Neurodegenerative tauopathies characterized by hyperphosphorylated tau include
frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's …

Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins
depends on contributions from surrounding glia. Here we demonstrate that NF-κB signaling in …

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 …

Tauopathies, including frontotemporal dementia (FTD) and Alzheimer's disease (AD), are
neurodegenerative diseases in which tau fibrils accumulate. Recent evidence supports …

Neuronal expression of familial Alzheimer's disease–mutant human amyloid precursor
protein (hAPP) and hAPP-derived amyloid-β (Aβ) peptides causes synaptic dysfunction, …

Tau (MAPT) drives neuronal dysfunction in Alzheimer disease (AD) and other tauopathies.
To dissect the underlying mechanisms, we combined an engineered ascorbic acid …

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

Aging is the predominant risk factor for neurodegenerative diseases. One key phenotype as
the brain ages is an aberrant innate immune response characterized by proinflammation. …

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 …

Activation of microglia is a prominent pathological feature in tauopathies, including Alzheimer’s
disease. How microglia activation contributes to tau toxicity remains largely unknown. …