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Jung, Y.

https://orcid.org/0000-0001-9560-7822

Mayo Clinic

Mayo Clinic in Arizona

Citations 2

Regional β‐amyloid burden does not correlate with cognitive or language deficits in Alzheimer's disease presenting as aphasia
Jung, Y. , Whitwell, Jennifer L. , Senjem, Matthew L. , Jack, Clifford R. , Lowe, Val J. , Josephs, Keith A. , Duffy, Joseph R. , Strand, Edythe A. , Machulda, Mary M. , Jack, Clifford R , Senjem, Matthew L

European Journal of Neurology | June 23, 2015 | Volume: 23 | Issue: 2 | Pages: 313-319

10.1111/ene.12761 Get It

Background and purpose A subset of patients with Alzheimer's disease ( AD ) present with early and prominent language impairment (aphasic AD ). Our previous study demonstrated an association between global β‐amyloid burden measured on [ 11 C] Pittsburgh compound B (PiB) positron emission tomography and general cognitive impairment, but not with aphasia, in such subjects. As a follow‐up, whether there is any association between regional β‐amyloid burden, atrophy on magnetic resonance imaging ( MRI ) and global cognitive impairment, aphasia or other cognitive and functional impairment in aphasic AD is assessed. Methods Forty‐four aphasic AD subjects who underwent PiB scanning and volumetric MRI and were determined to be positive for β‐amyloid deposition were analyzed. All had completed detailed neurological, neuropsychological and language batteries. Spearman's rank‐order correlation was utilized to assess for associations. Results Greater visuospatial impairment was associated with increased β‐amyloid burden in the primary visual cortex ( P = 0.001). Although there were many trends for associations between neurocognitive and language deficits and regional β‐amyloid burden, there were no strong associations that survived correction for multiple comparisons. However, neurocognitive and language impairment in these subjects strongly correlated with the degree of left lateral temporal and inferior parietal atrophy ( P < 0.004). Conclusions The findings from this study suggest a close relation between the severity of regional atrophy and cognitive and language impairment, but argue against a strong association between regional β‐amyloid burden and such deficits in aphasic AD subjects. Hence, other pathological factors may be driving the previously identified association between global β‐amyloid deposition and general cognitive impairment in aphasic AD .
Amyloid burden correlates with cognitive decline in Alzheimer's disease presenting with aphasia
Jung, Y. , Whitwell, Jennifer L. , Senjem, Matthew L. , Lowe, Val J. , Josephs, Keith A. , Duffy, Joseph R. , Strand, Edythe A. , Machulda, Mary M. , Jack, Clifford R. , Senjem, Matthew L

European Journal of Neurology | December 16, 2013 | Volume: 21 | Issue: 7 | Pages: 1040-1043

10.1111/ene.12331 Get It

Background and purposeA subset of patients with Alzheimer's disease (AD) present with early and prominent language deficits. It is unclear whether the burden of underlying β‐amyloid pathology is associated with language or general cognitive impairment in these subjects.MethodsThe relationship between cortical β‐amyloid burden on [11C]Pittsburgh compound B (PiB) positron emission tomography (PET) and performance on the Montreal Cognitive Assessment (MoCA), the Wechsler Memory Scale − Third Edition (WMS‐III), the Boston Naming Test (BNT) and the Western Aphasia Battery (WAB) was assessed using regression and correlation analyses in subjects presenting with aphasia who showed β‐amyloid deposition on PiB PET.ResultsThe global PiB ratio was inversely correlated with MoCA (P = 0.02) and the WMS‐III Visual Reproduction (VR) subtest (VR I, P = 0.02; VR II, P = 0.04). However, the correlations between PiB ratio, BNT (P = 0.13), WAB aphasia quotient (P = 0.11) and WAB repetition scores (P = 0.34) were not significant.ConclusionThis study demonstrates that an increased cortical β‐amyloid burden is associated with cognitive impairment, but not language deficits, in AD subjects presenting with aphasia. The results suggest that β‐amyloid deposition could be partly contributing to impaired cognition in such patients whilst language dysfunction may be more influenced by other pathological mechanisms, perhaps downstream pathways of β‐amyloid deposition.