title: Amyloid-beta deposits in the cerebral cortex of the aged common marmoset (Callithrix jacchus): incidence and chemical composition.
abstract: The incidence, distribution and chemical composition of amyloid-beta (A beta) peptide-positive deposits were investigated in the lower primate species common marmoset (Callithrix jacchus). No A beta deposits were observed in the brains of 7 marmosets below 7 years of age. In 15 marmosets above 7 years, 60% displayed cortical A beta-immunoreactive plaques, 80% had A beta deposited in intracortical vessels and 87% displayed A beta deposits in meningeal vessels. The cerebral cortex of the oldest animal (15 years) contained a substantial density of deposits. A beta-immunoreactive plaques were found predominantly in association cortical zones followed by a lower density in paralimbic cortical areas. Deposits within vessels were most frequent in occipital cortex. A beta40 was found primarily in vascular deposits, while A beta42 was present in plaques. Approximately 20% of plaques and most vascular deposits displayed thioflavin S staining, indicative of the presence of fibrillar A beta. Varying proportions of A beta deposits contained acetylcholinesterase or butyrylcholinesterase activities and apolipoprotein E and alpha1-antichymotrypsin immunoreactivity. A few plaques contained immunoreactivity for amyloid precursor protein in swollen neurites. However, no abnormally phosphorylated tau immunoreactivity was present in these neurites. Survival analysis in a colony of marmosets indicated that only 6% of animals can be expected to survive beyond 7 years of age. These results indicate that the aged marmoset brain displays A beta deposits with a distribution and chemical composition similar to those found in the human. These similarities suggest that the aged marmoset may be a useful lower primate model for the study of the pathological effects of A beta. However, the relatively small number of animals which can be expected to reach old age severely limits the utility of this species as a model of A beta deposition.
authors.affiliation: Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. cgeula@caregroup.harvard.edu
authors.forename: Changiz
authors.initials: C
authors.lastname: Geula
authors.forename: Nicholas
authors.initials: N
authors.lastname: Nagykery
authors.forename: Chuang-Kuo
authors.initials: CK
authors.lastname: Wu
mesh_terms: D000375:Aging / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000032:analysis*; D000818:Animals; D001057:Apolipoproteins E / Q000032:analysis; D052160:Benzothiazoles; D001927:Brain Diseases / Q000453:epidemiology / Q000401:mortality / Q000473:pathology*; D002144:Callithrix; D002540:Cerebral Cortex / Q000737:chemistry / Q000201:enzymology / Q000473:pathology*; D002802:Cholinesterases / Q000032:analysis; D004195:Disease Models, Animal; D005260:Female; D015994:Incidence; D008297:Male; D016501:Neurites / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D010446:Peptide Fragments / Q000032:analysis*; D058225:Plaque, Amyloid / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D016019:Survival Analysis; D013844:Thiazoles / Q000032:analysis; D000514:alpha 1-Antichymotrypsin / Q000032:analysis
chemical_list: D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D052160:Benzothiazoles; D010446:Peptide Fragments; D013844:Thiazoles; D000514:alpha 1-Antichymotrypsin; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42); C009462:thioflavin T; D002802:Cholinesterases