Article citationsMore>>

Sompol, P., Ittarat, W., Tangpong, J., Chen, Y., Doubinskaia, I., Batinic-Haberle, I., Abdul, H.M., Butterfield, D.A. and St Clair, D.K. (2008) A Neuronal Model of Alzheimer’s Disease: An Insight into the Mechanisms of Oxidative Stress-Mediated Mitochondrial Injury. Neuroscience, 153, 120-130.
https://doi.org/10.1016/j.neuroscience.2008.01.044

has been cited by the following article:

• TITLE: The Peripheral Hypotheses of Hypothalamic Aging

  AUTHORS: Zi-Jian Cai

  KEYWORDS: Aging, Suprachiasmatic Nucleus, Slow Wave Sleep, Preoptic Sexually Dimorphic Nucleus, Testosterone, Paraventricular Nucleus

  JOURNAL NAME: Open Access Library Journal, Vol.5 No.3, March 26, 2018

  ABSTRACT: 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.