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Culling Less Fit Neurons Protects against Amyloid-β-Induced Brain Damage and Cognitive and Motor Decline.

Abstract：

:Alzheimer's disease (AD) is the most common form of dementia, impairing cognitive and motor functions. One of the pathological hallmarks of AD is neuronal loss, which is not reflected in mouse models of AD. Therefore, the role of neuronal death is still uncertain. Here, we used a Drosophila AD model expressing a secreted form of human amyloid-β42 peptide and showed that it recapitulates key aspects of AD pathology, including neuronal death and impaired long-term memory. We found that neuronal apoptosis is mediated by cell fitness-driven neuronal culling, which selectively eliminates impaired neurons from brain circuits. We demonstrated that removal of less fit neurons delays β-amyloid-induced brain damage and protects against cognitive and motor decline, suggesting that contrary to common knowledge, neuronal death may have a beneficial effect in AD.

journal_name

Cell Rep

journal_title

Cell reports

authors

Coelho DS,Schwartz S,Merino MM,Hauert B,Topfel B,Tieche C,Rhiner C,Moreno E

doi

10.1016/j.celrep.2018.11.098

subject

Has Abstract

pub_date

2018-12-26 00:00:00

pages

3661-3673.e3

issue

13

issn

2211-1247

pii

S2211-1247(18)31889-8

journal_volume

25

pub_type

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