Aging brain

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

Inflammation Combined with Ischemia Produces Myelin Injury and Plaque-Like Aggregates of Myelin, Amyloid-β and AβPP in Adult Rat Brain.

Abstract: Background: Ischemia, white matter injury, and Alzheimer’s disease (AD) pathologies often co-exist in aging brain. How one condition predisposes to, interacts with, or perhaps causes the others remains unclear. Objectives: To better understand the link between ischemia, white matter injury, and AD, adult rats were administered lipopolysaccharide (LPS) to serve as an inflammatory stimulus, and 24 h later subjected to 20-min focal cerebral ischemia (IS) followed by 30-min hypoxia (H). Methods: Myelin and axonal damage, as well as amyloid-β (Aβ) and amyloid-β protein precursor (AβPP) deposition were examined by Western blot and immunocytochemistry following LPS/IS/H. Findings were compared to the 5XFAD mouse AD brain. Results: Myelin/axonal injury was observed bilaterally in cortex following LPS/IS/H, along with an increase in IL-1, granzyme B, and LPS. AβPP deposition was present in ischemic striatum in regions of myelin loss. Aβ1-42 and AβPP were deposited in small foci in ischemic cortex that co-localized with myelin aggregates. In the 5XFAD mouse AD model, cortical amyloid plaques also co-localized with myelin aggregates. Conclusions: LPS/IS/H produce myelin injury and plaque-like aggregates of myelin. AβPP and Aβ co-localize with these myelin aggregates.

Parahippocampal Cortex Mediates the Relationship between Lutein and Crystallized Intelligence in Healthy, Older Adults

Abstract: Introduction: Although diet has a substantial influence on the aging brain, the relationship between dietary nutrients and aspects of brain health remains unclear. This study examines the neural mechanisms that mediate the relationship between a carotenoid important for brain health across the lifespan, lutein, and crystallized intelligence in cognitively intact older adults. We hypothesized that higher serum levels of lutein are associated with better performance on a task of crystallized intelligence, and that this relationship is mediated by gray matter structure of regions within the temporal cortex. This investigation aims to contribute to a growing line of evidence, which suggests that particular nutrients may slow or prevent aspects of cognitive decline by targeting specific features of brain aging. Methods: We examined 75 cognitively intact adults between the ages of 65 and 75 to investigate the relationship between serum lutein, tests of crystallized intelligence (measured by the Wechsler Abbreviated Scale of Intelligence), and gray matter volume of regions within the temporal cortex. A three-step mediation analysis was implemented using multivariate linear regressions to control for age, sex, education, income, depression status, and body mass index. Results: The mediation analysis revealed that gray matter thickness of one region within the temporal cortex, the right parahippocampal cortex (Brodmann’s Area 34), partially mediates the relationship between serum lutein and crystallized intelligence. Conclusion: These results suggest that the parahippocampal cortex acts as a mediator of the relationship between serum lutein and crystallized intelligence in cognitively intact older adults. Prior findings substantiate the individual relationships reported within the mediation, specifically the links between (i) serum lutein and temporal cortex structure, (ii) serum lutein and crystallized intelligence, and (iii) parahippocampal cortex structure and crystallized intelligence. This report is the first to demonstrate a specific structural mediation between lutein status and crystallized intelligence, and therefore provides further evidence that specific nutrients may slow or prevent features of cognitive decline by hindering particular aspects of brain aging. Future work should examine the potential mechanisms underlying this mediation, including the antioxidant, anti-inflammatory, and membrane modulating properties of lutein.

The Cognitive Consequences of Structural Changes to the Aging Brain

Abstract: Publisher Summary This chapter reviews the history of the morphometric research on normal brain aging and examines in detail, the recently developed techniques for measuring the brain's structure and exploring structure- function association studies conducted within each neuroimaging modality in the context of aging. For comparison purposes, it reviews studies with participants showing “normal” aging, with a methodology in each technique following the most standard protocols. Because the state of the brain's structure affects the quality of its function, the study of changes in brain structure has proven fruitful in understanding cognitive aging. Brain's function ostensibly relies on the brain's structural integrity. Therefore, many studies have embarked on relating age differences in regional volume to their putative underlying function. The resulting literature is mixed in its findings because the brain's volume fluctuates over decades (incorporating growth and shrinkage), and because middle and older aged adults are probably able to compensate for degradation to the brain's structure over time or rely upon cognitive reserve resources to compensate for declines in structural integrity. Further, structure-cognition associations are not easily replicated and are sensitive to type of cognitive assessment and to sample composition. In this context, the chapter summarizes the volume cognition studies by cognitive domain. It concludes with a look toward needed future research directions with a particular focus on combined multimodality structure–function studies and a more careful selection and characterization of the health indices of the participants selected for cognitive aging studies.

Inflammation, Amyloid, and Atrophy in The Aging Brain: Relationships with Longitudinal Changes in Cognition.

Abstract: Amyloid deposition occurs in aging, even in individuals free from cognitive symptoms, and is often interpreted as preclinical Alzheimer's disease (AD) pathophysiology. YKL-40 is a marker of neuroinflammation, being increased in AD, and hypothesized to interact with amyloid-β (Aβ) in causing cognitive decline early in the cascade of AD pathophysiology. Whether and how Aβ and YKL-40 affect brain and cognitive changes in cognitively healthy older adults is still unknown. We studied 89 participants (mean age: 73.1 years) with cerebrospinal fluid samples at baseline, and both MRI and cognitive assessments from two time-points separated by two years. We tested how baseline levels of Aβ42 and YKL-40 correlated with changes in cortical thickness and cognition. Thickness change correlated with Aβ42 only in Aβ42+ participants (<600 pg/mL, n = 27) in the left motor and premotor cortices. Aβ42 was unrelated to cognitive change. Increased YKL-40 was associated with less preservation of scores on the animal naming test in the total sample (r = -0.28, p = 0.012) and less preservation of a score reflecting global cognitive function for Aβ42+ participants (r = -0.58, p = 0.004). Our results suggest a role for inflammation in brain atrophy and cognitive changes in cognitively normal older adults, which partly depended on Aβ accumulation.

Selective Impairments of Mitochondrial Respiratory Chain Activity During Aging and Ischemic Brain Damage

Abstract: Cumulative oxidative damage to mitochondrial deoxyribonucleic acid (DNA) with subsequent defects in oxidative phosphorylation may reduce the capacity of the aging brain to cope with metabolic stress. This may contribute to the age related increase in cerebral infarct size that has been documented following permanent middle cerebral artery occlusion (MCAO) in the rat. This hypothesis was evaluated by assessing mitochondrial respiratory chain complex activity in both ischemic and non ischemic brain tissue of adult (10 month) and aged (28 month) male Wistar rats, six hours after occlusion of the left middle cerebral artery. Aging was associated with a significant decline in cerebral mitochondrial function with impairment of the activities of complexes I, II and IV. The individual respiratory chain complexes also exhibited selective vulnerability to a focal cerebral ischemic lesion, with significant impairment of complex I activity in the lesioned hemisphere of both age groups. The age related decline in complex I activity may be important in the enhanced susceptibility of the aging brain to ischemic neuronal damage.