Alzheimer's disease (AD) is caused by synaptic and neuronal loss in the brain. One of the
characteristic hallmarks of AD is senile plaques containing amyloid β-peptide (Aβ). Aβ is …

Tau and amyloid beta (Aβ) are the prime suspects for driving pathology in Alzheimer's
disease (AD) and, as such, have become the focus of therapeutic development. Recent …

Alzheimer's disease (AD), the leading cause of dementia worldwide, is characterized by the
accumulation of the β-amyloid peptide (Aβ) within the brain along with hyperphosphorylated …

The amyloid β peptide (Aβ) is a critical initiator that triggers the progression of Alzheimer's
Disease (AD) via accumulation and aggregation, of which the process may be caused by Aβ …

A large body of evidence has implicated Aβ peptides and other derivatives of the amyloid
precursor protein (APP) as central to the pathogenesis of Alzheimer's disease (AD) …

An important pathological feature of Alzheimer's disease (AD) is the presence of
extracellular senile plaques in the brain. Senile plaques are composed of aggregations of …

Alzheimer's disease (AD) is characterized by the deposition of senile plaques (SPs) and
neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are composed of aggregated …

We studied the effect of microtubule-associated tau protein on trafficking of vesicles and
organelles in primary cortical neurons, retinal ganglion cells, and neuroblastoma cells. Tau …

The amyloid precursor protein (APP) is critical in the pathogenesis of Alzheimer's disease.
The question of its normal biological function in neurons, in which it is predominantly located …

Although amyloid‐β peptide (Aβ) is the neurotoxic species implicated in the pathogenesis of
Alzheimer's disease (AD), mechanisms through which intracellular Aβ impairs cellular …