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• W2885509648 abstract "The combination of genetics and genomics in Parkinson´s disease has recently begun to unveil molecular mechanisms possibly underlying disease onset and progression. In particular, catabolic processes such as autophagy have been increasingly gaining relevance as post-mortem evidence and experimental models suggested a participation in neurodegeneration and alpha-synuclein Lewy body pathology. In addition, familial Parkinson´s disease linked to LRRK2 and alpha-synuclein provided stronger correlation between etiology and alterations in autophagy. More detailed cellular pathways are proposed and genetic risk factors that associate with idiopathic Parkinson´s disease provide further clues in dissecting contributions of single players. Nevertheless, the fine-tuning of these processes remains elusive, as the initial stages of the pathways are not yet clarified.In this review, we collect literature evidence pointing to autophagy as the common, downstream target of Parkinsonian dysfunctions and augment current knowledge on the factors that direct the subsequent steps. Cell and molecular biology evidence indicate that p38 signaling underlies neurodegeneration and autoptic observations suggest a participation in neuropathology. Moreover, alpha-synuclein and LRRK2 also appear involved in the p38 pathway with additional roles in the regulation of GTPase signaling. Small GTPases are critical modulators of p38 activation and thus, their functional interaction with aSyn and LRRK2 could explain much of the detailed mechanics of autophagy in Parkinson´s disease.We propose a novel hypothesis for a more comprehensive working model where autophagy is controlled by upstream pathways, such as GTPase-p38, that have been so far underexplored in this context. In addition, etiological factors (LRRK2, alpha-synuclein) and risk loci might also combine in this common mechanism, providing a powerful experimental setting to dissect the cause of both familial and idiopathic disease." @default.
• W2885509648 created "2018-08-22" @default.
• W2885509648 creator A5009676465 @default.
• W2885509648 creator A5046641112 @default.
• W2885509648 creator A5068037007 @default.
• W2885509648 creator A5072580730 @default.
• W2885509648 creator A5089174016 @default.
• W2885509648 date "2018-08-02" @default.
• W2885509648 modified "2023-10-17" @default.
• W2885509648 title "A new hypothesis for Parkinson’s disease pathogenesis: GTPase-p38 MAPK signaling and autophagy as convergence points of etiology and genomics" @default.
• W2885509648 cites W1495804697 @default.
• W2885509648 cites W1523693806 @default.
• W2885509648 cites W1527671059 @default.
• W2885509648 cites W1544196343 @default.
• W2885509648 cites W1584602900 @default.
• W2885509648 cites W1611134798 @default.
• W2885509648 cites W1753110664 @default.
• W2885509648 cites W1764833860 @default.
• W2885509648 cites W1781925048 @default.
• W2885509648 cites W1786270771 @default.
• W2885509648 cites W1787368831 @default.
• W2885509648 cites W1851334881 @default.
• W2885509648 cites W1858544150 @default.
• W2885509648 cites W1882508453 @default.
• W2885509648 cites W1928236782 @default.
• W2885509648 cites W1942332138 @default.
• W2885509648 cites W1963643632 @default.
• W2885509648 cites W1964548627 @default.
• W2885509648 cites W1965006448 @default.
• W2885509648 cites W1965095016 @default.
• W2885509648 cites W1965778124 @default.
• W2885509648 cites W1965938007 @default.
• W2885509648 cites W1965942744 @default.
• W2885509648 cites W1967111894 @default.
• W2885509648 cites W1968378620 @default.
• W2885509648 cites W1971394915 @default.
• W2885509648 cites W1974247591 @default.
• W2885509648 cites W1978793506 @default.
• W2885509648 cites W1980235553 @default.
• W2885509648 cites W1981172305 @default.
• W2885509648 cites W1981289966 @default.
• W2885509648 cites W1983402821 @default.
• W2885509648 cites W1984394485 @default.
• W2885509648 cites W1985462906 @default.
• W2885509648 cites W1986178012 @default.
• W2885509648 cites W1987155530 @default.
• W2885509648 cites W1987484120 @default.
• W2885509648 cites W1990387678 @default.
• W2885509648 cites W1990473626 @default.
• W2885509648 cites W1992101582 @default.
• W2885509648 cites W1992937812 @default.
• W2885509648 cites W1992982674 @default.
• W2885509648 cites W1993094339 @default.
• W2885509648 cites W1993513350 @default.
• W2885509648 cites W1998334997 @default.
• W2885509648 cites W1998385521 @default.
• W2885509648 cites W1999893655 @default.
• W2885509648 cites W1999923500 @default.
• W2885509648 cites W2001410943 @default.
• W2885509648 cites W2002700767 @default.
• W2885509648 cites W2003695808 @default.
• W2885509648 cites W2005734278 @default.
• W2885509648 cites W2006544096 @default.
• W2885509648 cites W2006840724 @default.
• W2885509648 cites W2009556855 @default.
• W2885509648 cites W2010119513 @default.
• W2885509648 cites W2012089318 @default.
• W2885509648 cites W2015445654 @default.
• W2885509648 cites W2015913654 @default.
• W2885509648 cites W2017642230 @default.
• W2885509648 cites W2023215532 @default.
• W2885509648 cites W2024431122 @default.
• W2885509648 cites W2024782183 @default.
• W2885509648 cites W2029735360 @default.
• W2885509648 cites W2031884668 @default.
• W2885509648 cites W2032700869 @default.
• W2885509648 cites W2034433559 @default.
• W2885509648 cites W2035939787 @default.
• W2885509648 cites W2040000631 @default.
• W2885509648 cites W2042920992 @default.
• W2885509648 cites W2043291430 @default.
• W2885509648 cites W2046250764 @default.
• W2885509648 cites W2047558130 @default.
• W2885509648 cites W2048484492 @default.
• W2885509648 cites W2049277771 @default.
• W2885509648 cites W2051728587 @default.
• W2885509648 cites W2052047416 @default.
• W2885509648 cites W2053066346 @default.
• W2885509648 cites W2053206193 @default.
• W2885509648 cites W2055652883 @default.
• W2885509648 cites W2057358353 @default.
• W2885509648 cites W2057654279 @default.
• W2885509648 cites W2059073522 @default.
• W2885509648 cites W2060023105 @default.
• W2885509648 cites W2062065799 @default.
• W2885509648 cites W2063116259 @default.
• W2885509648 cites W2063127941 @default.
• W2885509648 cites W2063377136 @default.
• W2885509648 cites W2065236536 @default.
• W2885509648 cites W2068043905 @default.

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