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Chromatin structure in dementia.

D R McLachlan, P N Lewis, W J Lukiw

    Annals of Neurology
    |April 1, 1984
    PubMed
    Summary
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    Alzheimer's disease is linked to altered chromatin structure, specifically increased linker histones (H1o, H1oo) in brain cell nuclei. This change, unlike in other neurodegenerative diseases, may serve as a potential biomarker for Alzheimer's.

    Area of Science:

    • Neuroscience
    • Molecular Biology
    • Biochemistry

    Background:

    • Alzheimer's disease (AD) is a progressive neurodegenerative disorder.
    • Chromatin structure plays a crucial role in gene regulation within brain cells.
    • Alterations in chromatin may underlie the pathogenesis of neurodegenerative diseases.

    Purpose of the Study:

    • To investigate potential changes in chromatin structure in the neocortex of Alzheimer's disease patients.
    • To determine if specific histone modifications are associated with Alzheimer's disease.
    • To explore the potential of chromatin alterations as a biomarker for Alzheimer's disease.

    Main Methods:

    • Nuclei were extracted from the neocortex of Alzheimer's disease patients and age-matched controls.
    • Micrococcal nuclease digestion was used to release chromatin fragments, including dinucleosomes.

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  • Histone content and salt-induced release from chromatin were analyzed.

    • Main Results:

    • Nuclei from Alzheimer's disease patients showed an increased presence of linker histones H1o and H1oo in dinucleosomes.
    • These specific histone changes were not observed in other neurodegenerative diseases, except for an increase in H1 in Pick's disease.
    • Histones from Alzheimer's disease patients exhibited greater resistance to salt-induced release from chromatin compared to controls.

    Conclusions:

    • An alteration in chromatin structure, marked by specific changes in linker histones, is associated with Alzheimer's disease.
    • These findings suggest that chromatin structural changes may serve as a potential biomarker for Alzheimer's disease.
    • The observed resistance of histones to salt-induced release further supports a distinct chromatin state in Alzheimer's disease.