Viewpoint: Crosstalks between neurofibrillary tangles and amyloid plaque formation.
Since its discovery, the hallmarks of Alzheimer's disease (AD) brain have been recognised as the formation of amyloid plaques and neurofibrillary tangles (NFTs). Mounting evidence has suggested the active interplay between the two pathways. Studies have shown that β-amyloid (Aβ) can be internalized and generated intracellularly, accelerating NFT formation. Conversely, tau elements in NFTs are observed to affect Aβ and amyloid plaque formation. Yet the precise mechanisms which link the pathologies of the two brain lesions remain elusive. In this review, we discuss recent evidence that support five putative mechanisms by which crosstalk occurs between amyloid plaque and NFT formation in AD pathogenesis. Understanding the crosstalks in the formation of AD pathologies could provide new clues for the development of novel therapeutic strategies to delay or halt the progression of AD.
Department of Cell Biology and Anatomy, Southern Alberta Cancer Research and Hotchkiss Brain Institutes, University of Calgary, Alberta, Canada.
Kailie
K
Luan
Jesusa L
JL
Rosales
Ki-Young
KY
Lee
D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D006801:Humans; D016874:Neurofibrillary Tangles / Q000473:pathology*; D058225:Plaque, Amyloid / Q000473:pathology*; D016875:tau Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology
D016229:Amyloid beta-Peptides; D016875:tau Proteins