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Neuronal apoE4 induces early hyperexcitability in select populations of hippocampal neurons by altering Nell2 expression

Jang, S.-S.; Tabuena, D. R.; Grone, B.; Yip, O.; Blumenfeld, J.; Koutsodendris, N.; Ding, L.; Xu, Q.; Yoon, S. Y.; Huang, Y.; Zilberter, M.

2023-08-29 neuroscience
10.1101/2023.08.28.555153 bioRxiv
Show abstract

The full impact of apolipoprotein E4 (APOE4), the strongest genetic risk factor for Alzheimers disease (AD), on neuronal and network function remains unclear. We found hippocampal region-specific network hyperexcitability in young APOE4 knock-in (E4-KI) mice which predicted cognitive deficits at old age. Network hyperexcitability in young E4-KI mice was mediated by hippocampal region-specific subpopulations of smaller and hyperexcitable neurons that were eliminated by selective removal of neuronal APOE4. Aged E4-KI mice exhibited hyperexcitable granule cells, a progressive inhibitory deficit, and E/I imbalance in the dentate gyrus, exacerbating hippocampal hyperexcitability. Single-nucleus RNA-sequencing revealed neuronal cell type-specific and age-dependent transcriptomic changes, including Nell2 overexpression in E4-KI mice. Reducing Nell2 expression in specific neuronal types of E4-KI mice with CRISPRi rescued their abnormal excitability phenotypes, implicating Nell2 overexpression as a cause of APOE4-induced hyperexcitability. These findings highlight the early transcriptomic and electrophysiological alterations underlying APOE4-induced hippocampal network dysfunction and its contribution to AD pathogenesis with aging.

Published in Nature Aging (predicted rank #21) · training set

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