Endocytic uptake of monomeric amyloid-β peptides is clathrin- and dynamin-independent and results in selective accumulation of Aβ(1–42) compared to Aβ(1–40)

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Affected albumin endocytosis as a new neurotoxicity mechanism of amyloid beta

IJMS, Free Full-Text

Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases, Molecular Neurodegeneration

Frontiers Membrane interaction to intercellular spread of pathology in Alzheimer's disease

The amyloid-β degradation intermediate Aβ34 is pericyte-associated and reduced in brain capillaries of patients with Alzheimer's disease, Acta Neuropathologica Communications

Misfolded protein oligomers: mechanisms of formation, cytotoxic effects, and pharmacological approaches against protein misfolding diseases, Molecular Neurodegeneration

Misfolded amyloid-β-42 impairs the endosomal–lysosomal pathway

Frontiers Role of Clathrin and Dynamin in Clathrin Mediated Endocytosis/Synaptic Vesicle Recycling and Implications in Neurological Diseases

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Alzheimer's disease linked Aβ42 exerts product feedback inhibition on γ-secretase impairing downstream cell signaling

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