TREM2 and Risk of Alzheimer’s Disease — Friend or Foe?  

Oleh:

Tanzi, Rudolph E.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The New England Journal of Medicine (keterangan: ada di Proquest) vol. 372 no. 26 (Jun. 2015), page 2564-2565.

Ketersediaan

Perpustakaan FK Nomor Panggil: N08.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Alzheimer’s disease is a genetically complex and heterogeneous disorder. Genomewide association studies aimed at identifying gene variants that influence the risk of Alzheimer’s disease have implicated several innate immunity genes, including those involved in microglial activation, neuroinflammation, and clearance of the toxic peptide amyloid-beta 42 (Aß-42). For example, one of these genes, CD33, encodes a protein that, when active in microglia, inhibits microglial uptake and clearance of Aß-42, thereby promoting the pathological features of Aß-42,1 which are characterized by the accumulation of Aß-42 peptides in plaques. Neurofibrillary tangles, partly made up of the hyperphosphorylated tau protein, constitute another prominent feature of the disease.

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