title: Vascular change of hippocampal capillary is associated with vascular change of retinal capillary in aging.
abstract: Vascular deficiency, such as deleterious change of endothelial cells, becomes the prominent feature of hippocampal microvessels during the processes of aging in rodents and it seems to be associated with deficiency of intellectual behavior in aged subjects. The hippocampal microvessels and hippocampal pyramidal neurons form and accumulate intermediates of advanced Maillard reaction (glycation) end products, specifically N()-carboxymethyl lysine (CML) and CML in rodents during the processes of aging. CML facilitates proliferation of endothelial cells in culture. However, further conjugation of CML with the substance(s) seems to occur in the microvessels and pyramidal neurons of hippocampus and it brings about deleterious change of endothelial cells and pyramidal neuron death. This would cause deficiency of recognition and reference memory in rodents during the processes of aging. In man in Alzheimer's disease (AD), one might speculate that formation and accumulation of CML in the hippocampal microvessels initiate the accumulation of amyloid to produce cerebral amyloid angiopathy and it brings about hypoglycemia and hypoxia in the hippocampal pyramidal neurons. Furthermore, formation and accumulation of CML in the hippocampal pyramidal neurons initiate the deposition of neurofibrillary tangles and senile plaques which cause neuronal death. In this way, vascular deficiency of hippocampal microvessels seems to be associated with the demented disease, the atrophic process of the brain and accumulation of amyloid in the brain in man. In terms of vascular deficiency concerns, the vascular change of the retinal capillaries becomes also a prominent feature during the processes of aging and it has a positive correlation with the vascular change of hippocampal capillary. In man during senescence, one might also speculate that vascular change of eye capillaries would become the early market for diagnosis of dementia in AD.
authors.affiliation: Laboratory of Kampo Medicine and Neuroendocrinology, Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900, USA. hagino@uthscsa.edu
authors.forename: Nobuyoshi
authors.initials: N
authors.lastname: Hagino
authors.forename: Shinjiro
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Taiki
authors.initials: T
authors.lastname: Tsutsumi
authors.forename: Seikoh
authors.initials: S
authors.lastname: Horiuchi
authors.forename: Ryoji
authors.initials: R
authors.lastname: Nagai
authors.forename: Gyury
authors.initials: G
authors.lastname: Setalo
authors.forename: Erizabet
authors.initials: E
authors.lastname: Dettrich
mesh_terms: D000375:Aging / Q000473:pathology*; D000818:Animals; D002196:Capillaries / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000473:pathology; D006624:Hippocampus / Q000098:blood supply* / Q000473:pathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000473:pathology*