Aging

2019 ◽  
pp. 105-112
Author(s):  
Risto Näätänen ◽  
Teija Kujala ◽  
Gregory Light
Keyword(s):  
Hearing Loss ◽  
Speech Perception ◽  
Cognitive Decline ◽  
Temporal Processing ◽  
Brain Aging ◽  
Brain Plasticity ◽  
Part Of Speech ◽  
Memory Traces ◽  
Age Related ◽  
The Brain

This chapter shows that MMN and its magnetoencephalographic (MEG) equivalent MMNm are sensitive indices of aging-related perceptual and cognitive decline. Importantly, the age-related neural changes are associated with a decrease of general brain plasticity, i.e. that of the ability of the brain to form and maintain sensory-memory traces, a necessary basis for veridical perception and appropriate cognitive brain function. MMN/MMNm to change in stimulus duration is particularly affected by aging, suggesting the increased vulnerability of temporal processing to brain aging and accounting, for instance, for a large part of speech-perception difficulties of the aged beyond the age-related peripheral hearing loss.

Hearing and Cognitive Aging

2020 ◽  
Author(s):  
Margaret Kathleen Pichora-Fuller
Keyword(s):  
Older Adults ◽  
Hearing Loss ◽  
Cognitive Decline ◽  
Cognitive Aging ◽  
Brain Plasticity ◽  
Everyday Functioning ◽  
Ongoing Research ◽  
People With Dementia ◽  
Age Related ◽  
Sensory Motor

Age-related hearing loss is heterogeneous. Multiple causes can damage the auditory system from periphery to cortex. There can be changes in thresholds for detecting sound and/or in the perception of supra-threshold sounds. Influenced by trends in neuroscience and gerontology, research has shifted from a relatively narrow modality-specific focus to a broader interest in how auditory aging interacts with other domains of aging. The importance of the connection between sensory and cognitive aging was reported based on findings from the Berlin Aging Study in the mid-1990s. Of the age-related sensory and motor declines that become more prevalent with age, hearing loss is the most common, and it is the most promising as an early marker for risk of cognitive decline and as a potentially modifiable mid-life risk factor for dementia. Hearing loss affects more than half of the population by 70 years of age and about 80% of people over 80 years of age. It is more prevalent in people with dementia than in peers with normal cognition. People with hearing loss can be up to five times more likely to develop dementia compared to those with normal hearing. Evidence from cross-sectional studies has confirmed significant correlations between hearing loss and cognitive decline in older adults. Longitudinal studies have demonstrated that hearing loss is associated with incident cognitive decline and dementia. Various biological, psychological, and social mechanisms have been hypothesized to account for these associations, but the causes remain unproven. Nevertheless, it is widely believed that there is a meaningful interface among sensory, motor, and cognitive dysfunctions in aging, with implications for issues spanning brain plasticity to quality of life. Experimental research investigating sensory-motor-cognitive interactions provides insights into how age-related declines in these domains may be exacerbated or compensated. Ongoing research on auditory aging and how it interfaces with cognitive aging is expected to increase knowledge of the neuroscience of aging, provide insights into how to optimize the everyday functioning of older adults, and inspire innovations in clinical practice and social policy.

scholarly journals Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth cohort

2019 ◽  
Author(s):  
Maxwell L. Elliott ◽  
Daniel W. Belsky ◽  
Annchen R. Knodt ◽  
David Ireland ◽  
Tracy R. Melzer ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Birth Cohort ◽  
Brain Aging ◽  
Chronological Age ◽  
Biological Aging ◽  
Imaging Data ◽  
Cross Sectional ◽  
Cohort Differences ◽  
Age Related ◽  
The Brain

AbstractAn individual’s brainAGE is the difference between chronological age and age predicted from machine-learning models of brain-imaging data. BrainAGE has been proposed as a biomarker of age-related deterioration of the brain. Having an older brainAGE has been linked to Alzheimer’s, dementia, and mortality. However, these findings are largely based on cross-sectional associations which can confuse age differences with cohort differences. To illuminate the validity of brainAGE as a biomarker of accelerated brain aging, a study is needed of a large cohort all born in the same year who nevertheless vary on brainAGE. In the Dunedin Study, a population-representative 1972–73 birth cohort, we measured brainAGE at age 45 years, as well as the pace of biological aging and cognitive decline in longitudinal data from childhood to midlife (N = 869). In this cohort, all chronological age 45 years, brainAGE was measured reliably (ICC = 0.81) and ranged from 24 to 72 years. Those with older midlife brainAGEs tended to have poorer cognitive function in both adulthood and childhood, as well as impaired brain health at age 3. Furthermore, those with older brainAGEs had an accelerated pace of biological aging, older facial appearance, and early signs of cognitive decline from childhood to midlife. These findings help to validate brainAGE as a potential surrogate biomarker for midlife intervention studies that seek to measure dementia-prevention efforts in midlife. However, the findings also caution against the assumption that brainAGE scores represent only age-related deterioration of the brain as they may also index central nervous system variation present since childhood.

scholarly journals Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth-cohort

2019 ◽  
Author(s):  
Maxwell L. Elliott ◽  
Daniel W. Belsky ◽  
Annchen R. Knodt ◽  
David Ireland ◽  
Tracy R. Melzer ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Birth Cohort ◽  
Brain Aging ◽  
Chronological Age ◽  
Biological Aging ◽  
Imaging Data ◽  
Cohort Differences ◽  
Age Related ◽  
Brain Age ◽  
The Brain

AbstractAn individual’s brain-age is the difference between chronological age and age predicted from machine-learning models of brain-imaging data. Brain-age has been proposed as a biomarker of age-related deterioration of the brain. Having an older brain-age has been linked to Alzheimer’s, dementia and mortality. However, these findings are largely based on cross-sectional associations which can confuse age differences with cohort differences. To illuminate the validity of brain-age a biomarker of accelerated brain aging, a study is needed of a large cohort all born the same year who nevertheless vary on brain-age. In a population-representative 1972-73 birth cohort we measured brain-age at age 45, as well as the pace of biological aging and cognitive decline in longitudinal data from childhood to midlife (N=869). In this cohort, all chronological age 45 years, brain-age was measured reliably (ICC=.81) and ranged from 24 to 72 years. Those with older midlife brain-ages tended to have poorer cognitive function in both adulthood and childhood, as well as impaired brain health at age 3. Furthermore, those with older brain-ages had an accelerated pace of biological aging, older facial appearance and early signs of cognitive decline from childhood to midlife. These findings help to validate brain-age as a potential surrogate biomarker for midlife intervention studies that seek to measure treatment response to dementia-prevention efforts in midlife. However, the findings also caution against the assumption that brain-age scores represent only age-related deterioration of the brain as they may also index central nervous system variation present since childhood.

scholarly journals Polyphenol-rich extract from grape and blueberry attenuates cognitive decline and improves neuronal function in aged mice

2018 ◽  
Vol 7 ◽  
Author(s):  
Julien Bensalem ◽  
Stéphanie Dudonné ◽  
David Gaudout ◽  
Laure Servant ◽  
Frédéric Calon ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Learning And Memory ◽  
High Performance ◽  
Brain Plasticity ◽  
Memory Deficits ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Native Form ◽  
Age Related ◽  
The Brain

AbstractAgeing is characterised by memory deficits, associated with brain plasticity impairment. Polyphenols from berries, such as flavan-3-ols, anthocyanins, and resveratrol, have been suggested to modulate synaptic plasticity and cognitive processes. In the present study we assessed the preventive effect of a polyphenol-rich extract from grape and blueberry (PEGB), with high concentrations of flavonoids, on age-related cognitive decline in mice. Adult and aged (6 weeks and 16 months) mice were fed a PEGB-enriched diet for 14 weeks. Learning and memory were assessed using the novel object recognition and Morris water maze tasks. Brain polyphenol content was evaluated with ultra-high-performance LC-MS/MS. Hippocampal neurotrophin expression was measured using quantitative real-time PCR. Finally, the effect of PEGB on adult hippocampal neurogenesis was assessed by immunochemistry, counting the number of cells expressing doublecortin and the proportion of cells with dendritic prolongations. The combination of grape and blueberry polyphenols prevented age-induced learning and memory deficits. Moreover, it increased hippocampal nerve growth factor (Ngf) mRNA expression. Aged supplemented mice displayed a greater proportion of newly generated neurons with prolongations than control age-matched mice. Some of the polyphenols included in the extract were detected in the brain in the native form or as metabolites. Aged supplemented mice also displayed a better survival rate. These data suggest that PEGB may prevent age-induced cognitive decline. Possible mechanisms of action include a modulation of brain plasticity. Post-treatment detection of phenolic compounds in the brain suggests that polyphenols may act directly at the central level, while they can make an impact on mouse survival through a potential systemic effect.

scholarly journals Aging-associated deficit in CCR7 is linked to worsened glymphatic function, cognition, neuroinflammation, and β-amyloid pathology

2021 ◽  
Vol 7 (21) ◽  
pp. eabe4601
Author(s):  
Sandro Da Mesquita ◽  
Jasmin Herz ◽  
Morgan Wall ◽  
Taitea Dykstra ◽  
Kalil Alves de Lima ◽  
...  
Keyword(s):  
T Cells ◽  
Cognitive Decline ◽  
Brain Aging ◽  
Therapeutic Potential ◽  
T Cell Response ◽  
Age Related ◽  
Lymphatic Vasculature ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
Old Mice

Aging leads to a progressive deterioration of meningeal lymphatics and peripheral immunity, which may accelerate cognitive decline. We hypothesized that an age-related reduction in C-C chemokine receptor type 7 (CCR7)–dependent egress of immune cells through the lymphatic vasculature mediates some aspects of brain aging and potentially exacerbates cognitive decline and Alzheimer’s disease–like brain β-amyloid (Aβ) pathology. We report a reduction in CCR7 expression by meningeal T cells in old mice that is linked to increased effector and regulatory T cells. Hematopoietic CCR7 deficiency mimicked the aging-associated changes in meningeal T cells and led to reduced glymphatic influx and cognitive impairment. Deletion of CCR7 in 5xFAD transgenic mice resulted in deleterious neurovascular and microglial activation, along with increased Aβ deposition in the brain. Treating old mice with anti-CD25 antibodies alleviated the exacerbated meningeal regulatory T cell response and improved cognitive function, highlighting the therapeutic potential of modulating meningeal immunity to fine-tune brain function in aging and in neurodegenerative diseases.

Bidirectional Association Between Depression and Hearing Loss: Evidence From the China Health and Retirement Longitudinal Study

2021 ◽  
pp. 073346482110423
Author(s):  
Chao Wu
Keyword(s):  
Hearing Loss ◽  
Longitudinal Study ◽  
Cognitive Decline ◽  
Age Related ◽  
Bidirectional Association ◽  
Health Related ◽  
Clinically Significant ◽  
Using Data ◽  
Bidirectional Associations ◽  
Age Related Hearing Loss

The relationship between depression and age-related hearing loss (ARHL) is not fully understood. This study tested the bidirectional associations between clinically significant depressive symptoms (CSDSs) and ARHL in middle-aged and older adults using data from the China Health and Retirement Longitudinal Study. Among 3,418 participants free of baseline ARHL, baseline CSDS was associated with an increased odds of incident ARHL (odds ratio [OR]: 1.51). Cognitive decline, BMI, and arthritis partially mediated the longitudinal CSDS–ARHL association and explained 24% of the variance in the total effect. Among 4,921 participants without baseline CSDS, baseline ARHL was associated with an increased odds of incident CSDS (OR: 1.37). The bidirectional associations remained significant after adjustments for baseline demographic factors, comorbidities, and other health-related covariates. Depression may contribute to the development of ARHL, and vice versa. Interventions in depression, cognitive decline, and arthritis may delay the onset of ARHL and break the vicious circle between them.

scholarly journals Impairments in Brain Bioenergetics in Aging and Tau Pathology: A Chicken and Egg Situation?

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2531
Author(s):  
Amandine Grimm
Keyword(s):  
Brain Metabolism ◽  
Brain Aging ◽  
Cognitive Impairments ◽  
Tau Phosphorylation ◽  
The Body ◽  
Tau Pathology ◽  
Age Related ◽  
Energy Consuming ◽  
Effects Of Aging ◽  
The Brain

The brain is the most energy-consuming organ of the body and impairments in brain energy metabolism will affect neuronal functionality and viability. Brain aging is marked by defects in energetic metabolism. Abnormal tau protein is a hallmark of tauopathies, including Alzheimer’s disease (AD). Pathological tau was shown to induce bioenergetic impairments by affecting mitochondrial function. Although it is now clear that mutations in the tau-coding gene lead to tau pathology, the causes of abnormal tau phosphorylation and aggregation in non-familial tauopathies, such as sporadic AD, remain elusive. Strikingly, both tau pathology and brain hypometabolism correlate with cognitive impairments in AD. The aim of this review is to discuss the link between age-related decrease in brain metabolism and tau pathology. In particular, the following points will be discussed: (i) the common bioenergetic features observed during brain aging and tauopathies; (ii) how age-related bioenergetic defects affect tau pathology; (iii) the influence of lifestyle factors known to modulate brain bioenergetics on tau pathology. The findings compiled here suggest that age-related bioenergetic defects may trigger abnormal tau phosphorylation/aggregation and cognitive impairments after passing a pathological threshold. Understanding the effects of aging on brain metabolism may therefore help to identify disease-modifying strategies against tau-induced neurodegeneration.

scholarly journals Association of Age-Related Hearing Loss with Cognitive Decline

2020 ◽  
Vol 63 (4) ◽  
pp. 145-153
Author(s):  
Juyong Chung
Keyword(s):  
Hearing Loss ◽  
Cognitive Decline ◽  
Cochlear Implants ◽  
Hearing Aids ◽  
Microvascular Disease ◽  
Single Mechanism ◽  
Hearing Aid Use ◽  
Age Related ◽  
Age Related Hearing Loss

A number of studies have demonstrated a significant association between age-related hearing loss (ARHL) and cognitive decline. However their relationship is not clear. In this review, we focused on the etiological mechanisms between ARHL and cognitive decline to explain the nature of this relationship: 1) causal mechanisms (e.g., cognitive load hypothesis, cascade hypothesis); 2) common cause mechanisms (e.g., microvascular disease); 3) overdiagnosis or harbinger hypothesis. We conclude that no single mechanism is sufficient and hearing and cognition related to each other in several different ways. In addition, we reviewed the effectiveness of hearing intervention (e.g., hearing aids and cochlear implants) on cognition function, and the role of hearing aid use and cochlear implant depends on the relevant mechanism.

scholarly journals Nutrients, Microglia Aging, and Brain Aging

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zhou Wu ◽  
Janchun Yu ◽  
Aiqin Zhu ◽  
Hiroshi Nakanishi
Keyword(s):  
Oxidative Stress ◽  
Cognitive Decline ◽  
Systemic Inflammation ◽  
Brain Aging ◽  
Oxygen Species ◽  
Cellular Activation ◽  
Proinflammatory Mediators ◽  
The World ◽  
Age Dependent ◽  
The Brain

As the life expectancy continues to increase, the cognitive decline associated with Alzheimer’s disease (AD) becomes a big major issue in the world. After cellular activation upon systemic inflammation, microglia, the resident immune cells in the brain, start to release proinflammatory mediators to trigger neuroinflammation. We have found that chronic systemic inflammatory challenges induce differential age-dependent microglial responses, which are in line with the impairment of learning and memory, even in middle-aged animals. We thus raise the concept of “microglia aging.” This concept is based on the fact that microglia are the key contributor to the acceleration of cognitive decline, which is the major sign of brain aging. On the other hand, inflammation induces oxidative stress and DNA damage, which leads to the overproduction of reactive oxygen species by the numerous types of cells, including macrophages and microglia. Oxidative stress-damaged cells successively produce larger amounts of inflammatory mediators to promote microglia aging. Nutrients are necessary for maintaining general health, including the health of brain. The intake of antioxidant nutrients reduces both systemic inflammation and neuroinflammation and thus reduces cognitive decline during aging. We herein review our microglia aging concept and discuss systemic inflammation and microglia aging. We propose that a nutritional approach to controlling microglia aging will open a new window for healthy brain aging.

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