scholarly journals Aging Brain and Hearing: A Mini-Review

2022 ◽  
Vol 13 ◽  
Author(s):  
Yasue Uchida ◽  
Yukiko Nishita ◽  
Rei Otsuka ◽  
Saiko Sugiura ◽  
Michihiko Sone ◽  
...  

Brain reserve is a topic of great interest to researchers in aging medicine field. Some individuals retain well-preserved cognitive function until they fulfill their lives despite significant brain pathology. One concept that explains this paradox is the reserve hypothesis, including brain reserve that assumes a virtual ability to mitigate the effects of neuropathological changes and reduce the effects on clinical symptoms flexibly and efficiently by making complete use of the cognitive and compensatory processes. One of the surrogate measures of reserve capacity is brain volume. Evidence that dementia and hearing loss are interrelated has been steadily accumulating, and age-related hearing loss is one of the most promising modifiable risk factors of dementia. Research focused on the imaging analysis of the aged brain relative to auditory function has been gradually increasing. Several morphological studies have been conducted to understand the relationship between hearing loss and brain volume. In this mini review, we provide a brief overview of the concept of brain reserve, followed by a small review of studies addressing brain morphology and hearing loss/hearing compensation, including the findings obtained from our previous study that hearing loss after middle age could affect hippocampal and primary auditory cortex atrophy.

2006 ◽  
Vol 28 (2) ◽  
pp. 243 ◽  
Author(s):  
J. Taylor ◽  
G. Brown ◽  
C. De Miguel ◽  
M. Henneberg ◽  
F. J. Rühli

The ratio of brain volume to cranial volume of Phascolarctos cinereus has been reported to be low (60% encephalization) compared to other marsupials and eutherians. This MRI study indicates a substantial difference between the living P. cinereus brain (83% - 90% encephalization) and ones of cadaver specimens. This highlights the importance of in vivo morphological studies.


2021 ◽  
Author(s):  
Roxanna Korologou-Linden ◽  
Bing Xu ◽  
Elizabeth Coulthard ◽  
Esther Walton ◽  
Alfie Wearn ◽  
...  

Neuropathological changes associated with Alzheimers disease (AD) can occur decades before clinical symptoms. We investigated whether neurodevelopment and/or neurodegeneration affects the risk of AD, through reducing structural brain reserve and/or accelerating brain atrophy, respectively. We used bidirectional two-sample Mendelian randomization to estimate the effects of genetic liability to AD on global and regional cortical thickness, total intracranial volume, volume of subcortical structures and cerebral white matter in 36,842 participants aged eight to 81 years across five independent cohorts, and the effects of global and regional cortical thickness and subcortical volumes on AD risk in 94,337 participants. Our findings show that AD risk alleles have an age-dependent effect on a range of cortical and subcortical brain measures that starts in mid-life, in non-clinical populations. Evidence for such effects across childhood and young adulthood is weak. We also found little evidence to suggest brain morphology alters AD risk. Thus, genetic liability to AD is likely to alter mechanisms and/or rates of neurodegeneration, rather than reduce structural brain reserve.


2017 ◽  
Vol 22 (2) ◽  
pp. 96-103 ◽  
Author(s):  
Qiuhong Huang ◽  
Yongkang Ou ◽  
Hao Xiong ◽  
Haidi Yang ◽  
Zhigang Zhang ◽  
...  

Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.


2021 ◽  
Vol 13 ◽  
Author(s):  
Eva Pettemeridou ◽  
Eleni Kallousia ◽  
Fofi Constantinidou

Objective: The aim of this study was twofold. First, to investigate the relationship between age, gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) volumes, brain reserve (BR), and specific regions of interest (ROIs) with global cognitive function in healthy older adults participating in a longitudinal study on aging in the island country of Cyprus. Second, to assess the contribution of important demographic and psychosocial factors on brain volume. Specifically, the effects of sex and years of education and the association between depression symptoms on brain volume were also explored in this Mediterranean cohort.Methods: Eighty-seven healthy older adults (males = 37, females = 50) scoring ≥24 on the Mini-Mental State Examination (MMSE) were included, with a mean age of 72.75 years and a mean educational level of 10.48 years. The Geriatric Depression Scale was used to assess depression. T1-weighted magnetic resonance images were used to calculate global and regional volumes.Results: Age was negatively correlated with GM, WM, BR, MMSE scores, and ROIs, including the hippocampus, amygdala, entorhinal cortex, prefrontal cortex, anterior cingulate gyrus, and positively with CSF. Higher MMSE scores positively correlated with GM volume. Women exhibited greater levels of depression than men. Depression was also negatively correlated with GM volume and MMSE scores. Men had greater ventricular size than women and participants with higher education had greater ventricular expansion than those with fewer years in education.Conclusions: The reported structural changes provide evidence on the overlap between age-related brain changes and healthy cognitive aging and suggest that these age changes affect certain regions. Furthermore, sex, depressive symptomatology, and education are significant predictors of the aging brain. Brain reserve and higher education accommodate these changes and works against the development of clinical symptoms.


2019 ◽  
Vol 23 ◽  
pp. 233121651985726 ◽  
Author(s):  
Mark A. Eckert ◽  
Kenneth I. Vaden ◽  
Judy R. Dubno

Age-related hearing loss has been associated with varied auditory cortex morphology in human neuroimaging studies. These findings have suggested that peripheral auditory system declines cause changes in brain morphology but could also be due to latent variables that affect the auditory periphery and brain. The current longitudinal study was designed to evaluate these explanations for pure-tone threshold and brain morphology associations. Thirty adults (mean age at Time 1 = 64.12 ± 10.32 years) were studied at two time points (average duration between visits = 2.62 ± 0.81 years). Small- to medium-effect size associations were observed between high-frequency pure-tone thresholds and auditory cortex gray matter volume at each time point. Although there were significant longitudinal changes in low- and high-frequency hearing measures and brain morphology, those longitudinal changes were not significantly correlated across participants. High-frequency hearing measures at Time 1 were significantly related to more lateral ventricle expansion, such that participants with higher measures exhibited larger increases in ventricle size. This ventricle effect was statistically independent of high-frequency hearing associations with auditory cortex morphology. Together, these results indicate that there are at least two mechanisms for associations between age-related hearing loss and brain morphology. Potential explanations for a direct hearing loss effect on brain morphology, as well as latent variables that likely affect both the inner ear and brain, are discussed.


2019 ◽  
Author(s):  
Gavin M. Bidelman ◽  
Caitlin N. Price ◽  
Dawei Shen ◽  
Stephen R. Arnott ◽  
Claude Alain

ABSTRACTAge-related hearing loss leads to poorer speech comprehension, particularly in noise. Speech-in-noise (SIN) deficits among the elderly could result from weaker neural activity within, or poorer signal transmission between brainstem and auditory cortices. By recording neuroelectric responses from brainstem (BS) and primary auditory cortex (PAC), we show that beyond simply attenuating neural activity, hearing loss in older adults compromises the transmission of speech information between subcortical and cortical hubs of the auditory system. The strength of afferent BS→PAC neural signaling (but not the reverse efferent flow; PAC→BS) varied with mild declines in hearing acuity and this “bottom-up” functional connectivity robustly predicted older adults’ SIN perception. Our neuroimaging findings underscore the importance of brain connectivity, particularly afferent neural communication, in understanding the biological basis of age-related hearing deficits in real-world listening environments.


Metabolites ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 450
Author(s):  
Janusz Wiesław Błaszczyk

There is a growing body of evidencethat indicates that the aging of the brain results from the decline of energy metabolism. In particular, the neuronal metabolism of glucose declines steadily, resulting in a growing deficit of adenosine triphosphate (ATP) production—which, in turn, limits glucose access. This vicious circle of energy metabolism at the cellular level is evoked by a rising deficiency of nicotinamide adenine dinucleotide (NAD) in the mitochondrial salvage pathway and subsequent impairment of the Krebs cycle. A decreasing NAD level also impoverishes the activity of NAD-dependent enzymes that augments genetic errors and initiate processes of neuronal degeneration and death.This sequence of events is characteristic of several brain structures in which neurons have the highest energy metabolism. Neurons of the cerebral cortex and basal ganglia with long unmyelinated axons and these with numerous synaptic junctions are particularly prone to senescence and neurodegeneration. Unfortunately, functional deficits of neurodegeneration are initially well-compensated, therefore, clinical symptoms are recognized too late when the damages to the brain structures are already irreversible. Therefore, future treatment strategies in neurodegenerative disorders should focus on energy metabolism and compensation age-related NAD deficit in neurons. This review summarizes the complex interrelationships between metabolic processes on the systemic and cellular levels and provides directions on how to reduce the risk of neurodegeneration and protect the elderly against neurodegenerative diseases.


2013 ◽  
Vol 27 (1) ◽  
pp. 48-59 ◽  
Author(s):  
Eva M. Müller-Oehring ◽  
Tilman Schulte ◽  
Torsten Rohlfing ◽  
Adolf Pfefferbaum ◽  
Edith V. Sullivan

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