Morphological alterations in the amygdala and hippocampus of mice during ageing

Eur J Neurosci. 2002 Dec;16(12):2434-40. doi: 10.1046/j.1460-9568.2002.02405.x.

Abstract

Declines in memory function and behavioural dysfunction accompany normal ageing in mammals. However, the cellular and morphological basis of this decline remains largely unknown. It was assumed for a long time that cell losses in the hippocampus accompany ageing. However, recent stereological studies have questioned this finding. In addition, the effect of ageing is largely unknown in another key structure of the memory system, the amygdala. In the present study, we have estimated neuronal density and total neuronal numbers as well as density of fragments of degenerated axons in different hippocampal subfields and amygdaloid nuclei. Comparisons were made among aged (21-26 months old) mice and normal adult littermates (8 months old). No significant volume loss occurs in the hippocampus of aged mice. Small but insignificant reductions in total neuronal numbers were found in the hippocampus and in the amygdaloid nuclei. In contrast to the mild effects of ageing upon neuronal numbers, fragments of degenerated axons were increased in both hippocampus and amygdala of aged mice. These data suggest that ageing does not induce prominent cell loss in the hippocampus or amygdala, but leads to degeneration of axons that innervate these forebrain structures. Thus, mechanisms underlying age-related dysfunction depend on parameters other than neuronal numbers, at least in the hippocampal formation and the amygdala.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Afferent Pathways / pathology*
  • Afferent Pathways / physiopathology
  • Aging / pathology*
  • Amygdala / pathology*
  • Amygdala / physiopathology
  • Animals
  • Axons / pathology*
  • Cell Count
  • Hippocampus / pathology*
  • Hippocampus / physiopathology
  • Male
  • Memory Disorders / pathology*
  • Memory Disorders / physiopathology
  • Mice
  • Wallerian Degeneration / etiology
  • Wallerian Degeneration / pathology*
  • Wallerian Degeneration / physiopathology