Despite considerable progress in the understanding of its neuropathology, Alzheimer's
disease (AD) remains a complex disorder with no effective treatment that counteracts the …

Evidence from neuropathological, genetic, animal model, and biochemical studies has
indicated that the accumulation of amyloid‐beta (Aβ) is associated with, and probably …

Alzheimer's disease (AD) manifests as a progressive loss in memory, cognition, and
language that is commonly associated with elevated levels of amyloid-beta (A𝛽) peptide …

It is essential to identify the neuronal mechanisms of Alzheimer's Disease (AD)-associated
neuropsychiatric symptoms, eg, apathy, before improving the life quality of AD patients …

The hallmarks of Alzheimer's disease (AD) pathology include senile plaques accumulation
and neurofibrillary tangles, which is thought to underlie synaptic failure. Recent evidence …

Amyloid-beta (Aβ) and tau protein are both involved in the pathogenesis of Alzheimer's
disease. Aβ produces synaptic deficits in wild-type mice that are not seen in Mapt−/− mice …

In our previous studies, phosphorylation‐dependent tau mislocalization to dendritic spines
resulted in early cognitive and synaptic deficits. It is well known that amyloid beta (Aβ) …

Pathological accumulation of Aβ oligomers has been linked to neuronal networks
hyperexcitability, potentially underpinned by glutamatergic AMPA receptors (AMPARs) …

Glutamate excitotoxicity has long been related to Alzheimer's disease (AD) pathophysiology,
and it has been shown to affect the major AD-related hallmarks, amyloid-β peptide (Aβ) …

Alzheimer's disease (AD) is a devastating neurodegenerative disorder that impairs memory
and causes cognitive and psychiatric deficits. New evidences indicate that AD is …