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Diagonal Earlobe Crease is a Visible Sign for Cerebral Small Vessel Disease and Amyloid-β

We investigated the frequency and clinical significance of diagonal earlobe crease (DELC) in cognitively impaired patients using imaging biomarkers, such as white matter hyperintensities (WMH) on MRI and amyloid-β (Aβ) PET. A total of 471 cognitively impaired patients and 243 cognitively normal (CN)...

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Detalles Bibliográficos
Autores principales: Lee, Jin San, Park, Seongbeom, Kim, Hee Jin, Kim, Yeshin, Jang, Hyemin, Kim, Ko Woon, Rhee, Hak Young, Yoon, Sung Sang, Hwang, Kyoung Jin, Park, Key-Chung, Moon, Seung Hwan, Kim, Sung Tae, Lockhart, Samuel N., Na, Duk L., Seo, Sang Won
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5645376/
https://www.ncbi.nlm.nih.gov/pubmed/29042572
http://dx.doi.org/10.1038/s41598-017-13370-8
Descripción
Sumario:We investigated the frequency and clinical significance of diagonal earlobe crease (DELC) in cognitively impaired patients using imaging biomarkers, such as white matter hyperintensities (WMH) on MRI and amyloid-β (Aβ) PET. A total of 471 cognitively impaired patients and 243 cognitively normal (CN) individuals were included in this study. Compared with CN individuals, cognitively impaired patients had a greater frequency of DELC (OR 1.6, 95% CI 1.1–2.2, P = 0.007). This relationship was more prominent in patients with dementia (OR 1.8, 95% CI 1.2–2.7, P = 0.002) and subcortical vascular cognitive impairment (OR 2.4, 95% CI 1.6–3.6, P < 0.001). Compared with Aβ-negative cognitively impaired patients with minimal WMH, Aβ-positive patients with moderate to severe WMH were significantly more likely to exhibit DELC (OR 7.3, 95% CI 3.4–16.0, P < 0.001). We suggest that DELC can serve as a useful supportive sign, not only for the presence of cognitive impairment, but also for cerebral small vessel disease (CSVD) and Aβ-positivity. The relationship between DELC and Aβ-positivity might be explained by the causative role of CSVD in Aβ accumulation.