Chronic Neuroinflammation and Cognitive Decline in Patients with Cardiac Disease: Evidence, Relevance, and Therapeutic Implications.
Jan TraubAnna FreyStefan StoerkPublished in: Life (Basel, Switzerland) (2023)
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.
Keyphrases
- mild cognitive impairment
- cognitive decline
- cognitive impairment
- cerebral ischemia
- positron emission tomography
- white matter
- induced apoptosis
- traumatic brain injury
- lipopolysaccharide induced
- left ventricular
- lps induced
- end stage renal disease
- drug induced
- bone marrow
- resting state
- cell cycle arrest
- inflammatory response
- heart failure
- peritoneal dialysis
- subarachnoid hemorrhage
- cell therapy
- oxidative stress
- acute myeloid leukemia
- blood brain barrier
- ejection fraction
- emergency department
- chronic kidney disease
- single cell
- atrial fibrillation
- stem cells
- cell death
- patient safety
- quality improvement
- intensive care unit
- cell proliferation
- immune response
- hepatitis b virus
- multiple sclerosis
- patient reported outcomes
- spinal cord injury