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Adaptation to Hypoxia Prevents Beta‐Amyloid (Ab) Toxicity: Role of Nitric Oxide

Impaired synthesis of nitric oxide (NO) in cerebral blood vessels (CBV) results in endothelial dysfunction and brain hypoperfusion and thereby contributes to progression of Alzheimer’s disease (AD). Previously we have shown that adaptation to intermittent hypoxia (AH) can stimulate endothelial NO synthesis. We proposed that prior AH (simulated altitude 4,000 m; 4 h daily, 14 days) may restrict NO‐dependent disorders in experimental AD. AD was modeled in rats by a bilateral injection of Ab peptide fragment (25–35) into n. basalis magnocellularis. Dead neurons were revealed by Niessle staining. Memory retention was evaluated using the conditioned passive avoidance test. NO production was assessed by plasma level of NO2 and NO3. Endothelium‐dependent vasodilation was reflected by changes of local cerebral blood flow in response to acetylcholine using a laser Doppler probe. AH restricted cortical neuron death, memory retention loss, decrease in NO production and endothelial dysfunction. Inhibition of NO synthesis by L‐NNA aggravated the retention loss, whereas the NO donor dinitrosyl iron complex improved memory in Ab‐treated rats. Therefore stimulation of NO synthesis by AH can prevent neurodegeneration, cognitive disorders and endothelial dysfunction of CBV in experimental AD.