Aging brain

About: Aging brain is a(n) research topic. Over the lifetime, 1255 publication(s) have been published within this topic receiving 66405 citation(s).

The Adaptive Brain: Aging and Neurocognitive Scaffolding

Abstract: There are declines with age in speed of processing, working memory, inhibitory function, and long-term memory, as well as decreases in brain structure size and white matter integrity. In the face of these decreases, functional imaging studies have demonstrated, somewhat surprisingly, reliable increases in prefrontal activation. To account for these joint phenomena, we propose the scaffolding theory of aging and cognition (STAC). STAC provides an integrative view of the aging mind, suggesting that pervasive increased frontal activation with age is a marker of an adaptive brain that engages in compensatory scaffolding in response to the challenges posed by declining neural structures and function. Scaffolding is a normal process present across the lifespan that involves use and development of complementary, alternative neural circuits to achieve a particular cognitive goal. Scaffolding is protective of cognitive function in the aging brain, and available evidence suggests that the ability to use this mechanism is strengthened by cognitive engagement, exercise, and low levels of default network engagement.

Life and Death of Neurons in the Aging Brain

Abstract: Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.

Altered Histone Acetylation Is Associated with Age-Dependent Memory Impairment in Mice

Abstract: As the human life span increases, the number of people suffering from cognitive decline is rising dramatically. The mechanisms underlying age-associated memory impairment are, however, not understood. Here we show that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation and fail to initiate a hippocampal gene expression program associated with memory consolidation. Restoration of physiological H4K12 acetylation reinstates the expression of learning-induced genes and leads to the recovery of cognitive abilities. Our data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the aging mouse brain.

Oxidative stress in brain aging: Implications for therapeutics of neurodegenerative diseases

Abstract: Age has a powerful effect on enhanced susceptibility to neurodegenerative diseases, including susceptibility to stroke and cognitive impairment (CI) even in optimally healthy individuals We critically evaluated the notion that oxidative stress increases in aging brain Rigorous studies show logarithmic age-dependent increases in oxidized proteins and oxidized DNA lesions Decreased activity of antioxidant protective enzymes does not account for the observed increases The reactivity of the lipid oxidation product 4-hydroxy-2-nonenal (HNE) with key mitochondria enzymes may be important in the age-dependent loss in energy generation and enhanced susceptibility of neurons to apoptosis Age-dependent enhanced neuroinflammatory processes may play an important role in toxin generation that causes death or dysfunction of neurons in neurodegenerative diseases Non-steroidal anti-inflammatory drugs (NSAIDs) show significant promise Vitamin E supplementation did not show major beneficial effect on cognitive functions Major clinical trials for Alzheimer's disease (AD) involving cycloxygenase-II (COX II) inhibitors and amyloid-beta vaccination have been discontinued Novel therapeutics based on blocking neuron damaging neuroinflammatory processes show great promise for abating dementia progression although they have yet to make it to clinical practice

Neuron numbers and dendritic extent in normal aging and Alzheimer's disease

Abstract: Factors which limit the interpretation of studies of aging brain include: secular trends, species and strain differences, effects of tissue processing, and bias which may be introduced at many levels of an experimental design With these limitations considered, evidence is reviewed regarding neuron numbers and dendritic extent in normally aging rodent, monkey and human brain and in Alzheimer's disease It is concluded that neuron loss and change in dendritic extent in normal aging are regionally specific, and that corresponding brain regions do not always change in similar ways in rodents and primates It is suggested that such differences may, in part, be due to inconsistent definitions of ‘aged’ among species In Alzheimer's disease there is excess neuron loss and dendritic regression in some, but not all, brain regions Measures of the morphological substrates of brain function show appreciable overlap between AD and control groups It is hypothesized that the static, post-mortem status of brain morphology may not adequately reflect the functional capabilities of the dynamic morphology of the living brain