Aging brain

About: Aging brain is a research topic. Over the lifetime, 1255 publications have been published within this topic receiving 66405 citations.

Vascular Senescence: A Potential Bridge Between Physiological Aging and Neurogenic Decline

Abstract: The adult mammalian brain contains distinct neurogenic niches harboring populations of neural stem cells (NSCs) with the capacity to sustain the generation of specific subtypes of neurons during the lifetime. However, their ability to produce new progeny declines with age. The microenvironment of these specialized niches provides multiple cellular and molecular signals that condition NSC behavior and potential. Among the different niche components, vasculature has gained increasing interest over the years due to its undeniable role in NSC regulation and its therapeutic potential for neurogenesis enhancement. NSCs are uniquely positioned to receive both locally secreted factors and adhesion-mediated signals derived from vascular elements. Furthermore, studies of parabiosis indicate that NSCs are also exposed to blood-borne factors, sensing and responding to the systemic circulation. Both structural and functional alterations occur in vasculature with age at the cellular level that can affect the proper extrinsic regulation of NSCs. Additionally, blood exchange experiments in heterochronic parabionts have revealed that age-associated changes in blood composition also contribute to adult neurogenesis impairment in the elderly. Although the mechanisms of vascular- or blood-derived signaling in aging are still not fully understood, a general feature of organismal aging is the accumulation of senescent cells, which act as sources of inflammatory and other detrimental signals that can negatively impact on neighboring cells. This review focuses on the interactions between vascular senescence, circulating pro-senescence factors and the decrease in NSC potential during aging. Understanding the mechanisms of NSC dynamics in the aging brain could lead to new therapeutic approaches, potentially include senolysis, to target age-dependent brain decline.

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].

Neurosonology: a means of evaluating normal aging versus dementia

Abstract: The aging of the population and higher life expectancy have led to an increase in the incidence of cognitive changes and dementia. It is important to differentiate between cognitive changes associated with normal aging and those associated with dementia. Dementia is a syndrome caused by a heterogeneous group of disorders, the most common being Alzheimer’s disease and vascular dementia. While cardiovascular risk factors, such as diabetes mellitus, hypertension, hypercholesterolemia, atrial fibrillation and smoking, are particularly relevant in the development of vascular dementia, they may also play a role in Alzheimer’s disease. The control of these risk factors at an early stage may help to delay the onset and reduce the severity of vasculopathy. Cognitive changes and vasculopathy are correlated with decreased mean blood flow velocities in the main arteries of the brain. Intracranial hemodynamics of the aging brain can sucessfully be assessed by a number of methods, including transcranial Doppler sonogra...

Chapter 9 Changes in Neurotransmitter Signal Transduction Pathways in the Aging Brain

Abstract: Publisher Summary Cell to cell signaling in the brain propagates by ion flux-mediated electrical conduction and chemical stimulation of cell surface receptors. Chemical signaling by neurotransmitters represents the commonest mode of communication between nerve cells. A number of investigators have hypothesized that deficits in neurotransmission may underlie age-related changes in learning and memory and motor function and that these changes as well as other molecular and cellular alterations may promote or contribute to the development of age-related neurodegenerative diseases, including Alzheimer's Disease and Parkinson's Disease. This chapter discusses recent data from rodent, primate, and human studies that investigate age-related changes in interneuronal signaling by the classical neurotransmitters, acetylcholine, dopamine, norepinephrine, serotonin, glutamate, and GABA. It summarizes current research in this field as well as suggests future directions for investigation. The chapter discusses evidence that supports the presence of defective muscarinic cholinergic receptor G protein coupling in rat and human striata. In addition, it discusses evidence that suggests that age-related changes in neuronal membrane composition and structure contribute to changes in neurotransmitter signal conduction.

Chapter 5 Metabolism of the Aging Brain

Abstract: Publisher Summary This chapter discusses the effects of age on the metabolism of the nervous system are described both in unusually healthy individuals (successful aging) as well as in individuals who have diseases that are very common in the elderly (usual aging). The principles of neurobiology apply to the aging brain as they do to the adult and developing brain. The nervous system is complicated and regionally specialized. Dysfunction of the nervous system can often be documented at relatively early stages of disease or other damage, for instance by neuropsychological measurements or detailed neurological examination, and can often be mapped relatively precisely to specific parts of the brain, spinal cord, or peripheral nerves. The mechanisms of aging apply to the nervous system as they do to other tissues. In humans in vivo, cerebral metabolism tends to fall with aging, although it is possible to select a group of very healthy older subjects in whom measures of cerebral metabolism (cerebral metabolic rate for glucose [CMRglu] or for oxygen [CMRO 2 ] or for cerebral blood flow [CBF]) are comparable to those in younger subjects. A number of common diseases of aging can reduce cerebral metabolic rates, including cardiac disease, hypertension, strokes and other forms of cerebrovascular disease, and Alzheimer's disease. The decreases in metabolic rate in aged brain may be due to damage by reactive oxygen species (ROS), particularly to mitochondrial DNA (mtDNA) and to the cytochromes derived from mtDNA.