE) Dresden and Center for Regenerative Therapies Dresden (CRTD), Technische Universität Dresden, 01307 Dresden, Germany.
Cold Spring Harb Perspect Biol. 2015 Nov 2;7(11):a018929. doi: 10.1101/cshperspect.a018929.
Age and activity might be considered the two antagonistic key regulators of adult neurogenesis. Adult neurogenesis decreases with age but remains present, albeit at a very low level, even in the oldest individuals. Activity, be it physical or cognitive, increases adult neurogenesis and thereby seems to counteract age effects. It is, thus, proposed that activity-dependent regulation of adult neurogenesis might contribute to some sort of "neural reserve," the brain's ability to compensate functional loss associated with aging or neurodegeneration. Activity can have nonspecific and specific effects on adult neurogenesis. Mechanistically, nonspecific stimuli that largely affect precursor cell stages might be related by the local microenvironment, whereas more specific, survival-promoting effects take place at later stages of neuronal development and require the synaptic integration of the new cell and its particular synaptic plasticity.
年龄和活动可能被视为成体神经发生的两个相互拮抗的关键调节因子。成体神经发生随年龄增长而减少,但即使在最年长的个体中也依然存在,尽管水平极低。无论是身体活动还是认知活动,都会增加成体神经发生,从而似乎抵消了年龄的影响。因此,有人提出,成体神经发生的活动依赖性调节可能有助于某种“神经储备”,即大脑补偿与衰老或神经退行性变相关的功能丧失的能力。活动对成体神经发生可产生非特异性和特异性影响。从机制上讲,主要影响前体细胞阶段的非特异性刺激可能与局部微环境有关,而更具特异性的促存活效应则发生在神经元发育的后期阶段,并且需要新细胞的突触整合及其特定的突触可塑性。