{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T20:57:30Z","timestamp":1784667450043,"version":"3.55.0"},"reference-count":43,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2016,11,28]],"date-time":"2016-11-28T00:00:00Z","timestamp":1480291200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2017,1,12]]},"abstract":"<jats:p>Background: Of the three transforming growth factor (TGF)-\u03b2 isoforms known, TGF\u03b21 deficits have been widely reported in Alzheimer\u2019s disease (AD) and studied as a potential therapeutic target. In contrast, the status of TGF\u03b22, which has been shown to mediate amyloid-\u03b2 (A\u03b2)-mediated neuronal death, are unclear both in AD and in Lewy body dementias (LBD) with differential neuritic plaque and neurofibrillary tangle burden.<\/jats:p>\n                  <jats:p>Objective: To measure neocortical TGF\u03b22 levels and their correlations with neuropathological and clinical markers of disease severity in a well-characterized cohort of AD as well as two clinical subtypes of LBD, dementia with Lewy bodies (DLB) and Parkinson\u2019s disease dementia (PDD), known to manifest relatively high and low A\u03b2 plaque burden, respectively.<\/jats:p>\n                  <jats:p>\n                    Methods: Postmortem samples from temporal cortex (BA21) were measured for TGF\u03b22 using a Luminex-based platform, and correlated with scores for neuritic plaques, neurofibrillary tangles, \u03b1-synuclein pathology, dementia severity (as measured by annual decline of Mini-Mental State Examination scores) as well as soluble and total fractions of brain A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    .\n                  <\/jats:p>\n                  <jats:p>\n                    Results: TGF\u03b22 was significantly increased in AD and DLB, but not in PDD. TGF\u03b22 also correlated with scores for neurofibrillary tangles, Lewy bodies (within the LBD group), dementia severity, and soluble A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    concentration, but not with neuritic plaque scores, total A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    , or monomeric \u03b1-synuclein immunoreactivity.\n                  <\/jats:p>\n                  <jats:p>\n                    Conclusions: TGF\u03b22 is increased in the temporal cortex of AD and DLB, and its correlations with neuropathological and clinical markers of disease severity as well as with soluble A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    load suggest a potential pathogenic role in mediating the neurotoxicity of non-fibrillar A\u03b2. Our study also indicates the potential utility of targeting TGF\u03b22 in pharmacotherapeutic approaches to AD and DLB.\n                  <\/jats:p>","DOI":"10.3233\/jad-160781","type":"journal-article","created":{"date-parts":[[2016,11,29]],"date-time":"2016-11-29T11:43:14Z","timestamp":1480419794000},"page":"157-166","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":30,"title":["Increased Transforming Growth Factor \u03b22 in the Neocortex of Alzheimer\u2019s           Disease and Dementia with Lewy Bodies is\u00a0Correlated with Disease Severity and\u00a0Soluble             A\u03b2\n                    <sub>42<\/sub>\n                    Load"],"prefix":"10.1177","volume":"56","author":[{"given":"Joyce R.","family":"Chong","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Yong Loo Lin School of Medicine,\r            National University of Singapore, Singapore,\r            Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuek Ling","family":"Chai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Yong Loo Lin School of Medicine,\r            National University of Singapore, Singapore,\r            Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasinda H.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Yong Loo Lin School of Medicine,\r            National University of Singapore, Singapore,\r            Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Howlett","sequence":"additional","affiliation":[{"name":"Wolfson Centre for Age-Related Diseases, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Attems","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clive G.","family":"Ballard","sequence":"additional","affiliation":[{"name":"Wolfson Centre for Age-Related Diseases, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dag","family":"Aarsland","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Ward Sciences and Society,\r            Karolinska Institute, Stockholm,\r          Sweden"},{"name":"Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul T.","family":"Francis","sequence":"additional","affiliation":[{"name":"Wolfson Centre for Age-Related Diseases, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher P.","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Yong Loo Lin School of Medicine,\r            National University of Singapore, Singapore,\r            Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mitchell K.P.","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Yong Loo Lin School of Medicine,\r            National University of Singapore, Singapore,\r            Singapore"},{"name":"Wolfson Centre for Age-Related Diseases, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,11,28]]},"reference":[{"key":"ref001","doi-asserted-by":"publisher","DOI":"10.1042\/BST20140107"},{"key":"ref002","author":"Bourdenx M","year":"2015","journal-title":"Prog 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