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Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondr...

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondr...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_e4cca8864343441c862cd2169b11e9ee

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

About this item

Full title

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

Publisher

London: Nature Publishing Group UK

Journal title

Nature communications, 2022-08, Vol.13 (1), p.4444-4444, Article 4444

Language

English

Formats

Publication information

Publisher

London: Nature Publishing Group UK

More information

Scope and Contents

Contents

During the early stages of Alzheimer’s disease (AD) in both mouse models and human patients, soluble forms of Amyloid-β 1–42 oligomers (Aβ42o) trigger loss of excitatory synapses (synaptotoxicity) in cortical and hippocampal pyramidal neurons (PNs) prior to the formation of insoluble amyloid plaques. In a transgenic AD mouse model, we observed a sp...

Alternative Titles

Full title

Aβ42 oligomers trigger synaptic loss through CAMKK2-AMPK-dependent effectors coordinating mitochondrial fission and mitophagy

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_doaj_primary_oai_doaj_org_article_e4cca8864343441c862cd2169b11e9ee

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_e4cca8864343441c862cd2169b11e9ee

Other Identifiers

ISSN

2041-1723

E-ISSN

2041-1723

DOI

10.1038/s41467-022-32130-5

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