Neuroscience

Soluble Aβ Is Trouble, Too

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Science  29 Apr 2011:
Vol. 332, Issue 6029, pp. 514
DOI: 10.1126/science.332.6029.514-b
CREDIT: JIN ET AL., PROC. NATL. ACAD. SCI. U.S.A. 108, 5819, (2011)

Cognitive impairments from Alzheimer's disease cause considerable loss of independence among the elderly. Insoluble aggregates of amyloid β-protein (Aβ) characterize brains from persons afflicted with Alzheimer's disease. Accumulating evidence suggests, however, that the neurotoxicity is actually due to the soluble forms of Aβ. Jin et al. have now analyzed one particular soluble form, the Aβ dimer, and its effects on neurons. Aβ dimers isolated from human brain tissue induced degeneration and cytoskeletal disruption in cultured neurons derived from embryonic rat hippocampi. Aβ monomers were not as effective. Antibodies to soluble Aβ diminished the toxic effects on neurons, lending support to an immunotherapy strategy currently in clinical trials. Soluble Aβ mediated its effects at least in part through tau, which drives the formation of the neurofibrillary tangles that are also a hallmark of Alzheimer's disease pathology.

Proc. Natl. Acad. Sci. U.S.A. 108, 5819, (2011).

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