Poststroke dementia

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Post-stroke dementia (PSD) is currently defined as any dementia occurring after stroke. The overall statistic is striking as the incidence of stroke doubles the risk of dementia. There is also a direct link between stroke and development of Alzheimer's disease; although the latter is responsible only for part of the eventually developed dementias; the fraction of patients with Alzheimer's disease accounts for 20-60 per cent of those with PSD.

Brain defects that develop after stroke are directly associated with glial cells, as both astrocytes and microglia determine the size of the infarction, and through permissive astrogliosis they determine posttraumatic remodelling and regeneration of brain regions, which were not put to death by infarction (Chapter 9.1). Therefore, new therapeutic strategies aimed at glial cells may significantly affect the functional outcome and prevalence of PSD.

A particular type of post-stroke dementia is represented by Binswanger's disease, (or subcortical dementia), which is a form of vascular dementia characterized by diffuse white matter lesions; it leads to progressive loss of memory, cognition and behavioural adaptation. The infarct occurring in white matter triggers progressive death of oligodendrocytes, activation of microglia and degeneration of axons. The primary pathological steps most likely are associated with ischaemic death of oligodendrocytes.

Another relatively frequent and grim outcome of brain ischaemia-related disease is represented by periventricular leucomalacia; a condition that causes diffuse cerebral white matter injury. This occurs mostly in prematurely (<32 weeks) born infants; an especially high incidence (up to 20 per cent) of periventricular leucomalacia is observed among those born with very low weight (<1500g). The roots of this pathology can be found in (1) poor vascularization of white matter in premature infants and (2) prevalence of oligodendrocyte progenitors, which are particularly sensitive to ischaemia, reactive oxygen species and glutamate excito-toxicity. Thus, periods of even comparatively mild ischaemia result in profound damage to white matter and the demise of many oligodendrocyte progenitors. This, in turn, leads to defective myelination, with further defects in cerebral cortex development and impairment of pyramidal tracts, with subsequent neurological disorders, including cerebral palsy and cognitive defects.

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