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We aimed to evaluate the correlation between these factors using diffusion-weighted imaging (DWI) thermometry and blood tests of systemic inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>From July 2012 to Jun 2017, 103 patients with PD (44 men and 59 women; mean age, 60.43\u2009\u00b1\u20099.12\u00a0years) and 106 sex- and age-matched healthy volunteers (48 men and 58 women; mean age, 58.16\u2009\u00b1\u20098.45\u00a0years) retrospectively underwent magnetic resonance DWI thermometry to estimate brain intraventricular temperature (<jats:italic>T<\/jats:italic><jats:sub>v<\/jats:sub>). Subjects were divided into three subgroups in light of their ages. The tested inflammatory markers included plasma nuclear DNA, mitochondrial DNA, apoptotic leukocytes, and serum adhesion molecules. The correlations among the<jats:italic>T<\/jats:italic><jats:sub>v<\/jats:sub>values, clinical severity, and systemic inflammatory markers were then calculated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The PD patients did not show a natural trend of decline in<jats:italic>T<\/jats:italic><jats:sub>v<\/jats:sub>with age. Comparisons among the different age groups revealed that the younger PD subjects had significantly lower<jats:italic>T<\/jats:italic><jats:sub>v<\/jats:sub>values than the younger controls, but the older subjects had no significant group differences. Overall, the PD patients exhibited lower<jats:italic>T<\/jats:italic><jats:sub>v<\/jats:sub>values than the controls, as well as increased oxidative stress. The brain temperature showed positive correlations with inflammatory markers, including plasma nuclear DNA and L-selectin levels, in all the subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Possible pathophysiological correlations between systemic inflammation and brain temperature were indicated by the results of this study, a finding which may aid us in investigating the underlying pathogenesis of PD.<\/jats:p><\/jats:sec>","DOI":"10.1007\/s10072-019-04217-3","type":"journal-article","created":{"date-parts":[[2020,1,10]],"date-time":"2020-01-10T23:02:36Z","timestamp":1578697356000},"page":"1267-1276","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Alteration of brain temperature and systemic inflammation in Parkinson\u2019s disease"],"prefix":"10.1007","volume":"41","author":[{"given":"Hsiu-Ling","family":"Chen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kei","family":"Yamada","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Sakai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheng-Hsien","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng-Hsiang","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6945-5263","authenticated-orcid":false,"given":"Wei-Che","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,1,10]]},"reference":[{"issue":"Suppl 1","key":"4217_CR1","doi-asserted-by":"publisher","first-page":"216","DOI":"10.1111\/jnc.13731","volume":"139","author":"A Bose","year":"2016","unstructured":"Bose A, Beal MF (2016) Mitochondrial dysfunction in Parkinson\u2019s disease. 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