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Related Experiment Video

Updated: Jan 8, 2026

Abbiategrasso Brain Bank Protocol for Collecting, Processing and Characterizing Aging Brains
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A quantitative electron microscopic study of the ageing human cerebral cortex.

S Rees

    Acta Neuropathologica
    |December 21, 1976
    PubMed
    Summary

    Aging brains show increased dense deposits in oligodendrocytes, but not in neuronal inclusions. This study investigated age-related changes in brain cell inclusions in non-demented individuals.

    Area of Science:

    • Neuroscience
    • Neuropathology
    • Aging Research

    Background:

    • Atypical inclusions in neuronal and glial processes were previously identified in younger adults.
    • The age-related accumulation of these inclusions in the human brain remains largely uncharacterized.

    Purpose of the Study:

    • To investigate whether atypical inclusions and other cellular deposits accumulate with age in the human cerebral cortex.
    • To compare the age-related changes in neuronal processes versus glial cells, specifically oligodendrocytes.

    Main Methods:

    • Quantitative electron microscopy was employed on autopsy samples of frontal and temporal cortex from non-demented individuals aged 70-76 years.
    • Methods mirrored a previous study on younger individuals (15-54 years) to allow for direct age comparison.

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  • Cellular inclusions, dense deposits, corpora amylacea, and senile plaques were quantified.

    • Main Results:

    • The number of atypical inclusions in neuronal processes did not significantly increase with age.
    • A significant age-related increase in dense deposits within oligodendrocyte cell bodies and processes was observed.
    • Corpora amylacea were present in astrocytic processes, consistent with previous findings. Senile plaques were absent.

    Conclusions:

    • Oligodendrocytes, but not neurons, show age-related accumulation of dense deposits in the cerebral cortex.
    • These findings highlight specific cellular changes in aging non-demented brains, distinct from typical dementia pathologies.
    • Further research is warranted to understand the functional implications of these age-associated oligodendrocyte changes.