Although the linkage between vascular dysfunction and Alzheimer’s disease has received much attention, the
influence of beta-amyloid (Aβ) deposits on microcirculation in the chronic stage of ischemic brain injury is unknown. To
examine the relationship of Aβ with the microcirculation around Aβ deposits in the chronic stage of cerebral infarction,
Wistar rats were exposed to permanent middle cerebral artery occlusion (MCAo). Microangiography using albuminfluorescein
isothiocyanate was performed 3 months after MCAo, followed by immunohistochemistry with GFAP and Aβ.
Two types of atrophic changes were observed in the thalamus of ischemic brains: mild atrophy and severe atrophy with
tissue defects. In both types, the deposition of Aβ was observed in the ventroposterior lateral and ventroposterior medial
nuclei of the thalamus. Although various patterns of microcirculation were observed in the thalamus, a high density of enlarged
microvessels with reactive gliosis was often observed around Aβ deposits. Conversely, enlarged low-density microvessels
with less reactive gliosis were observed in the Aβ deposits. Because the regions with reactive gliosis without
Aβ deposits showed no changes in microcirculation and previous reports showed the proangiogenic and anti-angiogenic
effects of Aβ in in vitro studies, we hypothesize that continuous Aβ deposits act directly on microvessels, rather than via
reactive gliosis. Although further studies are necessary, therapeutic approaches to reduce Aβ deposits might be a promising
approach to improve microcirculation in the thalamus in the chronic stage of ischemic stroke.
Keywords: Amyloid Aβ, angiogenesis, blood-brain-barrier, cerebral ischemia, gliosis, microcirculation, microvessels, middle
cerebral artery occlusion, thalamus, APP23.
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