Showing papers on "Aging brain published in 1986"

Dendritic proliferation in the aging brain as a compensatory repair mechanism.

Abstract: Publisher Summary This chapter describes the alterations in dendritic extent as potential compensatory responses to age-related neuronal loss in selected brain regions and discusses the apparent breakdown of this compensatory response in Alzheimer's disease and in extreme old age in some brain regions. In considering alterations in dendritic extent as compensatory changes, changes taking place in the surrounding microenvironment of the dendritic trees being considered are also examined in the chapter. Scientists developed a model of two interacting classes of influences on dendritic extent in the aging brain. The loss of neighboring neurons is a proliferative influence in normal aging, at least up to some limit, which seems to be exceeded in very old age in some brain regions. This proliferative influence seems to be deficient in Alzheimer's disease. Partial denervation is a regressive influence in the aged brain, just as it is during earlier periods in the developmental continuum. There are brain regions in which both of these influences are operating. It is suggested that when both influences are operating on the same cell in the normally aging brain, the final effect on the dendritic tree will be a reflection of the net sum of these two influences. The rat cerebellar Purkinje cells represent one example in which there is both neighbor neuron death and an apparent loss of parallel fiber input.

Membrane Aging of the Brain Synaptosomes with Special Reference to Gangliosides

Abstract: Giacobini (1982) has proposed an idea of synaptic aging, according to which synapses are functionally developed to the maximal state in the developmental stage, and then may deteriorate in their function in senescence. Giacobini emphasized the relevance of reduced synaptic transmission to malfunction of the aging brain. Agerelated alterations of synaptic functions have been reported in terms of the levels, synthetic rates and releasing activities of neurotransmitters. Gibson and Peterson (1981a) reported the reduced synthetic rate of acetylcholine in aged mice with little change in acetylcholine content. Gibson and Peterson (1981b) also pointed out that the release of acetylcholine is severely affected with aging. We assumed that possible alterations of synaptic membranes would be responsible for the decrease In neurotransmission. We, therefore, have isolated synaptosomes from different age groups of mice and rats, and attempted to correlate the membrane changes with altered synaptic functions such as acetylcholine release.

Neurotransmitter Alterations in the Aging Brain

Abstract: This review of neurotransmitter alterations in aging brain is intended to focus on studies of human and animal material where one or more measurements were made of these special brain substances. There are several reasons to study neurotransmitter substances in aging nervous system: 1. neurotransmitters provide the means for communication between neurons in the CNS, and therefore, play a key role in the efficient processing of sensory, motor and integrative neural signals, as well as controlling the endocrine systems of the body [68–70]; 2. the loss of a particular neurotransmitter, dopamine, shows a strong correlation with age in man and animals, and is etiological for the age-related disease, Parkinsonism; 3. the means for detecting transmitters are easily adapted for quantitative analysis, allowing age vs transmitter level correlations, and 4. the potential for pharmacological intervention on brain aging is based, in part, on the known structure and metabolism of the neurotransmitters [41, 46].

Phospholipid Metabolism in Aging Brain

Abstract: The problem of aging may be considered from different points of view. Based on the main tendencies in the theoretical approach to aging, such points can be summarized as follows: a) predetermination (genetical?) of the maximal extent of life; b) result of random negative influences upon cells (Hocman, 1979). However, leaving aside the theoretical approach to the problem, valuable insight may be gained by studying the variety of metabolic changes during aging even though in these types of studies it is difficult to determine the causes and effects. Nevertheless, it is known that some biological functions are strictly connected with the membrane and that each modification of them may influence cellular functions. On this basis, we have studied some aspects of the metabolism of phospholipids in the brain, as these compounds influence the membrane status. In particular, we have determined the rate of the main phospholipid biosynthesis and turnover in aged rat brain with the final target of trying to connect some alterations of physiological functions to the variations of this metabolism. The knowledge of these metabolic changes connected with aging may also be useful for a pharmacological approach to the problem.

Biologic plasticity of the aging brain

Abstract: The study was performed to elucidate whether the biological plasticity of the brain is reduced with advancing age. Both glucose and energy metabolism in the brain cortex of male Wistar rats aged 6, 12, 24 and 30 months were investigated under normal conditions and in 12 and 24 months old rats under complete cerebral ischemia. Under physiological conditions, glucose, fructose-1,6-phosphate and ATP decreased from 6 to 12 months of age whereas pyruvate, malate and creatine phosphate fell from 12 to 30 months of age. It was concluded that glucose and energy metabolism in brain cortex may be slightly reduced with normal aging. Complete cerebral ischemia caused server reduction in cortical glucose, pyruvate, citrate, alpha-ketoglutarate, malate, oxaloacetate, ATP and creatine phosphate and an increase in fructose-1,6-phosphate, lactate, succinate and AMP. Differences between 12 and 24 month old animals became obvious. It is concluded that aged animals as compared to adult animals are not capable of reacting sufficiently to stress conditions. The biological capacity of the brain is assumed to be reduced with aging.

The Aging Brain

Abstract: This chapter discusses the relationship between functional alterations and brain metabolism in aging animals and humans and in the pathological conditions of Alzheimer’s disease (AD).

Treatment of cerebrovascular and aging brain disorders

Abstract: Compositions containing alpha -dihydroergocryptine and dihydroergocristine or their salts in association with a suitable pharmaceutical vehicle are useful for treating ailments associated with cerebral aging.