Lecanemab reduces hippocampal amyloid but fails to rescue pattern separation deficits in humanized APP/APOEε4 mouse models. (Neuroscience 2026) - Sep 27, 2026 - Abstract #PSTR010.07 / V16; Pres time: Nov 14, 2026; 01:00 PM - 05:00 PM; Location: WCC Halls A-C; "The persistence of cognitive impairment despite plaque reduction suggests that hippocampal neurogenic dysfunction, potentially driven or sustained by amyloid pathology, may better explain cognitive deficits than plaque burden alone. This platform provides a human-translatable approach for defining what lecanemab modifies, what remains resistant to treatment, and why amyloid clearance alone may be insufficient for disease modification."
Preclinical • Alzheimer's Disease • CNS Disorders • Cognitive Disorders • MAPT
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W. SHLEL1; A. A. BATALLÁN BURROWES1; A. ARRAR2; L. ROBAYO NOGUERA2; N. YALIKUN3; T. W. SCHMITZ4; M. A. PRADO5; T. J. BUSSEY6; L. M. SAKSIDA7; V. F. PRADO8
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