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Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal‐dominant Alzheimer's disease
Author(s) -
CarmonaIragui María,
Balasa Mircea,
Benejam Bessy,
Alcolea Daniel,
Fernández Susana,
Videla Laura,
Sala Isabel,
SánchezSaudinós María Belén,
MorenasRodriguez Estrella,
RibosaNogué Roser,
IllánGala Ignacio,
GonzalezOrtiz Sofía,
Clarimón Jordi,
Schmitt Frederick,
Powell David K.,
Bosch Beatriz,
Lladó Albert,
Rafii Michael S.,
Head Elizabeth,
Molinuevo José Luis,
Blesa Rafael,
Videla Sebastián,
Lleó Alberto,
SánchezValle Raquel,
Fortea Juan
Publication year - 2017
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.2017.03.007
Subject(s) - cerebral amyloid angiopathy , apolipoprotein e , cerebrospinal fluid , alzheimer's disease , amyloid (mycology) , early onset alzheimer's disease , pathology , medicine , disease , biomarker , pittsburgh compound b , dementia , genetics , biology
We aimed to investigate if cerebral amyloid angiopathy (CAA) is more frequent in genetically determined than in sporadic early‐onset forms of Alzheimer's disease (AD) (early‐onset AD [EOAD]). Methods Neuroimaging features of CAA, apolipoprotein ( APOE ), and cerebrospinal fluid amyloid β (Aβ) 40 levels were studied in subjects with Down syndrome (DS, n = 117), autosomal‐dominant AD (ADAD, n = 29), sporadic EOAD ( n = 42), and healthy controls ( n = 68). Results CAA was present in 31%, 38%, and 12% of cognitively impaired DS, symptomatic ADAD, and sporadic EOAD subjects and in 13% and 4% of cognitively unimpaired DS individuals and healthy controls, respectively. APOE ε4 genotype was borderline significantly associated with CAA in sporadic EOAD ( P = .06) but not with DS or ADAD. There were no differences in Aβ040 levels between groups or between subjects with and without CAA. Discussion CAA is more frequently found in genetically determined AD than in sporadic EOAD. Cerebrospinal fluid Aβ40 levels are not a useful biomarker for CAA in AD.