Search: onr:"swepub:oai:gup.ub.gu.se/326254" > APOE epsilon 4 gene...
Fältnamn | Indikatorer | Metadata |
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000 | 06881naa a2200745 4500 | |
001 | oai:gup.ub.gu.se/326254 | |
003 | SwePub | |
008 | 240910s2023 | |||||||||||000 ||eng| | |
009 | oai:prod.swepub.kib.ki.se:152373355 | |
024 | 7 | a https://gup.ub.gu.se/publication/3262542 URI |
024 | 7 | a https://doi.org/10.1186/s13195-023-01209-62 DOI |
024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1523733552 URI |
040 | a (SwePub)gud (SwePub)ki | |
041 | a eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Snellman, Anniinau Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xsnela |
245 | 1 0 | a APOE epsilon 4 gene dose effect on imaging and blood biomarkers of neuroinflammation and beta-amyloid in cognitively unimpaired elderly |
264 | 1 | c 2023 |
520 | a BackgroundNeuroinflammation, characterized by increased reactivity of microglia and astrocytes in the brain, is known to be present at various stages of the Alzheimer's disease (AD) continuum. However, its presence and relationship with amyloid pathology in cognitively normal at-risk individuals is less clear. Here, we used positron emission tomography (PET) and blood biomarker measurements to examine differences in neuroinflammation and beta-amyloid (A beta) and their association in cognitively unimpaired homozygotes, heterozygotes, or non-carriers of the APOE epsilon 4 allele, the strongest genetic risk for sporadic AD.MethodsSixty 60-75-year-old APOE epsilon 4 homozygotes (n = 19), heterozygotes (n = 21), and non-carriers (n = 20) were recruited in collaboration with the local Auria biobank. The participants underwent C-11-PK11195 PET (targeting 18-kDa translocator protein, TSPO), C-11-PiB PET (targeting A beta), brain MRI, and neuropsychological testing including a preclinical cognitive composite (APCC). C-11-PK11195 distribution volume ratios and C-11-PiB standardized uptake value ratios (SUVRs) were calculated for regions typical for early A beta accumulation in AD. Blood samples were drawn for measuring plasma glial fibrillary acidic protein (GFAP) and plasma A beta(1-42/1.40).ResultsIn our cognitively unimpaired sample, cortical C-11-PiB-binding increased according to APOE epsilon 4 gene dose (median composite SUVR 1.47 (range 1.38-1.66) in non-carriers, 1.55 (1.43-2.02) in heterozygotes, and 2.13 (1.61-2.83) in homozygotes, P = 0.002). In contrast, cortical composite C-11-PK11195-binding did not differ between the APOE epsilon 4 gene doses (P = 0.27) or between A beta-positive and A beta-negative individuals (P = 0.81) and associated with higher A beta burden only in APOE epsilon 4 homozygotes (Rho = 0.47, P = 0.043). Plasma GFAP concentration correlated with cortical C-11-PiB (Rho = 0.35, P = 0.040), but not C-11-PK11195-binding (Rho = 0.13, P = 0.47) in A beta-positive individuals. In the total cognitively unimpaired population, both higher composite C-11-PK11195-binding and plasma GFAP were associated with lower hippocampal volume, whereas elevated C-11-PiB-binding was associated with lower APCC scores.ConclusionsOnly A beta burden measured by PET, but not markers of neuroinflammation, differed among cognitively unimpaired elderly with different APOE epsilon 4 gene dose. However, APOE epsilon 4 gene dose seemed to modulate the association between neuroinflammation and A beta. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng |
653 | a Alzheimer's disease | |
653 | a Microglia | |
653 | a Astrocytes | |
653 | a Beta-amyloid | |
653 | a PET | |
653 | a TSPO | |
653 | a APOE | |
653 | a Apolipoprotein E | |
653 | a GFAP | |
653 | a Biomarker | |
653 | a microglial activation | |
653 | a alzheimers-disease | |
653 | a in-vivo | |
653 | a translocator | |
653 | a protein | |
653 | a neuronal function | |
653 | a burden | |
653 | a association | |
653 | a risk | |
653 | a impairment | |
653 | a deposition | |
653 | a Neurosciences & Neurology | |
700 | 1 | a Ekblad, L. L.4 aut |
700 | 1 | a Tuisku, J.4 aut |
700 | 1 | a Koivumaki, M.4 aut |
700 | 1 | a Ashton, Nicholas J.u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xashtn |
700 | 1 | a Lantero Rodriguez, Juanu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xrodri |
700 | 1 | a Karikari, Thomasu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xkarit |
700 | 1 | a Helin, S.4 aut |
700 | 1 | a Bucci, M.u Karolinska Institutet4 aut |
700 | 1 | a Loyttyniemi, E.4 aut |
700 | 1 | a Parkkola, R.4 aut |
700 | 1 | a Karrasch, M.4 aut |
700 | 1 | a Schöll, Michael,d 1980u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xschom |
700 | 1 | a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Wallenberg Centre for Molecular and Translational Medicine,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xzethe |
700 | 1 | a Blennow, Kaj,d 1958u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xbleka |
700 | 1 | a Rinne, J. O.4 aut |
710 | 2 | a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org |
773 | 0 | t Alzheimers Research & Therapyg 15:1q 15:1x 1758-9193 |
856 | 4 8 | u https://gup.ub.gu.se/publication/326254 |
856 | 4 8 | u https://doi.org/10.1186/s13195-023-01209-6 |
856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:152373355 |
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