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30 reviewsSUMMARYAlzheimer’s disease (AD) is initiated by amyloid-beta (Aβ) accumulation in the neocortex; however, thecortical layers and neuronal cell types first susceptible to Aβ remain unknown. Using in vivo two-photonCa2+ imaging in the visual cortex of AD mouse models, we found that cortical layer 5 neurons displayedabnormally prolonged Ca2+ transients before substantial plaque formation. Neuropixels recordings revealedthat these abnormal transients were associated with reduced spiking and impaired visual tuning of parvalbumin (PV)-positive fast-spiking interneurons (FSIs) in layers 5/6, whereas PV-FSIs in superficial layers remained unaffected. These dysfunctions occurred alongside a deep-layer-specific reduction in neuronal pentraxin 2 (NPTX2) within excitatory neurons, decreased GluA4 in PV-FSIs, and fewer excitatory synapses ontoPV-FSIs. Notably, NPTX2 overexpression increased excitatory input onto layers 5/6 PV-FSIs and rectifiedtheir spiking activity. Thus, our findings reveal an early selective impairment of deep cortical layers 5/6 inAD models and identify deep-layer PV-FSIs as therapeutic targets.
