Aggregates of β-amyloid peptide (βAP), the main constituent of amyloid plaques in Alzheimer's brain, kill neurons by a not yet defined mechanism, leading to apoptotic death. Here, we report that both full-length βAP(1–40) or (1–42) and its active fragment βAP(25–35) act as...
Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microglia. In Alzheimer's disease, microglia cluster around beta-amyloid deposits, suggesting that these cells are important for amyloid plaque formation, maintenance and/or clearance. We crossed two distinct APP ...
Nevertheless, it is clear from the obtained data that fibril formation is not beneficial to the affected cells and causes significant toxicity. This conclusion is consistent with histological observations that amyloid plaques within the brain are typically surrounded by halos of altered neuronal activity...
Amyloid β protein (Aβ) is the main component of neuritic plaques in Alzheimer’s disease (AD), and its accumulation has been considered as the molecular driver of Alzheimer’s pathogenesis and progression. Aβ has been the prime target for the development of AD therapy. However, the repeate...
However, it is still unclear what causes autophagic dysfunction in neurons and how it contributes to disease progression. Moreover, the role of autophagy in microglia, the innate immune cell and phagocyte of the CNS, has not been explored. We hypothesized that autophagy in microglia in AD is ...
The principal pathological features of Alzheimer's disease (AD), comprised of neurofibrilary tangles and amyloid plaques, are posited by the amyloid cascade hypothesis [1–3] to be pivotal in the clinical manifestations (impaired memory and cognition, dementia) of the disease. Current marketed ther...
The role of amyloid precursor protein (APP) as the precursor protein of the β-amyloid peptide, which accumulates in extracellular plaques in Alzheimer's disease (AD), is well established. By contrast, its physiological function is largely unresolved. Recent data suggest it functions as a kinesin...
In Alzheimer disease, the peptide amyloid-β (Aβ) and the protein tau aggregate to form plaques and tangles, respectively, which comprise the histopathological hallmarks of this disease. This Review discusses the complexity of Aβ biogenesis, trafficking, post-translational modifications and ...
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The dysfunctional accumulation of amyloid beta (Aβ) plaques in neuronal cells is widely regarded as a hallmark sign of Alzheimer's disease (AD). However, the mechanisms by which Aβ causes the rampant apoptosis that leads to the characteristic memory loss and dementia observed in AD patients ...