Accumulations of insoluble deposits of amyloid β-peptide are major pathological hallmarks
of Alzheimer disease. Amyloid β-peptide is derived by sequential proteolytic processing from …

Alzheimer's disease (AD) starts from pure cognitive impairments and gradually progresses
into degeneration of specific brain circuits. Although numerous factors initiating AD have …

Neuronal and synaptic loss is characteristic in many neurodegenerative diseases, such as
frontotemporal dementia and Alzheimer's disease. Recently, we showed that inducing …

Synaptic loss is the cardinal feature linking neuropathology to cognitive decline in
Alzheimer's disease (AD). However, the mechanism of synaptic damage remains …

The impact of inflammation suppressor pathways on Alzheimer's disease (AD) evolution
remains poorly understood. Human genetic evidence suggests involvement of the cardinal …

Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in
Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the …

The amyloid precursor protein (APP) has occupied a central position in Alzheimer's disease
(AD) pathophysiology, in large part due to the seminal role of amyloid-β peptide (Aβ), a …

Synapse loss is the strongest correlate for cognitive decline in Alzheimer's disease. The
mechanisms underlying synapse loss have been extensively investigated using mouse …

Alzheimer's disease (AD) is associated with defects of synaptic connectivity. Such defects
may not be restricted to local neuronal interactions but may extend to long-range brain …

Stem cell transplantation represents a promising therapy for central nervous system injuries,
but its application to Alzheimer's disease (AD) is still limited and the potential mechanism for …