Alzheimer's disease (AD) may result from the accumulation of amyloid-β (Aβ) peptides in the
brain. The cysteine protease cathepsin B (CatB) is associated with amyloid plaques in AD …

Impaired degradation of amyloid beta (Aβ) peptides could lead to Aβ accumulation, an early
trigger of Alzheimer's disease (AD). How Aβ-degrading enzymes are regulated remains …

Amyloid-β oligomers may cause cognitive deficits in Alzheimer’s disease by impairing
neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine …

Synapses between engram cells are believed to be substrates for memory storage, and the
weakening or loss of these synapses leads to the forgetting of related memories. We found …

Adult neurogenesis regulates plasticity and function in the hippocampus, which is critical for
memory and vulnerable to Alzheimer's disease (AD). Promoting neurogenesis may improve …

Progranulin (PGRN) is a widely expressed secreted protein that is linked to inflammation. In
humans, PGRN haploinsufficiency is a major inherited cause of frontotemporal dementia (…

Aberrant microglial activation has been proposed to contribute to the cognitive decline in
Alzheimer disease (AD), but the underlying molecular mechanisms remain enigmatic. …

Alzheimer’s disease (AD) is the most prevalent dementia, pathologically featuring abnormal
accumulation of amyloid-β (A β) and hyperphosphorylated tau, while sleep, divided into …

Microglia continuously survey the brain parenchyma and actively shift status following
stimulation. These processes demand a unique bioenergetic programme; however, little is known …

Amyloid β (Aβ) oligomer-induced aberrant neurotransmitter release is proposed to be a
crucial early event leading to synapse dysfunction in Alzheimer’s disease (AD). In the present …