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P1‐178: Frequency of cerebral infarcts in probable dementia with lewy bodies
Author(s) -
Sarro Lidia,
Radford Jonathan Graff,
Zuk Samantha M.,
Tosakulwong Nirubol,
Przybelski Scott A.,
Boeve Bradley,
Ferman Tanis J.,
Smith Glenn E.,
Knopman David S.,
Filippi Massimo,
Petersen Ronald C.,
Jack Clifford R.,
Kantarci Kejal
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2015.06.377
Subject(s) - dementia with lewy bodies , dementia , medicine , cardiology , fluid attenuated inversion recovery , population , cognitive decline , cohort , disease , magnetic resonance imaging , radiology , environmental health
published CSF total tau (T-Tau) cutoff values: T-Tau positive (n1⁄4145, males1⁄472) and T-Tau negative (n1⁄463, males1⁄448) patients, characterized by CSF T-Tau values above or below the 93 pg/mL threshold, respectively. Voxel-based morphometry (VBM) was applied to compare whole-brain patterns of GM and WM volume in T-Tau positive and negative patients. Statistical analyses were performed by using SPM12 software. Age, gender, education, MMSE score, MRI field strength and intracranial volume were included as nuisance variables in the analysis. Results:T-Tau positive and negative patients were comparable in terms of age, dementia clinical severity, ApoE4 phenotype, and neuropsychological impairment. Only T-tau positive AD exhibited significant (FWE corrected) and extensive WM volume loss in bilateral medial temporal regions compared to CN, in particular in the parahyppocampal WM. When compared to T-tau negative AD, T-tau positive patients showed no GM volume reduction. Instead, they presented extensive WM atrophy in bilateral fornix, corona radiata and centrum semiovale (p<0.001 uncorrected). Conclusions:This study supports the notion that the tau-induced pathogenic process specifically affects the WM integrity, and suggests a new radiological phenotype in a distinct population of AD patients whose brain structural changes are mainly driven by tau-induced neurodegeneration.