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• W2109366922 endingPage "569" @default.
• W2109366922 startingPage "541" @default.
• W2109366922 abstract "The increased expression and/or abnormal processing of the amyloid precursor protein (APP) is associated with the formation of amyloid plaques and cerebrovascular amyloid deposits, which are one of the major morphological hallmarks of Alzheimer's disease (AD). Among the processes regulating APP metabolism, the proteolytic cleavage of APP into amyloidogenic or nonamyloidogenic fragments is of special interest. The cleavage of the APP by the α-secretase within the β-amyloid sequence generates nonamyloidogenic C-terminal APP fragments and soluble APPsα, which has neurotrophic and neuroprotective activities. Proteolytic processing of APP by β-secretase, on the other hand, exposes the N-terminus of β-amyloid, which is liberated after γ-secretase cleavage at the variable amyloid C-terminus. The resulting 39–43 amino acid β-amyloid may be neurotoxic and disrupt neuronal connectivity after its accumulation in senile plaques. In this review, we discuss evidence derived from in vitro experiments, suggesting that the stimulation of protein kinase C (PKC)-coupled M1/M3 muscarinic acetylcholine receptors increases the nonamyloidogenic, secretory pathway of APP processing. It has also been shown in animal models that under conditions of reduced M1/M3 muscarinic acetylcholine receptor stimulation the secretory pathway of APP processing is inhibited and that constitutive upregulation of M1/M3-associated PKC increases APP secretion. Thus, the cortical cholinergic hypoactivity characteristic of AD may inhibit the nonamyloidogenic APP processing pathway and lead to increased β-amyloid generation. It has been shown in vitro that nerve growth factor (NGF)-associated signaling also influences the expression and catabolism of APP. Recent experiments with NGF-responsive cells revealed a specific role for the high-affinity NGF receptor, TrkA, in the increases in secretory APP processing and a role for the low-affinity neurotrophin receptor, p75NTR, in the transcriptional regulation of APP. Therefore, treatments with NGF could ameliorate cortical cholinergic dysfunction in AD. These findings may influence the design of therapeutic strategies aimed at stimulating cholinergic function and at increasing nonamyloidogenic APP processing without elevating APP expression." @default.
• W2109366922 created "2016-06-24" @default.
• W2109366922 creator A5001402241 @default.
• W2109366922 creator A5005145881 @default.
• W2109366922 creator A5051248527 @default.
• W2109366922 creator A5070096942 @default.
• W2109366922 creator A5090058992 @default.
• W2109366922 date "1998-12-01" @default.
• W2109366922 modified "2023-09-29" @default.
• W2109366922 title "The regulation of amyloid precursor protein metabolism by cholinergic mechanisms and neurotrophin receptor signaling" @default.
• W2109366922 cites W120263029 @default.
• W2109366922 cites W1276370372 @default.
• W2109366922 cites W1415841971 @default.
• W2109366922 cites W143657778 @default.
• W2109366922 cites W1481591018 @default.
• W2109366922 cites W148406203 @default.
• W2109366922 cites W1510308646 @default.
• W2109366922 cites W1510383592 @default.
• W2109366922 cites W1510793409 @default.
• W2109366922 cites W1510919372 @default.
• W2109366922 cites W1513751959 @default.
• W2109366922 cites W1517881466 @default.
• W2109366922 cites W1537950723 @default.
• W2109366922 cites W1539302044 @default.
• W2109366922 cites W1544102899 @default.
• W2109366922 cites W1550759106 @default.
• W2109366922 cites W1554535382 @default.
• W2109366922 cites W1554824558 @default.
• W2109366922 cites W1574959285 @default.
• W2109366922 cites W1576690422 @default.
• W2109366922 cites W1581006056 @default.
• W2109366922 cites W1597264233 @default.
• W2109366922 cites W1598870275 @default.
• W2109366922 cites W1600007560 @default.
• W2109366922 cites W1604272660 @default.
• W2109366922 cites W1605023308 @default.
• W2109366922 cites W1606587171 @default.
• W2109366922 cites W1609471181 @default.
• W2109366922 cites W1617304195 @default.
• W2109366922 cites W1627693029 @default.
• W2109366922 cites W1631745757 @default.
• W2109366922 cites W1638610891 @default.
• W2109366922 cites W1655404681 @default.
• W2109366922 cites W1671332310 @default.
• W2109366922 cites W1738253268 @default.
• W2109366922 cites W177887123 @default.
• W2109366922 cites W1794943105 @default.
• W2109366922 cites W1825726719 @default.
• W2109366922 cites W1828770259 @default.
• W2109366922 cites W1830398839 @default.
• W2109366922 cites W1836761553 @default.
• W2109366922 cites W1837897734 @default.
• W2109366922 cites W1856257340 @default.
• W2109366922 cites W1860556713 @default.
• W2109366922 cites W1885793991 @default.
• W2109366922 cites W189551846 @default.
• W2109366922 cites W1902701859 @default.
• W2109366922 cites W190615324 @default.
• W2109366922 cites W1919811763 @default.
• W2109366922 cites W1920580857 @default.
• W2109366922 cites W1930427841 @default.
• W2109366922 cites W1948740236 @default.
• W2109366922 cites W1949477754 @default.
• W2109366922 cites W1963793691 @default.
• W2109366922 cites W1964792461 @default.
• W2109366922 cites W1964972074 @default.
• W2109366922 cites W1965072630 @default.
• W2109366922 cites W1965496447 @default.
• W2109366922 cites W1966768311 @default.
• W2109366922 cites W1966822531 @default.
• W2109366922 cites W1967836806 @default.
• W2109366922 cites W1968675059 @default.
• W2109366922 cites W1969423869 @default.
• W2109366922 cites W1970848626 @default.
• W2109366922 cites W1971256323 @default.
• W2109366922 cites W1972718612 @default.
• W2109366922 cites W1972850922 @default.
• W2109366922 cites W1972988863 @default.
• W2109366922 cites W1973159287 @default.
• W2109366922 cites W1973238216 @default.
• W2109366922 cites W1973514804 @default.
• W2109366922 cites W1973863820 @default.
• W2109366922 cites W1975256554 @default.
• W2109366922 cites W1975627206 @default.
• W2109366922 cites W1975781078 @default.
• W2109366922 cites W1976526457 @default.
• W2109366922 cites W1977370575 @default.
• W2109366922 cites W1977405586 @default.
• W2109366922 cites W1977683347 @default.
• W2109366922 cites W1978000247 @default.
• W2109366922 cites W1978677685 @default.
• W2109366922 cites W1978751701 @default.
• W2109366922 cites W1979240613 @default.
• W2109366922 cites W1979543098 @default.
• W2109366922 cites W1979743454 @default.
• W2109366922 cites W1979773315 @default.
• W2109366922 cites W1980433009 @default.
• W2109366922 cites W1980906872 @default.

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