AIM: Although diabetes mellitus (DM) is considered to be one of the most consistent risks for developing dementia, it is not known if the pathology in dementia patients with DM is similar to or distinct from typical pathological features of Alzheimer's disease (AD). To discover the mechanism of developing dementia in AD patients with DM in a living state, we studied the distribution of amyloid β (Αβ) protein of diabetic AD patients. METHODS: To evaluate the accumulation of Aβ, we examined 14 normal controls, four diabetic patients with AD and 11 non-diabetic patients with AD by positron emission tomography (PET) using BF-227, a currently developed Aβ tracer. RESULTS: The analysis of PET images among the three groups showed an abundant aggregated Aβ accumulation in the cerebral cortex of both AD patients with and without DM. The extent and distributions of BF-227 accumulation in diabetic AD patients were not significantly different from these of non-diabetic AD patients. CONCLUSION: These results suggest that the degree and extent of Aβ deposition is not significantly different between AD with DM and AD alone.
AIM: Although diabetes mellitus (DM) is considered to be one of the most consistent risks for developing dementia, it is not known if the pathology in dementiapatients with DM is similar to or distinct from typical pathological features of Alzheimer's disease (AD). To discover the mechanism of developing dementia in ADpatients with DM in a living state, we studied the distribution of amyloid β (Αβ) protein of diabetic ADpatients. METHODS: To evaluate the accumulation of Aβ, we examined 14 normal controls, four diabeticpatients with AD and 11 non-diabeticpatients with AD by positron emission tomography (PET) using BF-227, a currently developed Aβ tracer. RESULTS: The analysis of PET images among the three groups showed an abundant aggregated Aβ accumulation in the cerebral cortex of both ADpatients with and without DM. The extent and distributions of BF-227 accumulation in diabetic ADpatients were not significantly different from these of non-diabetic ADpatients. CONCLUSION: These results suggest that the degree and extent of Aβ deposition is not significantly different between AD with DM and AD alone.
Authors: Eugene J Barrett; Zhenqi Liu; Mogher Khamaisi; George L King; Ronald Klein; Barbara E K Klein; Timothy M Hughes; Suzanne Craft; Barry I Freedman; Donald W Bowden; Aaron I Vinik; Carolina M Casellini Journal: J Clin Endocrinol Metab Date: 2017-12-01 Impact factor: 5.958
Authors: Jeremy J Pruzin; Julie A Schneider; Ana W Capuano; Sue E Leurgans; Lisa L Barnes; Rexford S Ahima; Steven E Arnold; David A Bennett; Zoe Arvanitakis Journal: Alzheimer Dis Assoc Disord Date: 2017 Jan-Mar Impact factor: 2.703
Authors: Steven E Arnold; Zoe Arvanitakis; Shannon L Macauley-Rambach; Aaron M Koenig; Hoau-Yan Wang; Rexford S Ahima; Suzanne Craft; Sam Gandy; Christoph Buettner; Luke E Stoeckel; David M Holtzman; David M Nathan Journal: Nat Rev Neurol Date: 2018-01-29 Impact factor: 42.937
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Authors: Timothy M Hughes; Kaycee M Sink; Jeff D Williamson; Christina E Hugenschmidt; Benjamin C Wagner; Christopher T Whitlow; Jianzhao Xu; S Carrie Smith; Lenore J Launer; Joshua I Barzilay; Faramarz Ismail-Beigi; R Nick Bryan; Fang-Chi Hsu; Donald W Bowden; Joseph A Maldjian; Jasmin Divers; Barry I Freedman Journal: J Diabetes Complications Date: 2018-05-29 Impact factor: 2.852