Showing papers on "Aging brain published in 1985"

Molecular biology of aging

Abstract: Symposium Lecture - I.- Aging Research: Challenge of the Twenty-First Century.- Wear and Tear Hypotheses.- Introductory Remarks: Session II.- Antioxidants and Longevity of Mammalian Species.- Relationship between Metabolic Rate, Free Radicals, Differentiation and Aging: A Unified Theory.- State of Knowledge on Action of Food Restriction and Aging.- The Endocrine Response to Dietary Restriction in the Rat.- Age Dependent Changes in Mitochondria.- Aging in Cellular Proteins.- Introductory Remarks: With Consideration of a T-Cell Model for Aging in Cellular Proteins.- Implications of 5?-Nucleotidase and its Inhibitor for Cellular Aging and Cancer.- The Effects of Dehydroepiandrosterone on the Rate of Development of Cancer and Autoimmune Processes in Laboratory Rodents.- The Alteration of Enzymes in Aging Animals.- Differential and Similar Responses Between Rodent and Human Cells to DNA-Damaging Agents: Possible Implications for Cellular Aging.- Symposium Lecture - II.- Living All Your Life.- Changes in DNA with Age - I.- Environmental and Genetic Factors that Influence Immunity and Longevity in Mice.- Cellular Senescence: Factors Modulating Cell Proliferation In Vitro.- Changes in Genetic Organisation and Expression in Aging Cells.- Changes in DNA with Age - II.- The Significance of DNA Methylation in Cellular Aging.- DNA Manipulating Genes and the Aging Brain.- In Vivo Studies on DNA Repair and Turnover with Age.- Hypersensitivity to DNA-Damaging Agents in Abiotrophies: A New Explanation for Degeneration of Neurons, Photoreceptors and Muscle in Alzheimer, Parkinson and Huntington Diseases, Retinitis Pigmentosa and Duchenne Muscular Dystrophy.- Reliability Theoretic Methods and Aging: Critical Elements, Hierarchies and Longevity-Interpreting Survival Curves.- Symposium Lecture - III.- The Odds on Normal Aging.- Diseases Featuring Altered Rates of Aging.- Introductory Remarks.- Progeria, A Model Disease for the Study of Accelerated Aging.- Amyloid, Immunopathology and Aging.- In Vitro Studies of Werner Syndrome Cells: Aberrant Growth and Chromosome behavior.- Molecular Basis of the Accumulation of Abnormal Proteins in Progeria and Aging Fibroblasts.- Future Directions in Aging Research.- Rapporteurs: R. W. Hart and A. Turturro.- L. Hayflick.- J. E. Seegmiller.- Participants.

Neuropathology of the Aging Brain and Dementia of the Alzheimer Type

Abstract: The two most prominent histopathological changes found in high numbers in the Alzheimer’s disease (AD) brain are the neurofibrillary tangle and the neuritic and amyloid plaque. Each of these lesions is characterized by an accumulation of proteinaceous fibrous profiles (the paired helical filaments) and amyloid fibers, respectively. These structures are not only distinguishable from each other but from all of the normal cellular filaments as well. Both lesions are also found, in low numbers, in the brains of aged, but otherwise clinically normal, individuals. This quantitative difference between age-associated pathology and the AD brain implies that the cause(s) responsible for the lesions may be fundamentally the same and differ only in degree.

Neurochemistry of the Aging Brain and Senile Dementia

Abstract: Neurochemical investigations demonstrate that normal brain aging is characterized by a moderate decrease in glycolytic turnover capacity. There is an age-dependent increase in soluble hexokinase activity and a significant decrease in activity of the key glycolytic enzyme phosphofructokinase. This decrease in the glycolytic turnover capacity lowers acetyl coenzyme A, necessary for the biosynthesis of acetylcholine. Therefore normal aging of the brain is additionally characterized by a moderate decline of the cholinergic activity. The monaminergic neurotransmitters also decrease, which results in a neurotransmitter imbalance.

Immunologic Factors Related to Cognitive/Behavioral Dysfunctions in Aging

Abstract: The loss of synapses (Bondareff 1976, 1980), the disappearance of neurotransmitter binding sites (Finch 1982; Lal and Carroll 1979; Severson and Finch 1980), and the mortality of neurons themselves (Colon 1973; Vogel 1969; Johnson and Erner 1972) are conspicuous changes observed in the normally aging mammalian CNS, and they have long been recognized as possible immediate causes for senescence-related declines in the capacity for adaptive behavior of both humans and animals (Landfield 1983; Rapport and Karpiak 1978). Continued research will no doubt further clarify the nature of degenerative changes in the normally aging brain, their contributions to normal senescence-related behavioral changes, and their relevance to senescence-related neuropsychopathology in humans.

Morphometrical and Microdensitometrical Studies on Monoaminergic and Peptidergic Neurons in the Aging Brain

Abstract: In a recent study we have characterized aging processes in transmitter-identified neurons demonstrated by immunocyto- chemistry or by radioreceptor autoradiography using computer assisted morphometry and microdensitomotry (Agnati et al. 1984). The results indicated the existence of heterogeneities in the degenerative patterns taking place in transmitter-identified nerve cells and receptors in relation to aging. It was i. a. discovered that the meso-striatal and meso-accumbens dopamine (DA) neurons underwent degeneration in the aging brain both pre- and postsynaptically, while the DA nerve terminal networks within the tuberculum olfactorium were resistant to the aging processes. Furthermore a marked and widespread disappearance of the μ- and Δ-type of opiate receptors were found in the aged brain, while the benzodiazepine binding was enhanced in several brain areas of the aging brain compared with the 3 month old rat brain. Thus, it is possible that in aging also supersensitivity development can take place in certain types of receptors such as the benzodiazepine receptors, which possibly represent co-transmitter binding sites in GABA synapses (see Guidotti et al. 1983). Instead, the GABA receptor binding sites are reduced in number in the aged brain, suggesting that some compensatory changes in aging may take place within the co-transmitter binding sites.

Trophic Factors in Brain Aging and Disease

Abstract: Success in treating and preventing infection and vascular disease has led to a significant increase in the number of people over the age of 65. This increase in the elderly population has focused attention on normal changes of the aging brain and the chronic disorders that may develop during the aging process. Clearly, such disorders are not inevitable consequences of aging, but they are present to a greater extent in aged individuals. The two common conditions which fall into this category are parkinsonism and Alzheimer’s disease. Both of these devastating diseases of the nervous system are degenerative disorders of unknown origin. In each, multiple etiologies, including viral or immunologic causes, have been implicated but never proven. Both conditions reflect pathologic changes in relatively limited pathways within the central nervous system. In Alzheimer’s disease and, to a much lesser extent, Parkinson’s disease, changes are noted which are known to occur in healthy older individuals. Thus, both conditions may represent accelerated aging of specific neuronal pathways. In order to understand the quantitative alterations in the brain of patients with these disorders, it is necessary to define the extent to which normal individuals demonstrate alterations in the number of neurons, in microscopic pathology, and in neurotransmitter metabolism during the aging process.

Effect of chronic treatment with phosphatidyl serine on phospholipase A1 and A2 activities in different brain areas of 4 month and 24 month old rats.

Abstract: The activities of phospholipase A1 and A2 were tested in mitochondria and microsomes from different cerebral areas of both 4 month and 24 month old rats, after 30 days i.p. treatment with ox Brain Cortex Phosphatidyl Serine (BC-PS). In the brain areas from control animals a rather great decline in its ability to hydrolize the fatty acids of the main phosphoglycerides was found. Taking into account only the effect of treatment with BC-PS on the modification of phospholipase activities caused by aging, we found that the treatment was able to balance the enzymatic functions altered by aging in several of the area examined. The importance of this result on the lipidic metabolism of the aging brain is also discussed.

Brain Plasticity and Aging

Abstract: The prevalence of most of the cerebral disorders in middle and old age has become obvious. Illnesses such as brain infarction, Parkinson’s disease, and the dementias, to mention only the most important ones, appear most frequently in later life. In addition to the burden they impose on the affected individuals and their families, such disorders consume socioeconomic resources. Both medical practice and research are challenged to alleviate disabilities originating in the diseased brain and to elucidate their underlying causes. To do this, it would seem necessary to determine whether aging per se inevitably leads to cerebral disorders such as those mentioned or whether such brain disorders occur in middle and old age independently of normal brain aging processes. Several findings support the view that normal cerebral aging is distinct from cerebral disorders of later life, particularly dementia (for review, see Hoyer 1982 b). For the normal brain, however, it has been possible to demonstrate certain differences between adulthood and senescence relating to mental capacities such as intelligence (Baltes and Schaie 1976; Baltes and Willis 1982; Horn and Cattell 1976; Horn and Donaldson 1976) and biological processes such as morphological and biochemical events (for review, see Hoyer 1982 a). It is therefore necessary to define the normal ranges of brain functions as they relate to age and to evaluate the effects of stress conditions on brain functions in later life in order to study the plasticity of the aging brain.

Blood Flow and Oxidative Metabolism of the Young Adult and Aging Brain

Abstract: During recent decades, an old desire of mankind seems to be fulfilled: that of becoming older and older. Progress in medical and social areas has increased the life expectancy of the population, at least in the highly developed countries. While in West Germany in 1974 about 13% of the population was 65 years and older (Lauter, 1974), this rate increased to about 16% by 1980. The estimated number of inhabitants aged 65 years and older will still be 16% in West Germany by the year 2000 although the population will decrease by 7% (Stat. Bundesamt, 1981). The process of aging is often a problem of the aging brain. However, physiological or normal cerebral aging should be strictly differentiated from pathological or abnormal cerebral aging. Different biological aspects will be discussed here in terms of normal cerebral aging to demonstrate similarities and differences in the young adult and aging brain.