TY  - JOUR
A1  - Traub, Jan
A1  - Grondey, Katja
A1  - Gassenmaier, Tobias
A1  - Schmitt, Dominik
A1  - Fette, Georg
A1  - Frantz, Stefan
A1  - Boivin-Jahns, Valérie
A1  - Jahns, Roland
A1  - Störk, Stefan
A1  - Stoll, Guido
A1  - Reiter, Theresa
A1  - Hofmann, Ulrich
A1  - Weber, Martin S.
A1  - Frey, Anna
T1  - Sustained increase in serum glial fibrillary acidic protein after first ST-elevation myocardial infarction
JF  - International Journal of Molecular Sciences
N2  - Acute ischemic cardiac injury predisposes one to cognitive impairment, dementia, and depression. Pathophysiologically, recent positron emission tomography data suggest astroglial activation after experimental myocardial infarction (MI). We analyzed peripheral surrogate markers of glial (and neuronal) damage serially within 12 months after the first ST-elevation MI (STEMI). Serum levels of glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were quantified using ultra-sensitive molecular immunoassays. Sufficient biomaterial was available from 45 STEMI patients (aged 28 to 78 years, median 56 years, 11% female). The median (quartiles) of GFAP was 63.8 (47.0, 89.9) pg/mL and of NfL 10.6 (7.2, 14.8) pg/mL at study entry 0–4 days after STEMI. GFAP after STEMI increased in the first 3 months, with a median change of +7.8 (0.4, 19.4) pg/mL (p = 0.007). It remained elevated without further relevant increases after 6 months (+11.7 (0.6, 23.5) pg/mL; p = 0.015), and 12 months (+10.3 (1.5, 22.7) pg/mL; p = 0.010) compared to the baseline. Larger relative infarction size was associated with a higher increase in GFAP (ρ = 0.41; p = 0.009). In contrast, NfL remained unaltered in the course of one year. Our findings support the idea of central nervous system involvement after MI, with GFAP as a potential peripheral biomarker of chronic glial damage as one pathophysiologic pathway.
KW  - myocardial infarction
KW  - STEMI
KW  - glial fibrillary acidic protein
KW  - GFAP
KW  - neurofilament light chain
KW  - NfL
KW  - glial damage
KW  - cardiac magnetic resonance imaging
KW  - MRI
KW  - infarction size
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-288261
SN  - 1422-0067
VL  - 23
IS  - 18
ER  - 
TY  - JOUR
A1  - Traub, Jan
A1  - Frey, Anna
A1  - Störk, Stefan
T1  - Chronic neuroinflammation and cognitive decline in patients with cardiac disease: evidence, relevance, and therapeutic implications
JF  - Life
N2  - Acute and chronic cardiac disorders predispose to alterations in cognitive performance, ranging from mild cognitive impairment to overt dementia. Although this association is well-established, the factors inducing and accelerating cognitive decline beyond ageing and the intricate causal pathways and multilateral interdependencies involved remain poorly understood. Dysregulated and persistent inflammatory processes have been implicated as potentially causal mediators of the adverse consequences on brain function in patients with cardiac disease. Recent advances in positron emission tomography disclosed an enhanced level of neuroinflammation of cortical and subcortical brain regions as an important correlate of altered cognition in these patients. In preclinical and clinical investigations, the thereby involved domains and cell types of the brain are gradually better characterized. Microglia, resident myeloid cells of the central nervous system, appear to be of particular importance, as they are extremely sensitive to even subtle pathological alterations affecting their complex interplay with neighboring astrocytes, oligodendrocytes, infiltrating myeloid cells, and lymphocytes. Here, we review the current evidence linking cognitive impairment and chronic neuroinflammation in patients with various selected cardiac disorders including the aspect of chronic neuroinflammation as a potentially druggable target.
KW  - neuroinflammation
KW  - cognitive impairment
KW  - dementia
KW  - myocardial infarction
KW  - heart failure
KW  - hypertension
KW  - coronary artery disease
KW  - atrial fibrillation
KW  - cardiac arrest
KW  - aortic valve stenosis
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-304869
SN  - 2075-1729
VL  - 13
IS  - 2
ER  -