Opposite patterns of age-associated changes in neurons and glial cells of the thalamus of human brain

Abstract In an autopsy series of 19 individuals, age-ranged 24–94, a relatively age-spared region, the anterior–ventral thalamus, was analyzed by immunohistochemical techniques to visualize neurons (neurofilament protein), astrocytes (glial fibrillary acidic protein), microglial cells (CD68) and amy...

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Published inNeurobiology of aging Vol. 29; no. 6; pp. 926 - 936
Main Authors Guidolin, D, Zunarelli, E, Genedani, S, Trentini, G.P, De Gaetani, C, Fuxe, K, Benegiamo, C, Agnati, L.F
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.06.2008
Subjects
Adult
Aged
Aged, 80 and over
Aging - metabolism
Aging - pathology
Amyloid precursor protein
Brain ageing
Glio-neuronal networks
Humans
Internal Medicine
Male
Medicin och hälsovetenskap
Middle Aged
Neuroglia - cytology
Neuroglia - metabolism
Neurology
Neurons - cytology
Neurons - metabolism
Thalamus - cytology
Thalamus - metabolism
Glio-neuronal networks
Brain ageing
Amyloid precursor protein
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Summary:Abstract In an autopsy series of 19 individuals, age-ranged 24–94, a relatively age-spared region, the anterior–ventral thalamus, was analyzed by immunohistochemical techniques to visualize neurons (neurofilament protein), astrocytes (glial fibrillary acidic protein), microglial cells (CD68) and amyloid precursor protein. The pattern of immunoreactivity was determined by surface fractal dimension and lacunarity , the size by the field area (FA) and the spatial uniformity by the uniformity index . From the normalized FA values of immunoreactivity for the four markers studied, a global parameter was defined to give an overall characterization of the age-dependent changes in the glio-neuronal networks. A significant exponential decline of the GP was observed with increasing age. This finding suggests that early in life (age < 50 years) an adaptive response might be triggered, involving the glio-neuronal networks in plastic adaptive adjustments to cope with the environmental challenges and the continuous wearing off of the neuronal structures. The slow decay of the GP observed in a later phase (age > 70 years) could be due to the non-trophic reserve still available.
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ISSN:0197-4580
1558-1497
1558-1497
DOI:10.1016/j.neurobiolaging.2006.12.015