What is it about?

Alzheimer’s disease is a progressive, irreversible neurodegenerative disorder, characterized by gradual decline of mental faculties, including learning capacity, emotional and behavioral alterations, serious decline of motor skills, and dysfunction of the autonomic nervous system with disruption of circadian rhythms. Among the potential modifiable risk factors, diabetes and obesity may play a considerable role in the pathogenetic background of the disease. We describe some of the morphological alterations of the hypothalamic nuclei in early cases of Alzheimer’s disease, using silver impregnation techniques and electron microscopy. The morphological and morphometric study revealed substantial decrease of the neuronal population, which was particularly marked in the suprachiasmatic, the supraoptic, and the paraventricular nuclei of the hypothalamus. The silver staining demonstrated an obvious shortage of the dendritic arborization of neurons, associated with marked spinal pathology and axonal dystrophy. It must be underlined that Alzheimer’s pathology, such as neuritic plaques and neurofibrillary degeneration, was minimal in the hypothalamus in comparison with other cortical and subcortical areas of the brain. Mitochondrial alterations and fragmentation of Golgi complex were observed by electron microscopy in a substantial number of neurons and astrocytes in the hypothalamic nuclei. The hypothalamic pathology may be related to instability of autonomic regulation which occurs gradually in Alzheimer’s disease.

Featured Image

Why is it important?

The hypothalamic pathology may be related to instability of autonomic regulation which occurs gradually in Alzheimer’s disease.

Perspectives

The support of the autonomic nervous system is important even from the initial stages of Alzheimer's disease

Professor Stavros J Baloyannis or Balogiannis or Balojannis or Baloyiannis or Mpalogiannis
Aristotle University of Thessaloniki

Read the Original

This page is a summary of: The Hypothalamus in Alzheimer’s Disease, December 2018, IntechOpen,
DOI: 10.5772/intechopen.81475.
You can read the full text:

Read

Contributors

The following have contributed to this page