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Synergistic Associa...
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Chiu, Ming-Jang
(författare)
Synergistic Association between Plasma Aβ1-42 and p-tau in Alzheimer's Disease but Not in Parkinson's Disease or Frontotemporal Dementia.
- Artikel/kapitelEngelska2021
Förlag, utgivningsår, omfång ...
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2021-04-07
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American Chemical Society (ACS),2021
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LIBRIS-ID:oai:gup.ub.gu.se/303458
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https://gup.ub.gu.se/publication/303458URI
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https://doi.org/10.1021/acschemneuro.1c00010DOI
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Ämneskategori:art swepub-publicationtype
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Beta-amyloid (Aβ1-42) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ1-42 in the blood is not elucidated. We investigated the association in individuals with AD (n = 62, including amnesic mild cognitive impairment and dementia), Parkinson's disease (n = 30), frontotemporal dementia (n = 25), and cognitively unimpaired controls (n = 41) using immunomagnetic reduction assays to measure plasma Aβ1-42 and p-tau181 concentrations. Correlation and regression analyses were performed to examine the relation between plasma levels, demographic factors, and clinical severity. Both plasma Aβ1-42 and p-tau concentrations were significantly higher in AD and frontotemporal dementia than in the controls and Parkinson's disease. A significant positive association was found between plasma p-tau and Aβ1-42 in controls (r = 0.579, P < 0.001) and AD (r = 0.699, P < 0.001) but not in frontotemporal dementia or Parkinson's disease. Plasma p-tau was significantly associated with clinical severity in the AD in terms of scores of clinical dementia rating (r = 0.288, P = 0.025) and mini-mental state examination (r = -0.253, P = 0.049). Regression analysis showed that plasma Aβ1-42 levels explain approximately 47.7% of the plasma p-tau levels in the AD after controlling age, gender, and clinical severity. While in non-AD participants, the clinical dementia rating explained about 47.5% of the plasma p-tau levels. The disease-specific association between plasma Aβ1-42 and p-tau levels in AD implies a possible synergic effect in mechanisms involving these two pathological proteins' genesis.
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Biuppslag (personer, institutioner, konferenser, titlar ...)
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Yang, Shieh-Yueh
(författare)
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Chen, Ta-Fu
(författare)
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Lin, Chin-Hsien
(författare)
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Yang, Fu-Chi
(författare)
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Chen, Wen-Ping
(författare)
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Zetterberg, Henrik,1973Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xzethe
(författare)
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Blennow, Kaj,1958Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xbleka
(författare)
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Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:ACS chemical neuroscience: American Chemical Society (ACS)12:8, s. 1376-13831948-7193
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