Premium
Inflammation and Breakdown of the Blood–Retinal Barrier During “Physiological Aging” in the Rat Retina: A Model for CNS Aging
Author(s) -
CHANLING TAILOI,
HUGHES SUZANNE,
BAXTER LOUISE,
ROSINOVA EMELIA,
McGREGOR IAIN,
MORCOS YVETTE,
VAN NIEUWENHUYZEN PETRA,
HU PING
Publication year - 2007
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680601073451
Subject(s) - microglia , retina , retinal , inflammation , neuroinflammation , blood–retinal barrier , occludin , central nervous system , blood–brain barrier , parenchyma , pathology , senescence , biology , infiltration (hvac) , tight junction , immunology , medicine , endocrinology , neuroscience , microbiology and biotechnology , ophthalmology , diabetic retinopathy , physics , thermodynamics , diabetes mellitus
Objective: To examine the possible contribution of inflammation and breakdown of the blood–brain barrier in the central nervous system (CNS) of physiologically aged rats showing cognitive decline. Methods: Young (3‐ to 6‐month‐old) and aged (24‐ to 30‐month‐old) Wistar rats were assessed by the novel object recognition test. Vascular and inflammatory changes in the CNS were investigated in whole‐mount preparations or sections of retinas from young adult or aged male Wistar rats. Results: Aged rats showed a significant impairment in short‐term memory compared with young adults. Deterioration of blood–retinal barrier function in aged rats was evidenced by leakage of intravascular tracer into the retinal parenchyma and reduced immunoreactivity for the tight junctional protein, occludin. Immunohistochemistry revealed the presence of major histocompatibility complex (MHC) class II‐positive resident microglia, activated T cells, and monocyte‐like cells in the retinal parenchyma of aged rats only. Microglia positive for the ED1 antigen, indicative of phagocytic activity, were also observed in these retinas. Conclusion: Breakdown of the blood–retinal barrier, MHC class II expression, microglial activation, and trafficking of activated T cells are associated with physiological aging. Such changes in the CNS may contribute to the pathogenesis of age‐related cognitive decline.