Age-dependent cerebrovascular dysfunction in a transgenic mouse model of cerebral amyloid angiopathy

摘要: The Tg2576 transgenic mouse model of human cerebral amyloid angiopathy is characterized by age-dependent cerebrovascular deposition amyloid- β (A ) starting from 9 months age and progressively worsening to involve most pial arterioles 18 months; soluble A levels are elevated long before vascular takes place in this model. It has been suggested that alone sufficient impair blood flow (CBF) regulation thereby contributing the early progression Alzheimer's disease. Using laser speckle flowmetry through an intact skull, we studied impact on a wide range CBF responses evaluate vasodilation vasoconstriction young or aged mice. Nineteen-month-old with severe deposits showed attenuated hyperaemic response during hypercapnia whisker stimulation compared wild-type littermates. anticipated increase due isoflurane anaesthesia was also suppressed, as were typical hypoperfusion cortical spreading depression α -chloralose anaesthesia. 8-month-old levels, but without deposition, did not differ age-matched controls. In conclusion, our data suggest associated impaired vasodilator well vasoconstrictor stimuli. These do controls when non-invasively prior thus challenging view cause dysfunction.