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A bell-shaped dependence between amyloidosis and GABA accumulation in astrocytes in a mouse model of Alzheimer’s disease

Brawek, Bianca, Chesters, Robert, Klement, Daniel, Müller, Julia, Lerdkrai, Chommanad, Hermes, Marina, Garaschuk, Olga·2018·Neurobiology of Aging
DOI 10.1016/j.neurobiolaging.2017.09.028
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Abstract

Functioning at the interface between the nervous and immune systems, in the amyloid-depositing brain, astrocytes become hypertrophic and accumulate around senile plaques. Moreover, hippocampal astrocytes upregulate their γ-aminobutyric acid (GABA) content and enhance tonic inhibition, likely causing local circuit imbalance. It remains, however, unclear whether this effect is hippocampus specific and how it is regulated during disease progression. Here, we studied changes in astrocytic morphology and GABA content in the frontal cortex and dentate gyrus of control and amyloid-depositing mice. Healthy aging was accompanied by a transient increase in astrocytic GABA content at middle age and region-specific alterations of soma size. In contrast, amyloid deposition caused a gradual cortex-accentuated increase in soma size. Importantly, our data uncovered a bell-shaped relationship between the mouse age and astrocytic GABA content in both brain regions. Moreover, in mice carrying an Alzheimer's disease-related mutation in presenilin 1, astrocytes accumulated GABA even in the absence of amyloidosis. These data question the proposed inhibition of astrocytic GABA synthesis as a universal strategy for treating network dysfunction in Alzheimer's disease.

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Crossref · 10.1016/j.neurobiolaging.2017.09.028

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  • Disturbances in glutamatergic and GABAergic systems have been heavily implicated in neurodegenerative pathology.

    “Indeed, disturbances in the glutamatergic and GABAergic systems have been heavily implicated in neurodegenerative pathology [86-88, 123, 126-128], and previous papers have reported an effect of SNX27 depletion on inhibitory synapse function through trafficking of the inhibitory synapse adhesion molecule Neuroligin-2 (NLG2) [77,129].”

    From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [127]

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Metadata

Authors
Brawek, B., Chesters, R., Klement, D., Müller, J., Lerdkrai, C., Hermes, M., & Garaschuk, O.
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2018-01
Volume
61
Pages
187-197
ISSN
0197-4580
DOI
10.1016/j.neurobiolaging.2017.09.028
Cited by
35
References
7
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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