β₂-Microglobulin coaggregates with Aβ and contributes to amyloid pathology and cognitive deficits in Alzheimer's disease model mice

b2-microglobulin functions as an endogenous NMDAR antagonist to impair synaptic function

Metabolic reprogramming in astrocytes results in neuronal dysfunction in intellectual disability

RAB39B Deficiency Impairs Learning and Memory Partially Through Compromising Autophagy

Overexpression of Human SNX27 Enhances Learning and Memory Through Modulating Synaptic Plasticity in Mice