Age-related loss of calbindin from human basal forebrain cholinergic neurons

Neuroreport. 1997 Jul 7;8(9-10):2209-13. doi: 10.1097/00001756-199707070-00024.

Abstract

Loss of basal forebrain cholinergic neurons (BFCN) occurs in many age-related neurological diseases. Although age is the common risk factor in these disorders, no consistent age-related changes have been reported in the human BFCN. We investigated age-related alterations in choline acetyltransferase (ChAT), low-affinity nerve growth factor receptor (p75LNGFR) and calbindin-D28k (CalBP) immunoreactivity in the human BFCN. No significant age-related changes were observed in ChAT or p75LNGFR immunoreactivity. By contrast, normal aging was accompanied by a selective, substantial and significant loss of CalBP immunoreactivity from the BFCN. Other CalBP-positive neurons were unchanged. Loss of the calcium buffering capacity conferred by CalBP may leave the BFCN vulnerable to damage in neurodegenerative disorders.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Aging / metabolism*
  • Calbindin 1
  • Calbindins
  • Choline O-Acetyltransferase / metabolism*
  • Female
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor / metabolism*
  • S100 Calcium Binding Protein G / metabolism*
  • Substantia Innominata / metabolism*

Substances

  • CALB1 protein, human
  • Calbindin 1
  • Calbindins
  • Receptor, Nerve Growth Factor
  • Receptors, Nerve Growth Factor
  • S100 Calcium Binding Protein G
  • Choline O-Acetyltransferase