絞り込み

オススメ書籍

15543

広告

【日病薬関東ブロック】問題解決能力が重要に‐6年制でシンポ - 薬事日報

【日病薬関東ブロック】問題解決能力が重要に‐6年制でシンポ薬事日報日本病院薬剤師会関東ブロック学術大会が8月30、31の両日、さいたま市で開かれた。学術大会では...

  1. 患者の副反応を追跡調査‐田村厚労相、HP...
  2. 【新製品】低刺激洗浄料「ミノン」シリーズ...
  3. アメリカに渡った日本人起業家が見た、日米...
  4. STAP現象「可能性ある」という専門家の...

ニュース一覧

Inflammatory Pathways in Parkinson's Disease; A BNE Microarray Study.

著者 Durrenberger PF , Grünblatt E , Fernando FS , Monoranu CM , Evans J , Riederer P , Reynolds R , Dexter DT
Parkinsons Dis.2012 ; 2012():214714.
この記事をPubMed上で見るPubMedで表示
この記事をGoogle翻訳上で見る Google翻訳で開く

Centre for Neuroscience, Division of Experimental Medicine, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.

スターを付ける スターを付ける     (144view , 1users)
  • このエントリーをはてなブックマークに追加

Full Text Sources

Miscellaneous

The aetiology of Parkinson's disease (PD) is yet to be fully understood but it is becoming more and more evident that neuronal cell death may be multifactorial in essence. The main focus of PD research is to better understand substantia nigra homeostasis disruption, particularly in relation to the wide-spread deposition of the aberrant protein α-synuclein. Microarray technology contributed towards PD research with several studies to date and one gene, ALDH1A1 (Aldehyde dehydrogenase 1 family, member A1), consistently reappeared across studies including the present study, highlighting dopamine (DA) metabolism dysfunction resulting in oxidative stress and most probably leading to neuronal cell death. Neuronal cell death leads to increased inflammation through the activation of astrocytes and microglia. Using our dataset, we aimed to isolate some of these pathways so to offer potential novel neuroprotective therapeutic avenues. To that effect our study has focused on the upregulation of P2X7 (purinergic receptor P2X, ligand-gated ion channel, 7) receptor pathway (microglial activation) and on the NOS3 (nitric oxide synthase 3) pathway (angiogenesis). In summary, although the exact initiator of striatal DA neuronal cell death remains to be determined, based on our analysis, this event does not remain without consequence. Extracellular ATP and reactive astrocytes appear to be responsible for the activation of microglia which in turn release proinflammatory cytokines contributing further to the parkinsonian condition. In addition to tackling oxidative stress pathways we also suggest to reduce microglial and endothelial activation to support neuronal outgrowth.
PMID: 22548201 [PubMed - in process]
印刷用ページを開く Endnote用テキストダウンロード