Asp664 cleavage of amyloid precursor protein induces tau phosphorylation by decreasing protein phosphatase 2A activity

Importance of the Caspase Cleavage Site in Amyloid-β Protein Precursor

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PP2A Regulates Tau Phosphorylation Directly and also Indirectly via Activating GSK-3β

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Aβ Accelerates the Spatiotemporal Progression of Tau Pathology and Augments Tau Amyloidosis in an Alzheimer Mouse Model

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Phosphorylation of Tau at Thr212, Thr231, and Ser262Combined Causes Neurodegeneration

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Many Neuronal and Behavioral Impairments in Transgenic Mouse Models of Alzheimer's Disease Are Independent of Caspase Cleavage of the Amyloid Precursor Protein

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A  Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines

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Caspase activation precedes and leads to tangles

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Caspase-3 triggers early synaptic dysfunction in a mouse model of Alzheimer's disease

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Caspase activation without apoptosis: insight into Aβ initiation of neurodegeneration

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Biguanide metformin acts on tau phosphorylation via mTOR/protein phosphatase 2A (PP2A) signaling

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Mechanism of cytotoxicity mediated by the C31 fragment of the amyloid precursor protein

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Advances in tau-focused drug discovery for Alzheimer's disease and related tauopathies

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Amyloid- 42 signals tau hyperphosphorylation and compromises neuronal viability by disrupting alkylacylglycerophosphocholine metabolism

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Tau phosphorylation: the therapeutic challenge for neurodegenerative disease

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Alzheimer's disease-type neuronal tau hyperphosphorylation induced by Aβ oligomers

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