Li Zhang1, Michael Chopp2, Yanlu Zhang2, Ye Xiong2, Chao Li2, Neema Sadry2, Imane Rhaleb2, Mei Lu2, Zheng Gang Zhang2. 1. From the Department of Neurology (L.Z., M.C., C.L., N.S., I.R., Z.G.Z.), Department of Neurosurgery (Y.Z., Y.X.), and Department of Biostatistics and Research Epidemiology (M.L.), Henry Ford Hospital, Detroit, MI; and Department of Physics, Oakland University, Rochester, MI (M.C.). lzhang@neuro.hfh.edu. 2. From the Department of Neurology (L.Z., M.C., C.L., N.S., I.R., Z.G.Z.), Department of Neurosurgery (Y.Z., Y.X.), and Department of Biostatistics and Research Epidemiology (M.L.), Henry Ford Hospital, Detroit, MI; and Department of Physics, Oakland University, Rochester, MI (M.C.).
Abstract
BACKGROUND AND PURPOSE: Diabetes mellitus (DM) is a common metabolic disease among the middle-aged and older population, which leads to an increase of stroke incidence and poor stroke recovery. The present study was designed to investigate the impact of DM on brain damage and on ischemic brain repair after stroke in aging animals. METHODS: DM was induced in middle-aged rats (13 months) by administration of nicotinamide and streptozotocin. Rats with confirmed hyperglycemia status 30 days after nicotinamide-streptozotocin injection and age-matched non-DM rats were subjected to embolic middle cerebral artery occlusion. RESULTS: Middle-aged rats subjected to nicotinamide-streptozotocin injection became hyperglycemic and developed cognitive deficits 2 months after induction of DM. Histopathologic analysis revealed that there was sporadic vascular disruption, including cerebral microvascular thrombosis, blood-brain barrier leakage, and loss of paravascular aquaporin-4 in the hippocampi. Importantly, middle-aged DM rats subjected to stroke had exacerbated sensorimotor and cognitive deficits compared with age-matched non-DM ischemic rats during stroke recovery. Compared with age-matched non-DM ischemic rats, DM ischemic rats exhibited aggravated neurovascular disruption in the bilateral hippocampi and white matter, suppressed stroke-induced neurogenesis and oligodendrogenesis, and impaired dendritic/spine plasticity. However, DM did not enlarge infarct volume. CONCLUSIONS: Our data suggest that DM exacerbates neurovascular damage and hinders brain repair processes, which likely contribute to the impairment of stroke recovery.
BACKGROUND AND PURPOSE:Diabetes mellitus (DM) is a common metabolic disease among the middle-aged and older population, which leads to an increase of stroke incidence and poor stroke recovery. The present study was designed to investigate the impact of DM on brain damage and on ischemic brain repair after stroke in aging animals. METHODS:DM was induced in middle-aged rats (13 months) by administration of nicotinamide and streptozotocin. Rats with confirmed hyperglycemia status 30 days after nicotinamide-streptozotocin injection and age-matched non-DMrats were subjected to embolic middle cerebral artery occlusion. RESULTS: Middle-aged rats subjected to nicotinamide-streptozotocin injection became hyperglycemic and developed cognitive deficits 2 months after induction of DM. Histopathologic analysis revealed that there was sporadic vascular disruption, including cerebral microvascular thrombosis, blood-brain barrier leakage, and loss of paravascularaquaporin-4 in the hippocampi. Importantly, middle-aged DMrats subjected to stroke had exacerbated sensorimotor and cognitive deficits compared with age-matched non-DM ischemicrats during stroke recovery. Compared with age-matched non-DM ischemicrats, DM ischemicrats exhibited aggravated neurovascular disruption in the bilateral hippocampi and white matter, suppressed stroke-induced neurogenesis and oligodendrogenesis, and impaired dendritic/spine plasticity. However, DM did not enlarge infarct volume. CONCLUSIONS: Our data suggest that DM exacerbates neurovascular damage and hinders brain repair processes, which likely contribute to the impairment of stroke recovery.
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