Showing papers in "Neurobiology of Aging in 1987"

TL;DR: In this article, the authors reviewed evidence regarding neuron numbers and dendritic extent in normal aging rodent, monkey and human brain and in Alzheimer's disease and concluded that neuron loss and change in dendric extent are regionally specific, and corresponding brain regions do not always change in similar ways in rodents and primates.

TL;DR: A better understanding of the interactions between calcium homeostasis and calcium-dependent processes during aging will likely help in the design of more effective therapeutic strategies.

TL;DR: It is proposed that an underlying cause of altered Ca2+ homeostasis during brain aging may be an increased membrane conductance to Ca2+.

TL;DR: This commentary proposes that neurobiology of aging must look beyond the issue of age related changes in calcium concentrations within the cytosol to studies of structure, function, and dynamics of membranes to give a better clue about underlying mechanisms of these changes.

TL;DR: The decline in visual recognition ability in aging monkeys parallels the decline in memory observed with advancing age in humans.

TL;DR: The authors' data suggest that the increase occurs or accelerates significantly after age 70, but the case numbers preclude reaching such a conclusion with statistical confidence, however, when the patients are divided into those less than 70 and those older, fibrous astrocytes in the cellular layer are shown to be significantly increased in the latter group compared to the former.

TL;DR: Results suggest that with respect to short-term memory and exploration, differences between aged and young rats may be influenced by a "complexity" factor and may be secondary to differences in motivation and reactions to novelty.

TL;DR: Aged squirrel monkeys develop senile plaques in the brain that are similar to those occurring in aged rhesus monkeys and aged humans.

TL;DR: Results suggest that rabbits as young as 2 1/2 years old show behavioral and correlated neural response deficits and Neural unit activity in the hippocampus modeled the behavioral eyelid response but took much longer to develop in the older animals.

TL;DR: One of the genes modified in schizophrenia is postulated to be directly or indirectly linked to the control of excitatory neurotransmission; possibly the normal switching on of the expression of the adult form of the NMDA receptor is altered, resulting in an inappropriate functioning of this receptor.

TL;DR: It is suggested that D-1 receptor density is up-regulated by loss of dopamine during aging, which result in an altered complement of dopamine receptors in older humans and may provide a basis for selective pharmacotherapy in disorders of the basal ganglia.

TL;DR: The results suggest that the motor cortex of the human brain is capable of synaptic plasticity in response to aging-induced synaptic loss, and this plasticity is not apparent in the somatosensory cortex, where there is no age-related synapse loss.

TL;DR: Although the basal release of ACh was not altered by age, K+-stimulated ACh release was reduced in striatum, and the age-related increases in basal GLU and DA release may be important in the pathophysiology of cell death during aging.

TL;DR: In this paper, a P300 event-related potential (P3a) was recorded to unexpected, deviant auditory stimuli requiring no behavioral response, and the brain potential underwent systematic latency prolongation and amplitude decrease with advancing age.

TL;DR: The preserved glucose metabolism of the resting aging brain in the presence of structural atrophic changes is suggested to be in line with normal aging.

TL;DR: The rate of decline in striatal dopamine receptors is closely related to the rate of aging and maximal life span of the species and may reflect both maturational and senescent processes modifying the behavior of animals as they age.

TL;DR: Patients with early onset disease exhibit a more severe and more widespread loss of neurons from cortical and sub-cortical regions and the neurochemical changes involve not only the cholinergic system, but also neurons containing GABA, somatostatin and norepinephrine.

TL;DR: The mechanisms underlying the beneficial effect of BC-PS treatment on neuronal connectivity might be explained on the basis of its pharmacological actions on neuronal membranes, neurotransmission and/or interaction with NGF.

TL;DR: The relationship between diminished noradrenergic innervation and diminished immune responsiveness in aging mammals, while not clear on a causal level, is presented as a hypothesis for further testing.

TL;DR: Learning ability in a complex sequential T-maze (Stone maze) progressively declined with increasing age in rats which were normally housed in standard caging, but environmental enrichment significantly improved maze performance but did not prevent the age-dependent impairment.

TL;DR: The role of immunogenicity of use of stem cells in perinatal asphyxia and the current status of stem cell treatments for cerebral palsy are discussed.

TL;DR: The decrease in the density of D-1 DA receptors in senescent rats may underlie some of the age-related alterations in dopaminergic functions in the rat brain.

TL;DR: The results indicate that as the rat ages the density of the muscarinic receptors is altered differently in the various brain regions: it is decreased in the cerebral cortex, hippocampus, striatum and olfactory bulb of both male and female rats, but is increased in the brain stem of senescent males while no significant change is observed for females.

TL;DR: The decreases in 3H-NE uptake and NE levels in the hypothalamus were apparent at 12 months, whereas the decrease in 3 H-NE release after high frequency stimulation was seen in the senile rats.

TL;DR: Phosphatidylserine appears to restore acetylcholine release in aging rats by maintaining an adequate acetyl choline supply in the slices.

TL;DR: Differences in deprivation history are probably not responsible for previous findings that radial maze training early in life prevents the appearance of age-related deficits in accurate spatial memory.

TL;DR: The results do not support the hypothesized roles of blood-brain barrier disruption or of immunologically-mediated injury of the central nervous system in the pathogenesis of AD.

TL;DR: In this paper, it was shown that cell numbers in human brain structures of more than a factor or two may be missed when only cell density is measured, and that the cell numbers may be increased or decreased by up to a factor of two.

TL;DR: Findings indicate that a series of age-related behavioral changes occurs in the cat, some of these may be related to morphological and neurophysiological alterations in neurons in the caudate nucleus.

TL;DR: The histopathology of the aged animals' hippocampus and fiber tracts supports the possibility that the delayed alternation impairment shown by these animals was a result of age related degenerative changes.