Showing papers on "Aging brain published in 1981"

Energy‐Metabolising Enzymes in Brain Regions of Adult and Aging Rats

Abstract: The regional enzyme activities of glucose metabolism in the rat brain were investigated. Hexokinase (EC 2.7.1.1) and pyruvate dehydrogenase (EC 1.2.4.1), key enzymes for glucose metabolism, showed no changes in activity in all the regions studied of the aging brain as compared with the adult brain. However, the activity of d-3-hydroxybutyrate dehydrogenase (EC 1.1.1.30) is low throughout the adult brain and, in contrast with hexokinase and pyruvate dehydrogenase, its activity decreases significantly during aging. Other enzymes that showed significant decreases during aging are aldolase (EC 4.1.2.13), lactate dehydrogenase (EC 1.1.1.27), citrate synthase (EC 4.1.3.7), and NAD+-linked isocitrate dehydrogenase (EC 1.1.1.41). The catabolic enzyme in cholinergic metabolism, acetylcholinesterase (EC 3.1.1.7), selected as an example of a non-energy-metabolising enzyme, also showed significant decreases in all regions of the brain in aging, although its highest activity remained in the striatum. These results are discussed with respect to the energy metabolism in various brain regions and their status with aging.

Aging and Cell Structure

Abstract: 1. Central Nervous System.- 1. Introduction.- 2. Dendritic Changes.- 3. Loss of Neurons.- 4. Changes in Dendritic Spines.- 5. Changes in Synaptic Populations.- 6. Changes in Cell Body and Nuclear Sizes.- 7. Changes in Nucleoplasm.- 8. Changes in Neuronal Cytoplasm.- 9. Neurofibrillary Tangles.- 10. Lipofuscin.- 11. Neuroglia.- 12. Choroid Plexus.- References.- 2. The Mammalian Peripheral Nervous System in Old Age.- 1. Introduction.- 2. Age-Related Changes in Man.- 2.1. General Comments.- 2.2. The Aging Sensory Unit.- 2.3. The Aging Motor Unit.- 2.4. The Aging Peripheral Autonomic System.- 2.5. The Aging Peripheral Nerve of Man.- 3. Age-Related Changes in Animals.- 3.1. General Comments.- 3.2. The Aging Sensory Unit.- 3.3. The Aging Motor Unit.- 3.4. The Aging Peripheral Autonomic System.- 3.5. The Aging Peripheral Nerve of Laboratory Animals.- 4. Concluding Remarks.- 4.1. Lipofuscin.- 4.2. Central-Peripheral Distal Axonopathy.- 4.3. Proximal Demyelination.- 4.4. Neuronal Loss.- 4.5. Epilogue.- References.- 3. Neurofibrillary and Synaptic Pathology in the Aged Brain.- 1. Age-Associated Changes in the Human Brain.- 2. Neurofibrillary Pathology.- 2.1. Normal Fibrillar Proteins in the CNS.- 2.2. Neurofibrillary Changes.- 2.3. Experimentally Induced and Naturally Occurring Neurofibrillary Changes.- 3. Synaptic Pathology and Glial Reactions.- 3.1. Morphology of the Neuritic Plaque.- 3.2. Pathogenesis of the Neuritic Plaque.- 3.3. Morphology of the Neuritic Changes.- 3.4. Role of Microglial Cells in Amyloid Deposition.- 3.5. Relationships between Amyloid Fibrils and PHFs.- References.- 4. Cytomorphological Alterations in the Aging Animal Brain with Emphasis on Golgi Studies.- 1. Introduction.- 1.1. The Use of Animal Models in Aging Research.- 1.2. Memory Deficits in Aging Animals.- 1.3. Neuronal Loss in Aging.- 2. The Aging Brain: A Golgi Perspective.- 2.1. The Dendritic Tree and Its Spines.- 2.2. A Survey of Golgi-Impregnated Neuronal Changes in the Aging Cerebral Cortex.- 2.3. Age-Related Alterations in the Cerebellum-Purkinje Cells.- 2.4. Golgi Studies of Dendritic Plasticity in the Adult and Aged Brain.- 3. Electron Microscopy of the Aging Brain.- 3.1. Lipofuscin.- 3.2. Nuclear Membrane Infolding.- 3.3. Filamentous Accumulation.- 3.4. Corpora Amylacea.- 3.5. Synaptic Alterations.- 3.6. Tubulovesicular Profiles.- 3.7. Alterations in Myelinated Fibers.- 4. Discussion.- 4.1. Golgi Studies.- 4.2. Electron Microscopy-Structural Changes in Aging Animal Brain.- 5. Summary and Conclusions.- References.- 5. Variation: Principles and Applications in the Study of Cell Structure and Aging.- 1. Origin of Variation.- 2. Analysis of Variation.- 3. Variation and Aging.- 4. Applications.- 4.1. Variation in Mouse Liver Cellular and Fine Structure: Effects of Aging, Alcohol, and Antioxidants.- 4.2. Variation in Vitality and Mortality.- 4.3. Time-Condensing in Experimental Aging Research through the Study of Variation.- 5. Concluding Remarks.- References.- 6. Ultrastructure of the Aging Kidney.- 1. Introduction.- 2. Materials and Methods.- 2.1. Rats.- 2.2. Humans.- 2.3. Ultrastructural Studies.- 3. Results.- 3.1. Rat Ultrastructural Studies.- 3.2. Clinicopathologic Correlations.- 4. Discussion.- References.- 7. Electron Microscopy of Skeletal Aging.- 1. Introduction.- 2. Bone 252.- 2.1. Periosteum.- 2.2. Endosteum.- 2.3. Osteocytes.- 2.4. Osteoclasts.- 2.5. Bone Surfaces.- 3. Cartilage.- 3.1. General Cartilage Aging.- 3.2. Electron Microscopy of Aging Cartilage.- 4. Summary and Conclusions.- References.- 8. The Cardiovascular System.- 1. Introduction.- 2. The Effect of Age on Physiological Parameters of the Cardiovascular System.- 2.1. Heart Rate and Electrocardiogram.- 2.2. Blood Pressure.- 2.3. Cardiac Output and Stroke Volume.- 2.4. Contractile Properties.- 2.5. Decline of Physical Work Capacity.- 3. The Effect of Age on the Structure of the Myocardium.- 3.1. Connective Tissue.- 3.2. Myocardial Cell.- 4. The Effect of Age on Coronary Vessels.- 5. The Effect of Age on the Reactivity of the Cardiovascular System to Drugs.- 5.1. Age-Associated Changes in Pharmacokinetics of Drugs.- 5.2. Digitalis Glycosides.- 5.3. Autonomic Drugs.- 5.4. Antiarrhythmic Agents.- 6. Summary.- References.- 9. Fine Structure of Aging Skeletal Muscle.- 1. Introduction.- 2. Structural Changes in Human Muscle.- 3. Freeze-Fracture Studies.- References.- 10. Insect vs. Mammalian Aging.- 1. Introduction.- 2. Comparison of Tissue and Body Organization in Insects and Mammals.- 3. Fine Structural Manifestations of Aging.- 3.1. Age Pigment.- 3.2. Mitochondria.- 3.3. Ribosomes, Endoplasmic Reticulum Membranes, and RNA.- 3.4. Nuclei.- 4. Comparison between Insect and Mammalian Aging.- 5. Conclusions.- References.

Neurofibrillary and Synaptic Pathology in the Aged Brain

Abstract: Normal aging in the human brain may be thought of as a state in which pathological alterations exist without obvious clinical expression. Unlike other organs in which there is a repetition of structural-functional units, the brain is a complex collection of groups of nerve cells, each with varying metabolic and functional characteristics (a multiorgan organ). A decline in the number of brain cells or key connections with one another, when below a critical reserve level, would be expected to result in a deterioration of function, and create difficulties in coping with additional noxious or infectious stress. At the same time, genetically programmed time-associated changes in aging brain cells may increase their susceptibility to harmful environmental effects (hormonal, infectious, immunological) and lead to various pathological changes found in the aged brain.

Blood-brain barrier, aging, brain blood flow, and sleep.

Abstract: We have shown that significant ultrastructural changes occur with increasing age in the BBB in the nonhuman primate. It is probable that similar changes occur in aging humans. Clearly, morphophysiological changes, i.e., structural changes in cerebral capillaries, may alter the BBB mechanism as well as capillary perfusion which, in turn, may affect cerebral energy metabolism and neuronal function. Thus neurological function may be affected and sensitive indices of function such as sleep patterns altered.