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. Author manuscript; available in PMC: 2014 May 5.
Published in final edited form as: Annu Rev Genet. 2013;47:601–623. doi: 10.1146/annurev-genet-110711-155524

Table 2.

Some possible explanations for late-onset neurodegeneration

1. Mitochondrial DNA mutations (26, 125)
2. Oxidative modifications of DNA, lipids, or proteins (87, 100)
3. Impaired autophagy (133)
4. Altered apoptosis (201)
5. Posttranslational chemical modification (201)
6. Modified innate immunity (186)
7. Accumulation of exogenous toxins, such as heavy metals, alcohol, drugs, and hormones (19)
8. Concomitant conditions, such as atherosclerosis (96)
9. RNA-DNA differences (107)
10. Chaperone malfunction (111)
11. Somatic mutations (100)
12. Altered regulation of transcription (8)
13. Haploinsufficiency (30, 153)
14. Postinfectious syndromes of the central nervous system, including late polio, subacute sclerosing leukoencephalitis, postencephalitic Parkinson’s disease, and Lyme disease (59, 89, 203)
15. Modifier genes, such as apolipoprotein E and LRRK2 (17, 25)
16. Polyglutamine expansions (101, 196)
17. Dipeptide repeat proteins (127)
18. Cu2+ binding to expanded PrP octarepeat region (177)
19. Prion formation and accumulation (134, 144)