Amyloid-beta 40 as a biomarker of cognitive impairment in acute ischemic stroke

Aim: to study the role of amyloid-beta 40 (Aβ 40) in the development of cognitive impairment in acute ischemic stroke.
Materials and methods. The study included 70 patients aged 33–86 years, 46 men and 24 women. In patients with acute ischemic stroke cognitive status was assessed with Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment Test (MoCA), Frontal Assessment Battery (FAB), Schulte tables, Clock Drawing Test, Test for Semantic Verbal Fluency and Five Words Test. The concentration of Aβ 40 in the cerebrospinal fluid was determined. Morphometric (size of the infarct and leukoaraiosis area, volume of the brain ventricles and hippocampus) and diffusion-tensor parameters of MRI (fractional anisotropy of putamen, thalamus, hippocampus, corpus callosum, limbs of the internal capsule, the cingulate, the superior longitudinal and inferior fronto-occipital tracts) were studied.
Results. The concentration of Aβ 40 in the cerebrospinal fluid was 436,4 (226,0–514,0) pg/ml. The protein level was associated with the result of subtests «Orientation» (MMSE) and «Attention» (MoCA), as well as indirect recall with cues in MoCA. Patients with MMSE score of 24–27 points were characterized by a lower concentration of Aβ 40 as compared to patients with a score less than 24 points. Aβ 40 concentration more than 436,4 pg/mL was associated with a more severe somatic co-morbidity of stroke (hypertension, lower hemoglobin and albumin level, higher erythrocyte sedimentation rate), a smaller volume of the brain ventricles, lower fractional anisotropy of the thalamus, cingulate tracts and contralateral hippocampus. Aβ 40 concentration more than 436,4 pg/mL was also associated with a lower global cognitive status (according to the MMSE and MoCA), as well as the reduction in certain cognitive functions, namely, attention, visual-spatial functions and memory.
Conclusions. The concentration of Aβ 40 in the cerebrospinal fluid is a biological marker of severity type of post-stroke cognitive impairment. This interaction is probably due to the damage to the hippocampus, thalamus and cingulate tracts. In our opinion, the biomarker reflects both ischemic and neurodegenerative components of the pathogenesis of cognitive impairment in acute ischemic stroke.

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