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<div><p>Amyloid precursor protein (APP)-null mice exhibit significant deficits in motor performance, including reduced grip strength and impaired locomotion; however, the underlying neurophysiological mechanisms remain unclear. In this study, we show that conditional knockdown of APP sel...

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Príomhchruthaitheoir:	Miao-Jin Ji (22676552) (author)
Rannpháirtithe:	Tong-Xuan Wu (22676555) (author), Chenhao Tian (10801643) (author), Xiang Cao (298023) (author), Ruyuan Wei (22676558) (author), Yin-Yin Yang (301866) (author), Xinran Meng (11537536) (author), Huanyao Tang (22676561) (author), Tiantao Cui (22676564) (author), Jiao Yang (623531) (author), Xin Tang (134573) (author), Chao Liu (43092) (author)
Foilsithe / Cruthaithe:	2025
Ábhair:	Biochemistry Cell Biology Molecular Biology Neuroscience Physiology Developmental Biology Infectious Diseases mediated sodium currents deep cerebellar nucleus aberrant firing patterns specific app reconstitution cerebellar motor control app deficiency leads electrophysiological analysis revealed 6 channel activity motor performance motor function motor deficits app selectively purkinje cells marked reduction impaired locomotion findings reveal exogenous expression essential role dcn ). conditional knockdown behavioral deficits
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