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Aging of the Brain

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Neuroscience in the 21st Century

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 aging-related 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.

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Abbreviations

AD:

Alzheimer’s disease

AHP:

Afterhyperpolarization

AKAP:

A-kinase-anchoring protein

AMI:

Aging-related memory impairment

AMPA:

Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid

ApoE:

Apolipoprotein E

APP:

Amyloid precursor protein

ARA:

Arachidonic acid

Arc:

Activity-regulated cytoskeletal gene

ATP:

Adenosine triphosphate

Aβ:

Amyloid beta

BDNF:

Brain-derived neurotrophic factor

BOLD:

Blood-oxygen level dependent (imaging)

CA1:

Cornu ammonis1 (2,3)

CAMK:

Calcium-calmodulin kinase

CNS:

Central nervous system

DA:

Dopamine

DHA:

Docosahexaenoic acid

fMRI:

Functional magnetic resonance imaging

GABA:

Gamma-aminobutyric acid

GAD:

Glutamic acid decarboxylase

IEG:

Immediate early genes

IL-1:

Interleukin-1 (4, 6, 10)

IP3:

Inositol triphosphate

LPS:

Lipopolysaccharide

LTP:

Long-term potentiation

MWM:

Morris water maze

NF-κB:

Nuclear factor kappa B

NGF:

Nerve growth factor

NMDA:

N-methyl d-aspartate

PFC:

Prefrontal cortex

PIP2:

Phosphatidylinositol-biphosphate

PKB:

Protein kinase B (Akt)

PKCγ:

Protein kinase C gamma

PUFA:

Polyunsaturated fatty acid

RACK:

Receptor for activated C-kinase

TIA:

Transient ischemic attack

TNF:

Tumor necrosis factor

VDCC:

Voltage-dependent calcium channel

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Author information

Authors and Affiliations

  1. Department of Molecular Neurobiology, University of Groningen, Nijenborgh 7, 9747 AG, Groningen, The Netherlands

    Dr. Paul Luiten, Prof. Csaba Nyakas, Prof. Ulrich Eisel & Prof. Eddy van der Zee

Authors
  1. Dr. Paul Luiten
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  2. Prof. Csaba Nyakas
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  3. Prof. Ulrich Eisel
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  4. Prof. Eddy van der Zee
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Corresponding author

Correspondence to Paul Luiten .

Editor information

Editors and Affiliations

  1. Laboratory of Neurobiology and Behavior, The Rockefeller University, New York, NY, USA

    Donald W. Pfaff

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Luiten, P., Nyakas, C., Eisel, U., van der Zee, E. (2013). Aging of the Brain. In: Pfaff, D.W. (eds) Neuroscience in the 21st Century. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-1997-6_84

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