الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Several common themes have driven prevailing notions about neurodegenerative diseases and their underlying etiology. Pathologically, a frequent characteristic of these diseases is the accumulation and aggregation of abnormal or misfolded proteins, as with amyloid-β (Aβ) in Alzheimer‘s disease (AD) (Karran et al., 2011), α-synuclein in Parkinson‘s disease (PD) (Eidson et al., 2017), huntingtin protein in Huntington‘s disease (HD) (Krainc, 2010) and transactive response DNA-binding protein 43 (TDP-43) in frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) (Rademakers et al., 2012). The discovery of genetic mutations causing rare, early onset, familial forms of these diseases, as with theAPP (amyloid precursor protein) gene in AD (Sleegers et al., 2010) and the α-synuclein (SNCA) gene in PD (Hardy, 2010), further focused attention on mechanisms directly connected to disease pathology.