Molecular neurodegeneration

Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury.

Correction: Mutations in α-synuclein, TDP-43 and tau prolong protein half-life through diminished degradation by lysosomal proteases.

Mutations in a-synuclein, TDP-43 and tau prolong protein half-life through diminished degradation by lysosomal proteases.

Solving neurodegeneration: common mechanisms and strategies for new treatments.

Processing of progranulin into granulins involves multiple lysosomal proteases and is affected in frontotemporal lobar degeneration.

Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1.

Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer's disease.

Proteolytic cleavage of Beclin 1 exacerbates neurodegeneration.

Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture.

Phosphorylation of tau at Y18, but not tau-fyn binding, is required for tau to modulate NMDA receptor-dependent excitotoxicity in primary neuronal culture.

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