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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004881naa a2200433 4500
001oai:gup.ub.gu.se/246420
003SwePub
008240528s2017 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/2464202 URI
0247 a https://doi.org/10.1001/jamaneurol.2016.32322 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Dean, Douglas C4 aut
2451 0a Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease.
264 1b American Medical Association (AMA),c 2017
520 a The accumulation of aggregated β-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer disease (AD). While plaque and tangle accumulation likely contributes to neuron and synapse loss, disease-related changes to oligodendrocytes and myelin are also suspected of playing a role in development of AD dementia. Still, to our knowledge, little is known about AD-related myelin changes, and even when present, they are often regarded as secondary to concomitant arteriosclerosis or related to aging.To assess associations between hallmark AD pathology and novel quantitative neuroimaging markers while being sensitive to white matter myelin content.Magnetic resonance imaging was performed at an academic research neuroimaging center on a cohort of 71 cognitively asymptomatic adults enriched for AD risk. Lumbar punctures were performed and assayed for cerebrospinal fluid (CSF) biomarkers of AD pathology, including β-amyloid 42, total tau protein, phosphorylated tau 181, and soluble amyloid precursor protein. We measured whole-brain longitudinal and transverse relaxation rates as well as the myelin water fraction from each of these individuals.Automated brain mapping algorithms and statistical models were used to evaluate the relationships between age, CSF biomarkers of AD pathology, and quantitative magnetic resonance imaging relaxometry measures, including the longitudinal and transverse relaxation rates and the myelin water fraction.The mean (SD) age for the 19 male participants and 52 female participants in the study was 61.6 (6.4) years. Widespread age-related changes to myelin were observed across the brain, particularly in late myelinating brain regions such as frontal white matter and the genu of the corpus callosum. Quantitative relaxometry measures were negatively associated with levels of CSF biomarkers across brain white matter and in areas preferentially affected in AD. Furthermore, significant age-by-biomarker interactions were observed between myelin water fraction and phosphorylated tau 181/β-amyloid 42, suggesting that phosphorylated tau 181/β-amyloid 42 levels modulate age-related changes in myelin water fraction.These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. We expect that clarifying the nature of myelin damage in preclinical AD may be informative on the disease's course and lead to new markers of efficacy for prevention and treatment trials.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
7001 a Hurley, Samuel A4 aut
7001 a Kecskemeti, Steven R4 aut
7001 a O'Grady, J Patrick4 aut
7001 a Canda, Cristybelle4 aut
7001 a Davenport-Sis, Nancy J4 aut
7001 a Carlsson, Cynthia M4 aut
7001 a Zetterberg, Henrik,d 1973u 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)xzethe
7001 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
7001 a Asthana, Sanjay4 aut
7001 a Sager, Mark A4 aut
7001 a Johnson, Sterling C4 aut
7001 a Alexander, Andrew L4 aut
7001 a Bendlin, Barbara B4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
7730 t JAMA neurologyd : American Medical Association (AMA)g 74:1, s. 41-49q 74:1<41-49x 2168-6157x 2168-6149
8564 u https://discovery.ucl.ac.uk/1538023/1/Zetterberg_jamaneurology_Dean_2016_oi_160067.pdf
8564 8u https://gup.ub.gu.se/publication/246420
8564 8u https://doi.org/10.1001/jamaneurol.2016.3232

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