Jenna M Tarasoff-Conway, Roxana O Carare, Ricardo S Osorio, Lidia Glodzik, Tracy Butler, Els Fieremans, Leon Axel, Henry Rusinek, Charles Nicholson, Berislav V Zlokovic, Blas Frangione, Kaj Blennow, Joël Ménard, Henrik Zetterberg, Thomas Wisniewski, Mony J de Leon
Accumulation of toxic protein aggregates-amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles-is the pathological hallmark of Alzheimer disease (AD). Aβ accumulation has been hypothesized to result from an imbalance between Aβ production and clearance; indeed, Aβ clearance seems to be impaired in both early and late forms of AD. To develop efficient strategies to slow down or halt AD, it is critical to understand how Aβ is cleared from the brain. Extracellular Aβ deposits can be removed from the brain by various clearance systems, most importantly, transport across the blood-brain barrier...
August 2015: Nature Reviews. Neurology