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- W2985002612 startingPage "345" @default.
- W2985002612 abstract "The complexity of neurodegeneration restricts the ability to understand and treat the neurological disorders affecting millions of people worldwide. Therefore, there is an unmet need to develop new and more effective therapeutic strategies to combat these devastating conditions and that will only be achieved with a better understanding of the biological mechanism associated with disease conditions. Recent studies highlight the role of DNA damage, particularly, DNA double-strand breaks (DSBs), in the progression of neuronal loss in a broad spectrum of human neurodegenerative diseases. This is not unexpected because neurons are prone to DNA damage due to their non-proliferative nature and high metabolic activity. However, it is not clear if DSBs is a primary driver of neuronal loss in disease conditions or simply occurs concomitant with disease progression. Here, we provide evidence that supports a critical role of DSBs in the pathogenesis of the neurodegenerative diseases. Among different kinds of DNA damages, DSBs are the most harmful and perilous type of DNA damage and can lead to cell death if left unrepaired or repaired with error. In this review, we explore the current state of knowledge regarding the role of DSBs repair mechanisms in preserving neuronal function and survival and describe how DSBs could drive the molecular mechanisms resulting in neuronal death in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. We also discuss the potential implications of DSBs as a novel therapeutic target and prognostic marker in patients with neurodegenerative conditions." @default.
- W2985002612 created "2019-11-22" @default.
- W2985002612 creator A5004364771 @default.
- W2985002612 creator A5010563838 @default.
- W2985002612 creator A5019225720 @default.
- W2985002612 creator A5031301181 @default.
- W2985002612 date "2019-11-09" @default.
- W2985002612 modified "2023-10-15" @default.
- W2985002612 title "DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases" @default.
- W2985002612 cites W1752089945 @default.
- W2985002612 cites W1783508367 @default.
- W2985002612 cites W1797572428 @default.
- W2985002612 cites W1841331176 @default.
- W2985002612 cites W1935951477 @default.
- W2985002612 cites W1952574243 @default.
- W2985002612 cites W1964951140 @default.
- W2985002612 cites W1965453486 @default.
- W2985002612 cites W1969309856 @default.
- W2985002612 cites W1970227011 @default.
- W2985002612 cites W1971419576 @default.
- W2985002612 cites W1973522156 @default.
- W2985002612 cites W1977861446 @default.
- W2985002612 cites W1982990473 @default.
- W2985002612 cites W1984093745 @default.
- W2985002612 cites W1985039849 @default.
- W2985002612 cites W1986830781 @default.
- W2985002612 cites W1989332533 @default.
- W2985002612 cites W1995178146 @default.
- W2985002612 cites W1998129814 @default.
- W2985002612 cites W1998621531 @default.
- W2985002612 cites W2001854547 @default.
- W2985002612 cites W2002501210 @default.
- W2985002612 cites W2011328869 @default.
- W2985002612 cites W2011902133 @default.
- W2985002612 cites W2014508690 @default.
- W2985002612 cites W2017061287 @default.
- W2985002612 cites W2018530963 @default.
- W2985002612 cites W2026709018 @default.
- W2985002612 cites W2028921845 @default.
- W2985002612 cites W2033674626 @default.
- W2985002612 cites W2034502973 @default.
- W2985002612 cites W2036760484 @default.
- W2985002612 cites W2048250731 @default.
- W2985002612 cites W2048553024 @default.
- W2985002612 cites W2056079743 @default.
- W2985002612 cites W2057495929 @default.
- W2985002612 cites W2065022250 @default.
- W2985002612 cites W2069613314 @default.
- W2985002612 cites W2072358340 @default.
- W2985002612 cites W2075224534 @default.
- W2985002612 cites W2079531196 @default.
- W2985002612 cites W2079658347 @default.
- W2985002612 cites W2080053685 @default.
- W2985002612 cites W2083101826 @default.
- W2985002612 cites W2086206949 @default.
- W2985002612 cites W2091307037 @default.
- W2985002612 cites W2092638438 @default.
- W2985002612 cites W2092647016 @default.
- W2985002612 cites W2101837274 @default.
- W2985002612 cites W2105567273 @default.
- W2985002612 cites W2116435487 @default.
- W2985002612 cites W2120211376 @default.
- W2985002612 cites W2121672398 @default.
- W2985002612 cites W2125644182 @default.
- W2985002612 cites W2127958463 @default.
- W2985002612 cites W2128817844 @default.
- W2985002612 cites W2134807701 @default.
- W2985002612 cites W2135144687 @default.
- W2985002612 cites W2139503512 @default.
- W2985002612 cites W2140345256 @default.
- W2985002612 cites W2142765322 @default.
- W2985002612 cites W2145200068 @default.
- W2985002612 cites W2147477441 @default.
- W2985002612 cites W2153466677 @default.
- W2985002612 cites W2153825225 @default.
- W2985002612 cites W2154375184 @default.
- W2985002612 cites W2160480808 @default.
- W2985002612 cites W2164995160 @default.
- W2985002612 cites W2167829409 @default.
- W2985002612 cites W2169505821 @default.
- W2985002612 cites W2171917960 @default.
- W2985002612 cites W2252783105 @default.
- W2985002612 cites W2256829667 @default.
- W2985002612 cites W2271326836 @default.
- W2985002612 cites W2292824768 @default.
- W2985002612 cites W2316716290 @default.
- W2985002612 cites W2329936440 @default.
- W2985002612 cites W2342148852 @default.
- W2985002612 cites W2363218275 @default.
- W2985002612 cites W2394888858 @default.
- W2985002612 cites W2396545524 @default.
- W2985002612 cites W2402648944 @default.
- W2985002612 cites W2423225083 @default.
- W2985002612 cites W2513448306 @default.
- W2985002612 cites W2521797369 @default.
- W2985002612 cites W2528746299 @default.
- W2985002612 cites W2543598768 @default.
- W2985002612 cites W2546800956 @default.