Aging brain

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

Multiple Brain Markers are Linked to Age-Related Variation in Cognition

Abstract: Age-related alterations in brain structure and function have been challenging to link to cognition due to potential overlapping influences of multiple neurobiological cascades. We examined multiple brain markers associated with age-related variation in cognition. Clinically normal older humans aged 65-90 from the Harvard Aging Brain Study (N = 186) were characterized on a priori magnetic resonance imaging markers of gray matter thickness and volume, white matter hyperintensities, fractional anisotropy (FA), resting-state functional connectivity, positron emission tomography markers of glucose metabolism and amyloid burden, and cognitive factors of processing speed, executive function, and episodic memory. Partial correlation and mediation analyses estimated age-related variance in cognition shared with individual brain markers and unique to each marker. The largest relationships linked FA and striatum volume to processing speed and executive function, and hippocampal volume to episodic memory. Of the age-related variance in cognition, 70-80% was accounted for by combining all brain markers (but only ∼20% of total variance). Age had significant indirect effects on cognition via brain markers, with significant markers varying across cognitive domains. These results suggest that most age-related variation in cognition is shared among multiple brain markers, but potential specificity between some brain markers and cognitive domains motivates additional study of age-related markers of neural health.

Astrocytes in the aging brain.

Abstract: Astrocytes have traditionally been viewed as passive supportive cells, which were primarily responsible for maintaining an optimal environment for electrical neuronal activity. Recent studies have, however, demonstrated that the activity of nerve cells can be modulated by astrocytes, in that neurons are recruited into astrocyte-initiated and propagated calcium waves, both in vitro and in situ. By this means, propagated shifts in cytosolic calcium within the astrocytic syncytium may regulate neuronal response and firing thresholds. In turn, astrocytes are actively modulated by neuronal activity, and the existence of astrocyte–neuron signaling loops has been established in several areas of the brain. As a result of these findings, it is now recognized that astrocytes play an active role in brain function, particularly within the highly coupled astrocytic syncytium of the neocortex and the hippocampus. The mechanisms by which calcium signaling is propagated and how it is evoked are the focus of intense research activity. It is known that gap junctions and the connexins, their constituent proteins, together with the local cytoskeleton, the calcium buffer capacity, and calcium waves triggered by purinergic transmitters, all cooperate to modulate astrocytic signaling to neighboring cells in young animals. What changes do astrocytes and their signaling machinery undergo during the aging process? This is a question of paramount importance; altered astrocytic dynamics in the aged brain may alter synaptic efficacy and neuronal survival and perhaps contribute to the cognitive decline observed during aging. In this review, we analyze our current understanding of astrocytic function during aging by reexamining the mechanisms by which astrocytes contribute to neuronal function and survival in normal brain and the changes they undergo in the aged brain.

Structural Changes in the Aging Brain

Abstract: Publisher Summary The phenomenon of aging is a part of a continuous developmental sequence commencing with embryogenesis and proceeding through a number of maturational phases during the life span of the organism. The process of aging exerts its effects on all organs of the body, and the brain is no exception. Some degree of loss of substance is the most obvious characteristic of the normal aging process, but the degree of alteration varies enormously among subjects. The unique combination of genetic and epigenetic factors each individual represents is powerfully reflected in brain structure and function. Indeed, the brain of a vigorous 80-year-old patient may show fewer changes than that of an individual 20 years his junior. This spectrum of age-related patterns is further enhanced by the range of dementing illnesses to which the individual is increasingly vulnerable as the course of life progresses. This chapter reviews some of these alterations. A broad range of age-related alterations occur from brain to brain in the structural matrix, just as there is marked variation in the degree of cognitive, motor, and psychosocial intactness among the aged. The chapter describes the structural characteristics of healthy aged brain tissue and describes how the latter contrasts with the manifestations of pathological aging.

Plasticity of the aging brain: New directions in cognitive neuroscience

Abstract: Cognitive neuroscience has revealed aging of the human brain to be rich in reorganization and change. Neuroimaging results have recast our framework around cognitive aging from one of decline to one emphasizing plasticity. Current methods use neurostimulation approaches to manipulate brain function, providing a direct test of the ways that the brain differently contributes to task performance for younger and older adults. Emerging research into emotional, social, and motivational domains provides some evidence for preservation with age, suggesting potential avenues of plasticity, alongside additional evidence for reorganization. Thus, we begin to see that aging of the brain, amidst interrelated behavioral and biological changes, is as complex and idiosyncratic as the brain itself, qualitatively changing over the life span.

In Vivo Tau, Amyloid, and Gray Matter Profiles in the Aging Brain

Abstract: We provide a comparative in vivo examination of the brain network-based distribution of two hallmarks of Alzheimer9s disease (AD) pathology in cognitively normal individuals: (1) Tau, detected with a novel positron emission tomography (PET) tracer known as 18F-AV-1451; and (2) amyloid-β, quantified with 11C-PiB PET. We used a high-resolution graph-based approach to investigate local-to-local and local-to-distributed cortical associations between the maps of Tau, amyloid-β, and gray matter intensity. Our study shows that Tau and amyloid-β deposits are associated with distinctive spatial patterns of brain tissue loss. Moreover, Tau and amyloid-β accumulations have strong network interdigitations in heteromodal and associative areas of the cortical mantle, particularly the inferior–lateral temporal lobe. These findings contribute significantly to our understanding of how these two main hallmarks of AD pathology propagate across the elderly human brain. SIGNIFICANCE STATEMENT It has been postulated that Alzheimer9s disease (AD) pathology interacts and resides within system-level circuits of the human brain, long before the onset of cognitive symptoms. However, a side-by-side comparison of tissue loss, amyloid-β, and Tau deposition in early stages of the disease has been precluded until the recent advent of Tau tracer-based neuroimaging. In this study, we used Tau positron emission tomography and network analyses to disentangle these pathological relationships. We found that Tau and amyloid-β deposits are associated with distinctive spatial patterns of brain tissue loss. Moreover, we uncovered the network interdigitations of Tau and amyloid-β in the cortical mantle. These findings contribute significantly to our understanding of how two main hallmarks of AD pathology propagate across the elderly human brain.