Titlebook: Etiopathogenesis; Yoshikuni Mizuno,Donald B. Calne (Director),R. Hor Book 1994 Birkh?user Boston 1994 cell.mortality.neurology.pathology.u

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書目名稱Etiopathogenesis影響因子(影響力)




書目名稱Etiopathogenesis影響因子(影響力)學科排名




書目名稱Etiopathogenesis網(wǎng)絡公開度




書目名稱Etiopathogenesis網(wǎng)絡公開度學科排名




書目名稱Etiopathogenesis被引頻次




書目名稱Etiopathogenesis被引頻次學科排名




書目名稱Etiopathogenesis年度引用




書目名稱Etiopathogenesis年度引用學科排名




書目名稱Etiopathogenesis讀者反饋




書目名稱Etiopathogenesis讀者反饋學科排名

犬儒主義者

Growth Factors in Parkinson’s Diseaseogical role and administration may have therapeutic effects (Hefti et al., 1989, 1990). Particular attention has been focused on Alzheimer’s disease (AD) and Parkinson’s disease (PD), the former because of the importance of nerve growth factor (NGF) in maintaining basal forebrain cholinergic neurons

教唆

Onerous

Neuroepidemiology of Parkinson’s Disease: Environmental InfluencesEtiological hypotheses need to be consistent with known epidemiologic factors, and descriptive epidemiologic observations may generate a new hypothesis. Analytic epidemiology seeks to identify risk factors that could lead to clues for causal associations with the disease.

Suggestions

Discussion: Session 8 — 9 A.M. - 8 February 1993. Specifically he wondered how many cases of Alzheimer’s disease would fall into the category of genetically determined familial Alzheimer’s disease, how many were sporadic cases predominantly caused by environmental factors, and how many cases would fall in between these categories. George-Hyslop t

協(xié)定

Manganese-Induced Neurotoxicity is the twelfth most common element in the earth’s crust and the fourth most widely used metal in the world. Eight million tons of manganese metal are extracted annually, of which 94% is employed in the manufacture of steel. Electrolytic high-temperature reduction converts manganese oxide to ferroma

協(xié)定

晚間

空洞

Jocose

Mitochondrial Dysfunction, Aging, and Huntington’s Diseasezheimer’s disease is advancing age. Huntington’s disease typically has a onset in the thirties and forties. A number of studies show age-dependent increases in mitochondrial DNA deletions, oxidative damage to mitochondrial DNA, and reductions in activities of mitochondrial enzymes.