Persistent neurological and cerebrovascular deficits following ischemic stroke in a transgenic mouse model of Alzheimer’s disease

Tissue nonspecific alkaline phosphatase (TNAP) is one of the most abundant enzymes in brain cerebral microvessels, although its function in human health and disease remains less clear. Our lab has demonstrated that the loss of TNAP activity in cerebral microvessels is linked to diminished blood‐brain barrier function and decreased cerebrovascular integrity in mouse models of sepsis, ischemic stroke, and Alzheimer’s disease (AD). While it is widely known that stroke and AD are comorbid, the relationship between existing AD and its impact on outcomes following ischemic stroke is less clear. The goal of this study was to assess the impact of a moderate cortical ischemic stroke on post‐stroke sensorimotor deficits and AD‐like neuropathology in a mouse model of AD. We hypothesized that post‐stroke loss of TNAP activity is accompanied by a persistent loss of cerebral blood flow (CBF), exacerbated sensorimotor deficits, elevated neuroinflammation, and increased beta‐amyloid deposition.