2014
DOI: 10.18632/oncotarget.2751
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Abstract: The amyloid cascade hypothesis posits that deposition of the amyloid β (Aβ) peptide in the brain is a key event in the initiation of Alzheimer's disease (AD). Nonetheless, it now seems increasingly unlikely that amyloid toxicity is the cause of sporadic AD, which leads to cognitive decline. Here, using accelerated-senescence nontransgenic OXYS rats, we confirmed that aggregation of Aβ is a later event in AD-like pathology. We showed that an age-dependent increase in the levels of Aβ1–42 and extracellular Aβ de… Show more

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Cited by 58 publications
(74 citation statements)
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“…In line with their hippocampus-dependent cognitive deficits, OXYS rats show a synaptic loss [31], prominent alterations of synaptic functions [33], and significant ultrastructural changes [28] in the hippocampus. Ultrastructural abnormalities in synaptic terminals of OXYS rats in the period of progression of AD-like pathology are characterized by decreased numbers of synaptic vesicles, by signs of their disorganization and destruction, by increased numbers of various vacuoles, and by swelling and disintegration of mitochondria [31].…”
Section: Resultsmentioning
confidence: 99%
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“…In line with their hippocampus-dependent cognitive deficits, OXYS rats show a synaptic loss [31], prominent alterations of synaptic functions [33], and significant ultrastructural changes [28] in the hippocampus. Ultrastructural abnormalities in synaptic terminals of OXYS rats in the period of progression of AD-like pathology are characterized by decreased numbers of synaptic vesicles, by signs of their disorganization and destruction, by increased numbers of various vacuoles, and by swelling and disintegration of mitochondria [31].…”
Section: Resultsmentioning
confidence: 99%
“…Because progressive accumulation of toxic amyloid-β species in the brain of OXYS rats starts at age 12 months [2728], we tested whether treatment with SkQ1 since 12 months of age affects amyloid-β 1-40 and amyloid-β 1-42 levels in the hippocampus of 18-month-old OXYS rats. Enzyme immunoassay analysis of amyloid-β 1-40 and amyloid-β 1-42 (Fig.…”
Section: Resultsmentioning
confidence: 99%
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“…18,19 Recent support for the amyloid hypothesis of AD came from a study which recapitulated the disease in a 3D human neuronal cell culture model, demonstrating that the appearance of prominent neurofibrillary tangles requires Ab generation, 20 a causality that is still controversial. 21 While APP triplication in trisomy 21 and mutations in APP and PSEN1 or PSEN2 of the g-secretase complex are known to engender familial AD, contributions of BACE1 polymorphisms remain to be established. 22 Nevertheless, the importance of BACE1 in AD pathogenesis has been demonstrated by mutations in APP, which either promote b-site cleavage causing a familial form of early-onset AD, or, contrarily, hinder APP b-cleavage and thus protect against the disease and even mild cognitive impairment.…”
Section: Role Of Bace1 In Admentioning
confidence: 99%