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Some antioxidants, for example, may theoretically interfere with the controlled oxidative environment that supports certain stages of follicular development

Increasing p16INK4a expression decreases forebrain progenitors and neurogenesis during ageing

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50,51 This energy deficiency triggers the collapse of the mitochondrial membrane potential ( m ) and the release of proapoptotic factors, which activate the caspase cascade and induce apoptosis or senescence

Other glutamate receptors, including kainate receptors (KARs) and metabotropic glutamate receptors, can control long-term and short-term synaptic plasticity [76, 77]