ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026
Kat5 cKO mouse replicates biological domain signatures associated with Alzheimer's disease.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionAlzheimer's disease (AD) can be caused by autosomal-dominant familial Alzheimer's disease (FAD) mutations in amyloid precursor protein (APP) or presenilin-1 and 2, which form an enzyme substrate complex. KAT5 binds to the APP intracellular domain. Recent reports of decreased γ-secretase activity in FAD mutants support KAT5 membrane sequestration.
methodsWe compare the hippocampal transcriptome profiles of the Kat5 brain-specific knockout (KO) mouse to multiple AD datasets through alignment with the TREAT-AD AD biological domains. We examine KAT5 subcellular localization in human wild-type and AD neurons.
resultsThe Kat5 KO mouse demonstrates downregulation of synaptic genes, metabolic pathways, and upregulation of DNA replication and repair, cell cycle, and immune response genes. We see similar profiles in Kat5 and comparative AD datasets. KAT5 is restricted to the cytosol in human AD neurons. DISCUSSION: This analysis supports the hypothesis that KAT5 nuclear signaling downstream of APP cleavage plays a pivotal role in neuronal homeostasis.
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