Cognitive Decline Clinical Trial
Official title:
Role of Th1-lymphocytes in the Development of Vascular Cognitive Impairment in Young Stroke Patients
In the present study, the investigators aim to elucidate the role of T-cells on cognitive decline in younger stroke patients, using repeated cognitive testing, brain imaging, and immunological analyses in the first 6 month after stroke. The examiners will investigate (i) the extent and duration of stroke-induced changes in T cell function within the peripheral blood of patients; and (ii) post-stroke cognitive functions.
Demands from society on stroke patients of younger age are in most cases higher than for
elderly stroke patients, because of occupational obligations and often their role as a
caregiver for a young family. For example, return to their former workplace may be impossible
even if cognitive deficits, e.g., in the memory domain, are only "minor" according to
standardized tests. Thus, cognitive function after stroke is of utmost importance for
activities of daily life and quality of life in young stroke patients. In order to prevent or
at least reduce post-stroke cognitive decline, the mechanisms underlying the decline need to
be further elucidated, to eventually develop new preventive and therapeutic approaches.
T-cell activation is associated with destruction of brain tissue. In neurodegenerative
diseases that primarily impair cognitive functions, e. g., Alzheimers Disease, T-cells were
identified as important mediators of disease pathology. Activation of cells of the adaptive
immune system, most importantly T-cells, has been also investigated in experimental stroke.
Here, these cells significantly contribute to secondary brain tissue damage. Stroke is
associated with massive changes of the central and peripheral immune response. The
investigators and other groups demonstrated that despite an overall lymphopenia, T-cells are
functionally intact and pro-inflammatorily polarized, for at least two weeks post-stroke.
Depletion of T cells has been shown to reduce infarct volume and to improve outcome in mice
post-experimental stroke.
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