It is well known that the hypothalamic changes in control of hormones determine the chronological
sequence of aging in mammals. For decades, it has
been demonstrated in humans that the hypothalamic nuclei manifest heterogeneity
in degeneration during aging, with the neuron number decreasing in both the
suprachiasmatic nucleus (SCN) and
the preoptic sexually dimorphic nucleus (SDN-POA) in the process of senescence, while the neuron number remains unchanged in the paraventricular nucleus (PVN). Recently, it was newly hypothesized some
peripheral mechanisms responsible for the senescent changes of the hypothalamic
nuclei. It was proposed by Cai that the decrease in slow-wave sleep (SWS) caused the
degeneration of the suprachiasmatic nucleus
(SCN). Besides, when reviewing the proposal by the European people in
television about the senescent pathway for male reproduction on the
degeneration of hypothalamic preoptic area by the common knowledge of reduction
of sperm production from adipose accumulation in the middle/old age, it was as
well demonstrated that the reduced testosterone level from the increased body fat caused the degeneration of the
male preoptic sexually dimorphic nucleus (SDN-POA). It seems both the
activity-dependent and hormonal regulation of the neuronal numbers are involved in the mechanisms
causing the senescence of the hypothalamic nuclei. It is further pointed out
that the paraventricular nucleus (PVN) maintaining its neuronal number unchanged in aging may cause many
cellular and molecular changes of aging from chronic stress. It is expected that these
preliminary considerations could elicit more investigations on the other
peripheral causes for the hypothalamic aging, such as the cholesterol, hypertension, and so on.
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