Aging brain

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

In vivo quantification of white matter microstructure for use in aging: a focus on two emerging techniques.

Abstract: Human brain imaging has seen many advances in the quantification of white matter in vivo. For example, these advances have revealed the association between white matter damage and vascular disease as well as their impact on risk for and development of dementia and depression in an aging population. Current neuroimaging methods to quantify white matter damage provide a foundation for understanding such age-related neuropathology; however, these methods are not as adept at determining the underlying microstructural abnormalities signaling at risk tissue or driving white matter damage in the aging brain. This review will begin with a brief overview of the use of diffusion tensor imaging (DTI) in understanding white matter alterations in aging before focusing in more detail on select advances in both diffusion-based methods and multi-component relaxometry techniques for imaging white matter microstructural integrity within myelin sheaths and the axons they encase. Although DTI greatly extended the field of white matter interrogation, these more recent technological advances will add clarity to the underlying microstructural mechanisms that contribute to white matter damage. More specifically, the methods highlighted in this review may prove more sensitive (and specific) for determining the contribution of myelin versus axonal integrity to the aging of white matter in brain.

Glutamate Receptors in Aging and Alzheimer's Disease

Abstract: The discovery that the stimulation of ionotropic glutamate receptors mediates not only the physiological action of glutamate but also a neurotoxic response provided the impetus for numerous investigations that sought to determine the role of glutamate in the pathophysiology of a number of neurodegenerative diseases, including Alzheimer's disease (AD). To date, nearly 200 articles have been published that specifically focus on the integrity and/or functional properties of the glutamate receptors in aging and AD. This chapter attempts to synthesize the results of these many studies and present them in as unbiased manner as possible. The chapter is divided into four main sections: (i) overview of the glutamate receptors, (ii) glutamate receptors in the aging (rodent) brain, (iii) glutamate receptors in the AD brain, and (iv) current topics of glutamate toxicity in AD. What will become obvious following the reading of this chapter is that data are at times inconsistent, with some investigators reporting that glutamate receptors are highly vulnerable in the aged and AD brain, whereas others state that these receptors are intact or even hyperfunctional. Contributing to these inconsistencies are a host of technical issues. To address this matter, the details of a number of studies (i.e., strain, species, age, brain region investigated, postmortem interval, when applicable) are presented in tabular form ( TABLE 20.1 , TABLE 20.2 , TABLE 20.3 , TABLE 20.4 , TABLE 20.5 , TABLE 20.6 , TABLE 20.7 , TABLE 20.8 , TABLE 20.9 , TABLE 20.10 , TABLE 20.11 , TABLE 20.12 , TABLE 20.13 , TABLE 20.14 ). By providing this information, it is our goal that the reader will be able to make some personal assessment of the extent to which technical details, may or may not, confound the biological relevance of the findings. It is also important to bear in mind that much of our knowledge of glutamate receptors in aging and AD has come about through studies employing autoradiographic techniques to investigate the anatomical distribution and density of various ligand-specific binding sites. Although these studies have been of considerable value in defining the role of glutamate in the aging brain and AD, it is clear from our knowledge of the molecular biology of the glutamate receptor that specific techniques are required allowing for the identification of individual glutamate receptor subtypes. Studies employing these latter techniques are currently underway in several laboratories and while much of the data remain unpublished it is clear that these works will play a critical role in the future in defining glutamates participation as an excitotoxic agent in the aging brain and AD.

Serotonergic ligand binding in aging brain of experimental animals.

Abstract: Although the use of aging experimental animals for studying serotonergic neuronal changes is limited because of species differences, cholinergic neuronal deterioration does appear to be a feature common to mammalian aging brains. In the present study, a recently introduced experimental animal, Suncus murinus (house musk shrew, an insectivore classified as being at the stem of the mammalian phylogenic tree) which in certain physiological characteristics is more closely related to the primate than is the rat, was used as an experimental animal model for serotonergic neuronal deterioration in aging brain. We examined the changes in binding to the membrane fraction of aging brain cortex of the experimental animals Suncus and Fischer rat of the serotonergic ligands, 5-HT, imipramine, and 8-OH-DPAT. Morphological study of the brain stem including the Nucleus raphae by immunohistochemical staining demonstrated that in Suncus all the serotonergic ligands had decreasing affinity to the membrane of aging brain; binding of 8-OH-DPAT and imipramine decreased to a greater extent than that of 5-HT. In contrast, the aging rat brain showed no appreciable change in the binding of serotonergic ligands.

Alcohol in the Aging Brain - The Interplay Between Alcohol Consumption, Cognitive Decline and the Cardiovascular System.

Abstract: As our society grows older new challenges for medicine and healthcare emerge. Age-related changes of the body have been observed in essential body functions, particularly in the loco-motor system, in the cardiovascular system and in cognitive functions concerning both brain plasticity and changes in behavior. Nutrition and lifestyle, such as nicotine intake and chronic alcohol consumption, also contribute to biological changes in the brain. This review addresses the effect of alcohol consumption on cognitive decline, changes in brain plasticity in the aging brain and on cardiovascular health in aging. Thus, studies on the interplay of chronic alcohol intake and either cognitive decline or cognitive preservation are outlined. Because of the inconsistency in the literature of whether alcohol consumption preserves cognitive functions in the aging brain or whether it accelerates cognitive decline, it is crucial to consider individual contributing factors such as culture, health and lifestyle in future studies.

Catechol-o-methyl transferase modulates cognition in late life: evidence and implications for cognitive enhancement.

Abstract: Aging is associated with deficits in several cognitive domains as well as a decline in brain dopamine activity. Catechol-O-methyl transferase (COMT), an enzyme involved in the degradation of dopamine, is a critical determinant of the availability of this neurotransmitter in the prefrontal cortex. A functional single nucleotide polymorphism in the COMT gene, Val158Met, modulates the activity of this enzyme and affects cognition and the brain regions underlying this function. The effects of COMT Val158Met polymorphism are magnified in the aging brain. Here, we review the evidence supporting a role of COMT genetic variation in cognitive as well as structural and functional brain changes associated with senescence. We will address the potential modulatory role of genetic and non-genetic factors on the neural and cognitive effects of COMT Val158Met in late life. Furthermore, we will discuss the viability of a COMT-targeted treatment for improving cognitive efficiency in aging.