Topographical localization of lipofuscin pigment in the brain of the aged fat-tailed dwarf lemur(Cheirogaleus Medius) and grey lesser mouse lemur(Microcebus Murinus): Comparison to iron localization

Abstract

The present study was undertaken to explore the distribution of lipofuscin in the brain of cheirogaleids by autofluorescence and compare it to other studies of iron distribution. Aged dwarf (Cheirogaleus medius) and mouse (Microcebus murinus) lemurs provide a reliable model for the study of normal and pathological cerebral aging. Accumulation of lipofuscin, an age pigment derived by lipid peroxidation, constitutes the most reliable cytological change correlated with neuronal aging. Brain sections of four aged (8–15 year old) and 3 young (2–3 year old) animals were examined. Lipofuscin accumulation was observed in the aged animals but not in the young ones. Affected regions include the hippocampus (granular and pyramidal cells), where no iron accumulation was observed, the olfactory nucleus and the olfactory bulb (mitral cells), the basal forebrain, the hypothalamus, the cerebellum (Purkinje cells), the neocortex (essentially in the pyramidal cells), and the brainstem. Even though iron is known to catalyse lipid oxidation, our data indicate that iron deposits and lipofuscin accumulation are not coincident. Different biochemical and morphological cellular compartments might be involved in iron and lipofuscin deposition. The nonuniform distribution of lipofuscin indicates that brain structures are not equally sensitive to the factors causing lipofuscin accumulation. The small size, the rapid maturity, and the relatively short life expectancy of the cheirogaleids make them a good model system in which to investigate the mechanisms of lipofuscinogenesis in primates. Am. J. Primatol. 49:183–193, 1999. © 1999 Wiley‐Liss, Inc.

Distinct Types of Lipofuscin Pigment in the Hippocampus and Cerebellum of Aged Cheirogaleid Primates

“…The purpose of our work was to use TEM to decipher the ultrastructure of lipofuscin within two different neuronal populations (hippocampal neurons and Purkinje cells), selected for their very different susceptibility to neurodegeneration, and in the same aged animals. Although lipofuscin accumulation did not appear to differ between 8‐year old and older cheirogaleid primate specimens (Gilissen et al, ), this study shows that dentate gyrus neurons and Purkinje cells accumulate lipofuscin granules of very different ultrastructures. Lipofuscin ultrastructure represents an anatomical outcome of the interaction between aging process and cellular physiology.…”

“…No lipofuscin was observed in the 3‐year old animal using confocal microscopy (see also Gilissen et al, ). This specimen was therefore not included in the EM study.…”

A Primer of Primate Pathology: Lesions and Nonlesions

“…All lemur species are endangered, but mouse and fat-tailed lemurs and bush babys are CITES II (of lower risk) (91). In current literature, the mouse lemur (Microcebus murinus) is suggested as a model for early Alzheimer's disease (79), and, along with the fat-tailed dwarf lemur (Cheirogaleus medius), as a model for age-related brain changes (41) and other aspects of neurobiology and neuropharmacology. Galagos including the lesser galago (Galago senegalensis) and the greater galago (Otolemur crassicaudatus) have also found a role in neuro-ophthalmologic research (48).…”

“…Several incidental lesions have been described in the brains of aging nonhuman primates including macaques, squirrel monkeys, and lemurs (28,41,42,79). These include lipofuscinosis, senile amyloid plaques, cerebrovascular amyloidosis, spheroids, and iron pigment.…”

Quantitation of sleep and spinal curvature in an unusually longevous owl monkey (Aotus azarae)

“…Brain iron and lipofuscin [17,18] Ring-tailed lemur 17 activity rhythm [51] data collected from few selected members of this colony. To remedy the then prevailing situation, we initiated our behavioral research program on this owl monkey colony in 2002.…”