Cerebrospinal Fluid C3a Increases with Age, But Does Not Increase Further in Alzheimer’s Disease

• Published in: Neurobiology of aging 1997-09, Vol.18 (5), p.555-557
• Main Authors: Loeffler, D.A, Brickman, C.M, Juneau, P.L, Perry, M.F, Pomara, N, LeWitt, P.A
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Aging; Aging - cerebrospinal fluid; Alzheimer Disease - cerebrospinal fluid; Alzheimer’s disease; Biological and medical sciences; Cerebrospinal fluid; Complement; Complement C3a - cerebrospinal fluid; Complement Membrane Attack Complex; Complement System Proteins - cerebrospinal fluid; Complement System Proteins - metabolism; Development. Senescence. Regeneration. Transplantation; Female; Fundamental and applied biological sciences. Psychology; Glycoproteins - cerebrospinal fluid; Glycoproteins - metabolism; Humans; Male; Middle Aged; Vertebrates: nervous system and sense organs
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/S0197-4580(97)00110-3

Complement activation is present in the brain in Alzheimer’s disease (AD), and C1q concentrations are decreased in AD cerebrospinal fluid (CSF). To determine whether concentrations of other complement proteins are also altered in AD CSF, we measured concentrations of C3a and SC5b-9 in CSF from patients with probable AD ( n = 19), normal aged controls ( n = 11), and normal younger controls ( n = 15). C3a concentrations were similar between AD and aged controls, but threefold higher than in younger controls ( p < 0.05 vs. both groups). A similar pattern was found with SC5b-9, though the increase was only twofold and statistically significant only for AD vs. younger controls. These results suggest that an increased generation of complement proteins in localized areas of the AD brain does not result in elevated concentrations of these proteins in CSF, compared with age-matched controls. Increased C3a (and, to a lesser extent, SC5b-9) in aged controls may be due to increased complement activation, increased central nervous system production, and/or blood–brain barrier leakage of these proteins.