Tau, prions and Aβ: the triad of neurodegeneration.
This article highlights the features that connect prion diseases with other cerebral amyloidoses and how these relate to neurodegeneration, with focus on tau phosphorylation. It also discusses similarities between prion disease and Alzheimer's disease: mechanisms of amyloid formation, neurotoxicity, pathways involved in triggering tau phosphorylation, links to cell cycle pathways and neuronal apoptosis. We review previous evidence of prion diseases triggering hyperphosphorylation of tau, and complement these findings with cases from our collection of genetic, sporadic and transmitted forms of prion diseases. This includes the novel finding that tau phosphorylation consistently occurs in sporadic CJD, in the absence of amyloid plaques.
Reiniger
Lilla
L
Division of Neuropathology, Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, WC1N 3BG, London, UK.
Lukic
Ana
A
Linehan
Jacqueline
J
Rudge
Peter
P
Collinge
John
J
Mead
Simon
S
Brandner
Sebastian
S
D016229:Amyloid beta-Peptides / Q000235:genetics / Q000502:physiology*; D000818:Animals; D002453:Cell Cycle / Q000235:genetics / Q000502:physiology; D016923:Cell Death / Q000235:genetics / Q000502:physiology; D006801:Humans; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D010766:Phosphorylation / Q000235:genetics / Q000502:physiology; D011328:Prions / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D016875:tau Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology
D016229:Amyloid beta-Peptides; D011328:Prions; D016875:tau Proteins
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