Showing papers on "Aging brain published in 1991"

Serotonin, memory, and the aging brain.

Abstract: Serotonin is widely distributed throughout the central nervous system and is implicated in a variety of neural functions such as pain, feeding, sleep, sexual behavior, cardiac regulation and cognition. This paper is concerned with the last of these. Abnormalities of the serotonergic nervous system are well documented in pathologic studies of Alzheimer's disease and there is evidence suggesting that changes in this system occur in association with non-disease aging. Data on the role of serotonin in learning and memory and on the effects of aging on brain serotonin function are reviewed and discussed in relation to pharmacologic treatment strategies for the memory impairments associated with advancing age.

Plasticity and regeneration of the nervous system

Abstract: Molecular and Cellular Aspects of Central and Peripheral Nervous System Development.- New Molecular Insights on the Development of the Peripheral Nervous System.- DNA Content Revealed by Cytophotometry in Neurons: Variability Related to Neuroplasticity.- Prenatal Development of the Rat Amygdaloid Complex: An Electron Microscopic Study.- Recent Findings on the Regulation of Axonal Calibre.- Hormones, Neurotransmitters, Xenobiotics, and Development.- The Biogenic Monoamines as Regulators of Early (Pre-Nervous) Embryogenesis: New Data.- Hormone-Dependent Plasticity of the Motoneurons of the Ischiocavernosus Muscle: An Ultrastructural Study.- Reactive Sprouting (Pruning Effect) Is Altered in the Brain of Rats Perinatally Exposed to Morphine.- Effects of Serotonin on Tyrosine Hydroxylase and Tau Protein in a Human Neuroblastoma Cell Line.- Critical Periods of Neuroendocrine Development: Effects of Prenatal Xenobiotics.- In Vivo and in Vitro Models of Development.- Cell Plasticity During In Vitro Differentiation of a Human Neuroblastoma Cell Line.- LN-10, A Brain Derived cDNA Clone: Studies Related to CNS Development.- Spinal Cord Slices with Attached Dorsal Root Ganglia: A Culture Model for the Study of Pathogenicity of Encephalitic Viruses.- Human Fetal Brain Cultures: A Model to Study Neural Proliferation, Differentiation, and Immunocompetence.- Development and Regulation of Glia.- Origin of Microglia and Their Regulation by Astroglia.- Neuronal-Astrocytic Interactions in Brain Development, Brain Function, and Brain Disease.- Structure and Function of Glia Maturation Factor Beta.- Neuromodulatory Actions of Glutamate, GABA and Taurine: Regulatory Role of Astrocytes.- C-6 Glioma Cells of Early Passage Have Progenitor Properties in Culture.- Regeneration.- Brain Extracellular Matrix and Nerve Regeneration.- Human Nerve Growth Factor: Biological and Immunological Activities, and Clinical Possibilities in Neurodegenerative Disease.- Schwann Cell Proliferation During Postnatal Development, Wallerian Degeneration and Axon Regeneration in Trembler Dysmyelinating Mutants.- Basic FGF and its Actions on Neurons: A Group Account with Special Emphasis on the Parkinsonian Brain.- Molecular and Morphological Correlates Following Neuronal Deafferentiation: A Cortico-Striatal Model.- Monosialoganglioside GM1 and Modulation of Neuronal Plasticity in CNS Repair Processes.- Nerve Growth Factor in CNS Repair and Regeneration.- Aging.- Ordered Disorder in the Aged Brain.- Plasticity in Expression of Co-Transmitters and Autonomic Nerves in Aging and Disease.- Nicotinic Cholinergic Receptors in Human Brain: Effects of Aging and Alzheimer.- Macromolecular Changes in the Aging Brain.- ADP-Ribosylation: Approach to Molecular Basis of Aging.- Mechanisms of Cell Death.

Determination of superoxide dismutase activity by the polarographic method of catalytic currents in the cerebrospinal fluid of aging brain and neurologic degenerative diseases.

Abstract: The activity of the superoxide dismutase was measured by the polarographic method of catalytic currents in the cerebrospinal fluid of patients with age-related neurologic degenerative diseases, namely, amyotrophic lateral sclerosis and Alzheimer's disease, and of a reference group of normal subjects. The superoxide dismutase activity was found to increase with age in reference subjects (r = 0.81) while no significant correlation was found in amyotrophic lateral sclerosis and Alzheimer's disease patients. The activity mean values were significantly lower (P < 0.01) in patients with neurologic degenerative diseases than in the reference subjects. The changes of superoxide dismutase activity in the aging brain and in age-related neurologic degenerative diseases are discussed.

Effect of acetyl-L-carnitine on the dopaminergic system in aging brain.

Abstract: We studied the effect of acetyl-L-carnitine (ALCAR) on dopamine release and the effect of long-term acetyl-L-carnitine treatment on age-related changes in striatal dopamine receptors and brain amino acid levels. In striatal tissue that had been incubated with [3H]dopamine, acetyl-L-carnitine increased the release of [3H]dopamine evoked by electrical stimulation. In striatal tissue from aged mice administered acetyl-L-carnitine for 3 months, the release of [3H]dopamine evoked by electrical stimulation was higher than that of its aged control; the release after a second stimulation was similar in the two groups. There was a significant decline in the number of D1 striatal dopamine receptors with age. The Bmax was 51% lower in 1.5-year-old mice than in 4-month-old animals. Administration of acetyl-L-carnitine for 3 months diminished the reduction in the binding of [3H]SCH-23390. [3H]Spiperone binding to D2 receptors was not decreased with age and was not affected by acetyl-L-carnitine treatment. Age-related decreases in levels of several amino acids were observed in several brain regions. Acetyl-L-carnitine lessened the reduction in the level of taurine only in the striatum. The findings confirm the multiple effects of acetyl-L-carnitine in brain, and suggest that its administration can have a positive effect on age-related changes in the dopaminergic system.

Senile Dementia: a Threshold Phenomenon of Normal Aging?

Abstract: Neurochemical investigations with normal aging brains show that in the first 70 years of life no major changes of the glycolytic pathway can be observed. Only in the following decades does a significant decrease of brain metabolic turnover occur. Changes in nerve cell size, one of the most relevant parameters in evaluating a diffuse nerve cell atrophy, appear in the brain cortex not earlier than between 85 and 94 years of age; a 21% nerve cell shrinkage is the mean. The results demonstrate that a significant decrease in turnover of the glycolytic pathway is followed by a significant but moderate shrinkage of the nerve cells after a delay of 10-15 years. Similar investigations in brains from senile demented subjects demonstrate that the change in glycolytic turnover is much more a quantitative than a qualitative phenomenon. In comparison with age-matched controls a decrease in glycolytic turnover of more than 60% is observed. Morphometric investigations of the nerve cell sizes in the brain cortex of senile demented subjects showed a decrease of 45-55% when compared with age-matched controls. When normal aging is compared with senile dementia it seems that old age dementia is a threshold phenomenon which starts if the glycolytic turnover drops below 50% of its value in young healthy adults. Physiological aging, however, stays within the range of the reserve capacity of normal brain performance. In conclusion, it seems that the exhaustion of the functional reserve capacity may shift an aging brain into a dementia syndrome.

Serotonergic ligand binding in aging brain of experimental animals.

Abstract: Although the use of aging experimental animals for studying serotonergic neuronal changes is limited because of species differences, cholinergic neuronal deterioration does appear to be a feature common to mammalian aging brains. In the present study, a recently introduced experimental animal, Suncus murinus (house musk shrew, an insectivore classified as being at the stem of the mammalian phylogenic tree) which in certain physiological characteristics is more closely related to the primate than is the rat, was used as an experimental animal model for serotonergic neuronal deterioration in aging brain. We examined the changes in binding to the membrane fraction of aging brain cortex of the experimental animals Suncus and Fischer rat of the serotonergic ligands, 5-HT, imipramine, and 8-OH-DPAT. Morphological study of the brain stem including the Nucleus raphae by immunohistochemical staining demonstrated that in Suncus all the serotonergic ligands had decreasing affinity to the membrane of aging brain; binding of 8-OH-DPAT and imipramine decreased to a greater extent than that of 5-HT. In contrast, the aging rat brain showed no appreciable change in the binding of serotonergic ligands.

Macromolecular changes in the aging brain.

Abstract: Several studies suggest that a decline in transcriptional and translational events may play a crucial role in the molecular mechanism underlying the aging process (for a review see Giuffrida and Lajtha, 1987).