Showing papers on "Aging brain published in 1983"

Accumulation of D-Aspartic Acid with Age in the Human Brain

Abstract: An age-related accumulation of D-aspartic acid was detected in the white matter of ten normal brains from individuals aged 30 to 80 years. Gray matter showed no systematic increase in D-aspartic acid. The rate constant for D-aspartate formation in the brain is equal to the predicted value calculated for 37 degrees C. Accumulation of the uncommon D-aspartate isomer in myelinated white matter implies that there is little or no turnover of this tissue, and this may have a bearing on dysfunction of the aging brain or on other diseases of myelin.

High Levels of Brain Dolichols in Neuronal Ceroid‐Lipofuscinosis and Senescence

Abstract: Dolichols as unesterified alcohols were identified as significant components of lipid extracts from storage cytosomes isolated post-mortem from the brains of patients with the infantile, late infantile, and juvenile types of neuronal ceroid-lipofuscinosis (NCL). Very small amounts of dolichols were present in the corresponding subcellular fractions of non-NCL brains. The nuclear fraction from NCL cerebral cortex contained the highest dolichol content expressed per milligram protein or lipid, whereas the crude mitochondrial fraction was the richest in normal brain. Highly significant elevations of dolichol levels were found in human cerebral cortex of patients with NCL and Alzheimer's disease compared with age-matched controls, but the levels were normal in Pick's disease. In human non-NCL cerebral cortex, dolichols increased from 16 micrograms/g at age 5 to over 200 at age 81. Rat cerebral cortex showed a similar progressive increase in dolichol content with age. The high dolichol values in NCL, Alzheimer's disease, and senescence appears to be related to the increase of lipofuscin in brain. This is the first time a uniform biochemical abnormality has been found in all childhood forms of NCL, but the enzyme defect is still unidentified. It may lie on pathways where dolichols and retinyl compounds are recycled in Golgi membranes and derived organelles during the biosynthesis of glycoproteins.

Biochemical changes of rat brain membranes with aging.

Abstract: Modification of membrane composition and enzymatic activities both in total brain homogenate and purified synaptic plasma membrane of 3 and 24 month old rats has been investigated. Protein, cholesterol and phospholipid content and (Na+, K+)ATPase and 2′, 3′ cyclic nucleotide phosphohydrolase activities were determined. The major changes occurred in the whole homogenate where a general increase in total protein and cholesterol content with age and a significant increase of the cholesterol/phospholipids molar ratio has been detected. In S.P.M. aging process induced a decrease of protein, cholesterol and phospholipids content associated with an increased membrane viscosity and a decrease of ΔE. These data are consistent with a change in the structural organization and in the distribution pattern of different cell population in the aging brain. A possible artifactual effect of freezing on the reported parameter is also discussed.

Exercise and the Aging Brain

Abstract: The clinical landmarks of an aging motor system closely resemble diseases of the extrapyramidal system, notably the basal ganglia. Similarly, mechanisms that appear to be related to one of these diseases, Parkinson's disease, also seem to be related to motor system aging. The nigrostriatal dopaminergic system, impaired in both Parkinson's disease and in aging, has been shown to be substantially involved in movement initiation. This involvement has been shown by analyzing nigrostriatal dopamine in fast vs slow responding animals, and by manipulating the dopaminergic system by pharmacological methods. Exercise may postpone the deterioration in response speed that is generally observed in the aged motor system, by maintaining the nigrostriatal dopamine system. This mechanism is suggested by differences in neurotransmitter function seen in exercise rats compared to sedentary rats, and in studies of dopamine metabolites obtained from exercised humans. These mechanisms suggest that an excellent physica...

DNA-polymerases in neuron and glial cells of developing and aging mouse brain.

Abstract: DNA-polymerases alpha and beta were studied in neuron and glial cells of mouse during developing and aging brain Maximum activity of alpha-enzyme was found to be prenatal, though a very low but significant level could be detected in aging brain Furthermore, this pattern was found to be dependent upon cell types that shift in peak activity just before birth in glial cells in contrast to neurons DNA-polymerase-beta remained high throughout the period studied though a second peak of activity was also observed at day 30 in both cell types, suggesting a possible role in DNA-replication in addition to DNA-repair It was found that beta-enzyme from glial cells behaves differently than the same enzyme from neurons

The Aging Brain: Cellular and Molecular Mechanisms of Aging in the Nervous System

Abstract: This monograph of 25 chapters, by a total of 74 contributors (39 of them outside North America), is dedicated to the memory of the famous teacher Guiseppe Levi, from the Institute of Normal Human Anatomy, University of Turin, Italy. The papers have been grouped into 5 major themes: cell mechanisms of ageing in the nervous system; ageing of membranes and the cytoskeleton; ageing of neurotransmitters; ageing involving receptor mechanisms; and human and clinical correlates of brain ageing. Use of the camera-ready (offset) reproduction method of printing has caused a noticeable unevenness of clarity in the type of certain chapters, but the tables, line-diagrams and small number of micrographs are reasonably clear. Some of the models presented seem rather remote from ageing of the brain for example, age-related changes in the iris muscle of the chick (Mussini et al), or a discussion of the latent period between initiation and appearance of cancers of the gastrointestinal tract in Cutler's treatise on the "dysdifferentiative hypothesis of mammalian longevity". On the other hand, some are highly topical: Bignami and Dahl on the neuronal cytoskeleton; acetylcholine synthesis and glucose metabolism, by the group from the Institute of Neurology, London; and changes in aminergic and GABA-ergic receptor binding function in ageing rats (Nomura et al; Kendall et al); as well as an important paper by Nordberg's group on both muscarinic and nicotinic cholinergic receptors in human tissues in normal ageing as well as in Alzheimer's and multi-infarct dementia. Almost every monograph on CNS ageing contains at least one chapter reviewing yet again the classical morphological lesions in the older human brain neuritic plaques, neurofibrillary tangles, etc. This book is no exception. The Staten Island group reiterates (for those who may still not have read about it) the usual discussion on the polypeptide triplets of the "paired helical filament" proteins making up the neurofibrillary degeneration seen in tangled nerve cells. However, in that other chapters demonstrate the increased breadth of experimentation embraced by the neurobiology of ageing (e.g,, neurotrophic factors from the regenerating retinae of goldfish, by some Weizmann Institute workers; or phospholipid biosynthesis studies in rat microsomes, by chemists at the University of Perugia), a selective romp through this text is probably justified, if only to see how very broad and sometimes fascinating the bandwagon of neural ageing has become in the more than 3 decades since Levi's "Growth and Aging" monograph suggested important affinities between early developmental differentiation and the later ageing phenomena within the nervous system.