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• W2136858260 abstract "Mechanisms of neuronal loss in Alzheimer's disease (AD) are poorly understood. Here we show that apoptosis is a major form of neuronal cell death in PS/APP mice modeling AD-like neurodegeneration. Pyknotic neurons in adult PS/APP mice exhibited apoptotic changes, including DNA fragmentation, caspase-3 activation, and caspase-cleaved alpha-spectrin generation, identical to developmental neuronal apoptosis in wild-type mice. Ultrastructural examination using immunogold cytochemistry confirmed that activated caspase-3-positive neurons also exhibited chromatin margination and condensation, chromatin balls, and nuclear membrane fragmentation. Numbers of apoptotic profiles in both cortex and hippocampus of PS/APP mice compared with age-matched controls were twofold to threefold higher at 6 months of age and eightfold higher at 21 to 26 months of age. Additional neurons undergoing dark cell degeneration exhibited none of these apoptotic features. Activated caspase-3 and caspase-3-cleaved spectrin were abundant in autophagic vacuoles, accumulating in dystrophic neurites of PS/APP mice similar to AD brains. Administration of the cysteine protease inhibitor, leupeptin, promoted accumulation of autophagic vacuoles containing activated caspase-3 in axons of PS/APP mice and, to a lesser extent, in those of wild-type mice, implying that this pro-apoptotic factor is degraded by autophagy. Leupeptin-induced autophagic impairment increased the number of apoptotic neurons in PS/APP mice. Our findings establish apoptosis as a mode of neuronal cell death in aging PS/APP mice and identify the cross talk between autophagy and apoptosis, which influences neuronal survival in AD-related neurodegeneration." @default.
• W2136858260 created "2016-06-24" @default.
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• W2136858260 date "2008-09-01" @default.
• W2136858260 modified "2023-10-16" @default.
• W2136858260 title "Neuronal Apoptosis and Autophagy Cross Talk in Aging PS/APP Mice, a Model of Alzheimer's Disease" @default.
• W2136858260 cites W1514558092 @default.
• W2136858260 cites W1528462551 @default.
• W2136858260 cites W1531145879 @default.
• W2136858260 cites W1533075111 @default.
• W2136858260 cites W1542061701 @default.
• W2136858260 cites W1560977824 @default.
• W2136858260 cites W1745634660 @default.
• W2136858260 cites W18034176 @default.
• W2136858260 cites W1836761553 @default.
• W2136858260 cites W1911014954 @default.
• W2136858260 cites W1918909705 @default.
• W2136858260 cites W1919353 @default.
• W2136858260 cites W1968776273 @default.
• W2136858260 cites W1970101770 @default.
• W2136858260 cites W1971003242 @default.
• W2136858260 cites W1972336737 @default.
• W2136858260 cites W1973231428 @default.
• W2136858260 cites W1973376874 @default.
• W2136858260 cites W1973541476 @default.
• W2136858260 cites W1980225806 @default.
• W2136858260 cites W1980786980 @default.
• W2136858260 cites W1981302459 @default.
• W2136858260 cites W1988022242 @default.
• W2136858260 cites W1988147472 @default.
• W2136858260 cites W1988695302 @default.
• W2136858260 cites W1992335590 @default.
• W2136858260 cites W1992484817 @default.
• W2136858260 cites W1994210846 @default.
• W2136858260 cites W1994539511 @default.
• W2136858260 cites W1995925086 @default.
• W2136858260 cites W1997426613 @default.
• W2136858260 cites W1998974178 @default.
• W2136858260 cites W2000483565 @default.
• W2136858260 cites W2000966665 @default.
• W2136858260 cites W2002984957 @default.
• W2136858260 cites W2003852184 @default.
• W2136858260 cites W2003887174 @default.
• W2136858260 cites W2006995322 @default.
• W2136858260 cites W2008958222 @default.
• W2136858260 cites W2012337697 @default.
• W2136858260 cites W2014155195 @default.
• W2136858260 cites W2017688136 @default.
• W2136858260 cites W2017945532 @default.
• W2136858260 cites W2031177524 @default.
• W2136858260 cites W2031293980 @default.
• W2136858260 cites W2032328804 @default.
• W2136858260 cites W2034132952 @default.
• W2136858260 cites W2034915619 @default.
• W2136858260 cites W2039402963 @default.
• W2136858260 cites W2045497115 @default.
• W2136858260 cites W2046848104 @default.
• W2136858260 cites W2047649942 @default.
• W2136858260 cites W2052853635 @default.
• W2136858260 cites W2054554778 @default.
• W2136858260 cites W2061473417 @default.
• W2136858260 cites W2063403801 @default.
• W2136858260 cites W2064470441 @default.
• W2136858260 cites W2066792703 @default.
• W2136858260 cites W2069233591 @default.
• W2136858260 cites W2077464099 @default.
• W2136858260 cites W2079282879 @default.
• W2136858260 cites W2083521073 @default.
• W2136858260 cites W2084609653 @default.
• W2136858260 cites W2084754412 @default.
• W2136858260 cites W2086539466 @default.
• W2136858260 cites W2087401867 @default.
• W2136858260 cites W2092808670 @default.
• W2136858260 cites W2093076184 @default.
• W2136858260 cites W2093618389 @default.
• W2136858260 cites W2094297139 @default.
• W2136858260 cites W2097364564 @default.
• W2136858260 cites W2097631517 @default.
• W2136858260 cites W2108086395 @default.
• W2136858260 cites W2113718307 @default.
• W2136858260 cites W2115772647 @default.
• W2136858260 cites W2121802881 @default.
• W2136858260 cites W2125172225 @default.
• W2136858260 cites W2135841642 @default.
• W2136858260 cites W2137690550 @default.
• W2136858260 cites W2138302361 @default.
• W2136858260 cites W2140955159 @default.
• W2136858260 cites W2141976152 @default.
• W2136858260 cites W2145206598 @default.
• W2136858260 cites W2147357406 @default.

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