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Reducing Endogenous Tau Ameliorates Amyloid B-Induced Deficits in an Alzheimer's Disease Mouse Model
Oleh:
Roberson, Erik D.
;
Scearce-levie, Kimberly
;
Palop, Jorge J.
;
Yan, Fengrong
;
Cheng, Irene H.
;
WU, Tiffany
;
Gerstein, Hilary
;
Yu, Gui-Qiu
;
Mucke, lennart
Jenis:
Article from Bulletin/Magazine
Dalam koleksi:
SCIENCE (keterangan: ada di Proquest) vol. 316 no. 5825 (May 2007)
,
page 750.
Topik:
Biomedicine
Ketersediaan
Perpustakaan FK
Nomor Panggil:
S01.K.2007.05
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
Many potential treatments for Alzheimer's disease target amyloid-B peptides (AB), which are widely presumed to cause the disease. The microtubule-associated protein tau is also involved in the disease, but it is unclear whether treatments aimed at tau could block AB-induced cognitive impairments. Here, we found that reducing endogenous tau levels prevented behavioral deficits in transgenic mice expressing human amyloid precursor protein, without altering their high AB levels. Tau reduction also protected both transgenic and nontransgenic mice against excitotoxicity. Thus, tau reduction can block AB- and excitotoxin-induced neuronal dysfunction and may represent an effective strategy for treating Alzheimer's disease and related conditions.
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