Journal of the American Heart Association · 2025
Cerebrospinal Fluid β-Amyloid and τ Levels in Patients With Iatrogenic Cerebral Amyloid Angiopathy, Sporadic Cerebral Amyloid Angiopathy, Alzheimer Disease, and Controls.
СтатьяСистематический обзорПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Jensen-Kondering Ulf, Margraf Nils G, Pikija Slaven, Rak-Frattner Kinga, Malojcic Branko, Frol Senta, Pretnar-Oblak Janja, de la Riva Patricia, Albajar Gomez Ines, DiFrancesco Jacopo C, Bersano Anna, Kuhlenbäumer Gregor, Storti Benedetta
Аннотация
BACKGROUND: Iatrogenic cerebral amyloid angiopathy (iCAA) is a subform of cerebral amyloid angiopathy caused by exposure to amyloid β. The aim of this study was to assess cerebrospinal fluid amyloid and τ concentrations in iCAA in comparison with sporadic cerebral amyloid angiopathy (sCAA), Alzheimer disease (AD), and controls.
METHODS: We conducted a systematic literature review to identify patients with iCAA with published cerebrospinal fluid marker concentrations. We then analyzed the cerebrospinal fluid concentrations of amyloid β40, amyloid β42, total τ, and phosphorylated τ 181, comparing them with the corresponding data of patients with sCAA, AD, and controls from our previous work.
RESULTS: The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study. Amyloid β40 concentrations did not differ significantly between iCAA and the other groups. Amyloid β42 concentration was significantly higher in controls than iCAA and the other groups. The amyloid β42/40 ratio was higher in iCAA than in AD and higher in controls than sCAA and AD. Total τ concentrations were lower in controls than iCAA but did not differ significantly between iCAA, sCAA, and AD. Phosphorylated τ concentrations were not significantly different in iCAA compared with controls, significantly higher in sCAA, and highest in AD.
CONCLUSIONS: The observation that phosphorylated τ concentrations in iCAA are not different from controls led us to the hypothesis that iCAA is characterized by amyloid plaque formation largely without concomitant phosphorylated τ aggregation, which is well compatible with most published pathologic studies.
METHODS: We conducted a systematic literature review to identify patients with iCAA with published cerebrospinal fluid marker concentrations. We then analyzed the cerebrospinal fluid concentrations of amyloid β40, amyloid β42, total τ, and phosphorylated τ 181, comparing them with the corresponding data of patients with sCAA, AD, and controls from our previous work.
RESULTS: The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study. Amyloid β40 concentrations did not differ significantly between iCAA and the other groups. Amyloid β42 concentration was significantly higher in controls than iCAA and the other groups. The amyloid β42/40 ratio was higher in iCAA than in AD and higher in controls than sCAA and AD. Total τ concentrations were lower in controls than iCAA but did not differ significantly between iCAA, sCAA, and AD. Phosphorylated τ concentrations were not significantly different in iCAA compared with controls, significantly higher in sCAA, and highest in AD.
CONCLUSIONS: The observation that phosphorylated τ concentrations in iCAA are not different from controls led us to the hypothesis that iCAA is characterized by amyloid plaque formation largely without concomitant phosphorylated τ aggregation, which is well compatible with most published pathologic studies.