Aging of the brain

Paul Luiten, C. Nyakas, Ulrich Eisel, Eddy van der Zee

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

An increasing number of persons live for nine or more decades and enjoy the benefits of a well-functioning brain until the end of their life. In that respect, the cognitive performance in later life and the quality maintenance of the brain are amazing biological phenomena. Since most nerve cells are generated during pregnancy and have to survive an active lifetime, the brain has to be endowed with a maintenance machinery of surprising long-term quality. During successful, that is, non-pathological, aging in most brain regions, there is very little or no evidence for a decrease in numbers of neurons. In some brain structures, a limited reduction of nerve cells may occur, but it is generally conceived that aging and aging-related cognitive impairments are not the result of massive cell loss but rather the result of synaptic changes, receptor dysfunction or signaling deficits, and metabolic decline. Besides, nerve cell loss during normal aging may be compensated by synaptogenesis, dendritic branching, or in certain brain structures like dentate gyrus by neurogenesis from progenitor stem cells. Yet most human individuals suffer from a mild but life-disturbing condition we call agingrelated memory impairment (AMI). In this chapter, some of the mechanisms will be shortly explored that are considered to be causal to non-pathological deterioration of cognitive faculties. In particular several cellular and molecular neuronal changes will be addressed that occur during aging, the consequences for interneuronal communication and membrane potential, the blood supply to the brain and cerebrovascular condition, and some observations on the protective neuroimmune system of the brain.

Original languageEnglish
Title of host publicationNeuroscience in the 21st Century
Subtitle of host publicationFrom Basic to Clinical, Second Edition
PublisherSpringer New York
Pages2755-2789
Number of pages35
ISBN (Electronic)9781493934744
ISBN (Print)9781493934737
DOIs
Publication statusPublished - Jan 1 2016

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Keywords

  • 5-hydroxytryptamine
  • Abolishment of LTP
  • Afterhyperpolarization (AHP)
  • Aging-related memory impairment (AMI)
  • Amyloid precursor protein (APP)
  • Axonal aberrations
  • Axonal aberrations
  • BDNF (brain-derived neurotrophic factor)
  • Blood flow in
  • Brain aging
  • Brain microvessels
  • Calcium homeostasis
  • CAMKIV gene
  • Cerebral blood flow
  • Changes of
  • Cholesterol
  • Cognitive dysfunction
  • Cortical microvascular decline
  • Degenerative changes
  • Gamma-aminobutyric acid (GABA)
  • Hippocampal volumetric loss
  • Innate inflammatory system
  • Memory impairment
  • Microglia
  • Morris water maze (MWM)
  • Nervous tissue
  • Neuroinflammatory processes
  • Neuronal loss
  • Neuronal membrane
  • Neurotransmitter serotonin
  • Neurotransmitter systems
  • Synaptic plasticity
  • Synaptic plasticity
  • Voltage-dependent calcium channels (VDCC)

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)
  • Agricultural and Biological Sciences(all)

Cite this

Luiten, P., Nyakas, C., Eisel, U., & van der Zee, E. (2016). Aging of the brain. In Neuroscience in the 21st Century: From Basic to Clinical, Second Edition (pp. 2755-2789). Springer New York. https://doi.org/10.1007/978-1-4939-3474-4_84