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• W4360864694 abstract "Increasingly prevalent acute and chronic human brain diseases are scourges for the elderly. Besides the lack of therapies, these ailments share a neuroinflammation that is triggered/sustained by different innate immunity-related protein oligomers called inflammasomes. Relevant neuroinflammation players such as microglia/monocytes typically exhibit a strong NLRP3 inflammasome activation. Hence the idea that NLRP3 suppression might solve neurodegenerative ailments. Here we review the recent Literature about this topic. First, we update conditions and mechanisms, including RNAs, extracellular vesicles/exosomes, endogenous compounds, and ethnic/pharmacological agents/extracts regulating NLRP3 function. Second, we pinpoint NLRP3-activating mechanisms and known NLRP3 inhibition effects in acute (ischemia, stroke, hemorrhage), chronic (Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, MS, ALS), and virus-induced (Zika, SARS-CoV-2, and others) human brain diseases. The available data show that (i) disease-specific divergent mechanisms activate the (mainly animal) brains NLRP3; (ii) no evidence proves that NLRP3 inhibition modifies human brain diseases (yet ad hoc trials are ongoing); and (iii) no findings exclude that concurrently activated other-than-NLRP3 inflammasomes might functionally replace the inhibited NLRP3. Finally, we highlight that among the causes of the persistent lack of therapies are the species difference problem in disease models and a preference for symptomatic over etiologic therapeutic approaches. Therefore, we posit that human neural cell-based disease models could drive etiological, pathogenetic, and therapeutic advances, including NLRP3’s and other inflammasomes’ regulation, while minimizing failure risks in candidate drug trials." @default.
• W4360864694 created "2023-03-25" @default.
• W4360864694 creator A5008110122 @default.
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• W4360864694 creator A5061275176 @default.
• W4360864694 date "2023-03-23" @default.
• W4360864694 modified "2023-09-27" @default.
• W4360864694 title "NLRP3 Inflammasome’s Activation in Acute and Chronic Brain Diseases—An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes" @default.
• W4360864694 cites W1529674879 @default.
• W4360864694 cites W1549316628 @default.
• W4360864694 cites W1561041814 @default.
• W4360864694 cites W1571275573 @default.
• W4360864694 cites W1606082686 @default.
• W4360864694 cites W1666339910 @default.
• W4360864694 cites W1699321428 @default.
• W4360864694 cites W1764212712 @default.
• W4360864694 cites W1825604636 @default.
• W4360864694 cites W1859128422 @default.
• W4360864694 cites W1914622032 @default.
• W4360864694 cites W1963947961 @default.
• W4360864694 cites W1966634013 @default.
• W4360864694 cites W1966914633 @default.
• W4360864694 cites W1970560893 @default.
• W4360864694 cites W1972431103 @default.
• W4360864694 cites W1977159891 @default.
• W4360864694 cites W1981472960 @default.
• W4360864694 cites W1981649246 @default.
• W4360864694 cites W1981893522 @default.
• W4360864694 cites W1985538633 @default.
• W4360864694 cites W1987329700 @default.
• W4360864694 cites W1993976394 @default.
• W4360864694 cites W1994167951 @default.
• W4360864694 cites W1995303995 @default.
• W4360864694 cites W1995605818 @default.
• W4360864694 cites W1997322387 @default.
• W4360864694 cites W2003618511 @default.
• W4360864694 cites W2005052262 @default.
• W4360864694 cites W2006558268 @default.
• W4360864694 cites W2007837046 @default.
• W4360864694 cites W2017639947 @default.
• W4360864694 cites W2018649598 @default.
• W4360864694 cites W2019495623 @default.
• W4360864694 cites W2026694335 @default.
• W4360864694 cites W2027047473 @default.
• W4360864694 cites W2030479443 @default.
• W4360864694 cites W2031964319 @default.
• W4360864694 cites W2037600884 @default.
• W4360864694 cites W2043361020 @default.
• W4360864694 cites W2049919805 @default.
• W4360864694 cites W2051329301 @default.
• W4360864694 cites W2056312916 @default.
• W4360864694 cites W2063758367 @default.
• W4360864694 cites W2064276033 @default.
• W4360864694 cites W2067406680 @default.
• W4360864694 cites W2068633454 @default.
• W4360864694 cites W2069172641 @default.
• W4360864694 cites W2070167771 @default.
• W4360864694 cites W2071517838 @default.
• W4360864694 cites W2080827095 @default.
• W4360864694 cites W2082890051 @default.
• W4360864694 cites W2084158898 @default.
• W4360864694 cites W2086406618 @default.
• W4360864694 cites W2096317294 @default.
• W4360864694 cites W2099901203 @default.
• W4360864694 cites W2100953877 @default.
• W4360864694 cites W2101134811 @default.
• W4360864694 cites W2108191354 @default.
• W4360864694 cites W2108829078 @default.
• W4360864694 cites W2109021011 @default.
• W4360864694 cites W2116854644 @default.
• W4360864694 cites W2119098586 @default.
• W4360864694 cites W2121830956 @default.
• W4360864694 cites W2127176298 @default.
• W4360864694 cites W2132960194 @default.
• W4360864694 cites W2133489393 @default.
• W4360864694 cites W2135695964 @default.
• W4360864694 cites W2139086927 @default.
• W4360864694 cites W2140882296 @default.
• W4360864694 cites W2142677020 @default.
• W4360864694 cites W2144241574 @default.
• W4360864694 cites W2146895123 @default.
• W4360864694 cites W2147546596 @default.
• W4360864694 cites W2151926428 @default.
• W4360864694 cites W2152672520 @default.
• W4360864694 cites W2153842328 @default.
• W4360864694 cites W2154445813 @default.
• W4360864694 cites W2158787641 @default.
• W4360864694 cites W2161771297 @default.
• W4360864694 cites W2161995310 @default.
• W4360864694 cites W2166865493 @default.
• W4360864694 cites W2169280749 @default.
• W4360864694 cites W2171212614 @default.
• W4360864694 cites W2197386596 @default.
• W4360864694 cites W2206384930 @default.
• W4360864694 cites W2254323294 @default.
• W4360864694 cites W2260110125 @default.

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