Cerebral microvascular pathology in aging and Alzheimer's disease.
By Eszter Farkas, P. Luiten. Progress in neurobiology, 2001
1,126 citations recorded by the source corpus.
The aging of the central nervous system and the development of incapacitating neurological diseases like Alzheimer's disease (AD) are generally associated with a wide range of histological and pathophysiological changes eventually leading to a compromised cognitive status. Although the diverse triggers of the neurodegenerative processes and their interactions are still the topic of extensive debate, the possible contribution of cerebrovascular deficiencies has been vigorously promoted in recent years. Various forms of cerebrovascular insufficiency such as reduced blood supply to the brain or disrupted microvascular integrity in cortical regions may occupy an initiating or intermediate position in the chain of events ending with cognitive failure. When, for example, vasoconstriction takes over a dominating role in the cerebral vessels, the perfusion rate of the brain can considerably decrease causing directly or through structural vascular damage a drop in cerebral glucose utilization. Consequently, cerebral metabolism can suffer a setback leading to neuronal damage and a concomitant suboptimal cognitive capacity. The present review focuses on the microvascular aspects of neurodegenerative processes in aging and AD with special attention to cerebral blood flow, neural metabolic changes and the abnormalities in microvascular ultrastructure. In this context, a few of the specific triggers leading to the prominent cerebrovascular pathology, as well as the potential neurological outcome of the compromised cerebral microvascular system are also going to be touched upon to a certain extent, without aiming at total comprehensiveness. Finally, a set of animal models are going to be presented that are frequently used to uncover the functional relationship between cerebrovascular factors and the damage to neural networks.
Subfields: Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/fce68004996cf0c57809d3a03c067eac25404f53
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Citations in the corpus
- Alterations in the BOLD fMRI signal with ageing and disease: a challenge for neuroimaging (2003, background): “Altered cerebrovascular dynamics Although cerebrovascular pathology is found in many medical, neurological and psychiatric disorders, extensive research has shown that the cerebrovascular system undergoes important changes in multiple components in a continuum throughout the human lifespan, proba”
- Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s disease (2009, background): “These are atrophy and irregularities of arterioles and capillaries, swelling and increased number of pinocytic vesicles in endothelial cells, increase in collagen IV, heparan sulfate proteoglycans and laminin deposition in the basement membrane, disruption of the basement membrane, reduced total mic”
- The blood-brain barrier: an engineering perspective (2013, background): “From transmission electron microscope images of rat brain capillaries, the endothelial cell thickness ranges from about 0.2 μm away from the nucleus to about 0.9 μm in the vicinity of the nucleus (Farkas and Luiten, 2001; Nicaise et al., 2009).”
- Alzheimer disease and cerebrovascular pathology: an update (2002, background): “…vessels (Claudio, 1996; Farkas et al., 2000) with increase of collagen IV (Kalaria and Pax, 1995) and breakdown of the BBB are considered important factors for disturbances of cerebral metabolism, reduced cerebral blood flow and neural metabolic changes (Shi et al., 2000; Farkas and Luiten, 2001).”
- Early age-related changes in adult hippocampal neurogenesis in C57 mice. (2010, background): “The vascular environment , which is affected by aging (Farkas and Luiten, 2001), is an important regulator of cell proliferation (Palmer et al., 2000).”
- The blood-brain barrier in Alzheimer's disease (2017, neutral): “VE-cadherinexpressionwas recently shown to be reduced in brain vessels that accumulate fi brino-gen-A β (Fg-A β ) complexes in a model of hyperhomocysteinemia, a pathology that may accompany cognitive disorders including AD (Muradashvili et al., 2014).”
- The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, neutral): “…fewer intact branches, atrophic string vessels, increased irregularity of capillary surfaces, marked changes in the vessel diameter, capillary basement membrane thickening, and collagen accumulation in the basement membrane have been described in AD (Farkas and Luiten, 2001; Bailey et al., 2004).”
- Neurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders (2011, background): “These changes include the appearance of string vessels (collapsed and acellular membrane tubes), a reduction in capillary density, a rise in endothelial pinocytosis , a decrease in mitochondrial content, accumulation of collagen and perlecans in the basement membrane, loss of tight junctions and/or”
- Central nervous system pericytes in health and disease (2011, background): “Some studies have suggested that Alzheimer's disease entails pericyte abnormalitie”