title: Similar ultrastructural breakdown of cerebrocortical capillaries in Alzheimer's disease, Parkinson's disease, and experimental hypertension. What is the functional link?
abstract: The brain, as an intensely active organ, is highly dependent on a sufficient nutrient and oxygen availability in order to reach its optimal working capacity. It is well known that the vital supply of energy substrates is provided by the circulatory system, which splits up into a fine, terminal capillary network in target tissues. These capillaries are considered as important sites, since the actual nutrient trafficking takes place through their walls. That is why an intact, preserved structure of the microvessels is crucial to fulfill their function. Since the brain is known to be particularly vulnerable to suboptimal oxygen and glucose delivery, the intact morphology of capillaries is of paramount importance. Several observations have indicated that the cerebral capillary ultrastructure is damaged in Alzheimer's disease (AD). Curiously, the regional cerebral blood flow of AD patients is also significantly lower than in age-matched control individuals. Based on these data, it has been suggested that the decreased blood supply and the cerebrovascular alterations contribute to the development of dementia. However, we have observed similar capillary damage in Parkinson's disease patients and chronically hypertensive rats in addition to AD cases, as presented here. These findings indicate that cerebral capillary damage is not exclusive for AD but occurs under other neurodegenerative disorders and hypertension, as well. We hypothesize that ultrastructural abnormalities of cerebral capillaries are causally related to decreased cerebral blood flow and create a condition that favors neurodegenerative mechanisms including the development of dementia.
authors.affiliation: Department of Animal Physiology, Graduate School of Behavioral and Cognitive Neurosciences, University of Groningen, The Netherlands. E.FARKAS@biol.rug.nl
authors.forename: E
authors.initials: E
authors.lastname: Farkas
authors.forename: G I
authors.initials: GI
authors.lastname: De Jong
authors.forename: E
authors.initials: E
authors.lastname: Apró
authors.forename: R A
authors.initials: RA
authors.lastname: De Vos
authors.forename: E N
authors.initials: EN
authors.lastname: Steur
authors.forename: P G
authors.initials: PG
authors.lastname: Luiten
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology; D000818:Animals; D001794:Blood Pressure; D002196:Capillaries / Q000473:pathology / Q000648:ultrastructure*; D002540:Cerebral Cortex / Q000098:blood supply* / Q000473:pathology*; D006801:Humans; D006973:Hypertension / Q000473:pathology* / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000473:pathology / Q000503:physiopathology; D010300:Parkinson Disease / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR