The relationship between self-reported sensory decline and cognitive frailty in older persons.

This study aimed to explore the relationship between self-reported sensory decline, including poor hearing and vision, and cognitive frailty in older persons. This cross-sectional study analyzed data from the 2020 National Survey of Living Conditions and Welfare Needs of Older Koreans. Binomial logistic regression analysis was performed to analyze the relationship between self-reported sensory decline and cognitive frailty. Of 9,692 participants, 39.8 % experienced sensory decline. The prevalence of cognitive frailty was 15.7 % among participants with poor hearing, 6.9 % among those with poor vision, and 17.9 % among those with combined poor hearing and vision. In our model, adjusted for sociodemographic and health-related variables, the cognitive frailty was significantly associated with poor hearing alone and combined poor hearing and vision. The findings suggest that healthcare professionals should prioritize their attention to the risk of cognitive frailty in older adults experiencing poor hearing alone and combined with poor vision.

Metabolic decline in an insect ear: correlative or causative for age-related auditory decline?

One leading hypothesis for why we lose our hearing as we age is a decrease in ear metabolism. However, direct measurements of metabolism across a lifespan in any auditory system are lacking. Even if metabolism does decrease with age, a question remains: is a metabolic decrease a cause of age-related auditory decline or simply correlative? We use an insect, the desert locust Schistocerca gregaria, as a physiologically versatile model to understand how cellular metabolism correlates with age and impacts on age-related auditory decline. We found that auditory organ metabolism decreases with age as measured fluorometrically. Next, we measured the individual auditory organ's metabolic rate and its sound-evoked nerve activity and found no correlation. We found no age-related change in auditory nerve activity, using hook electrode recordings, and in the electrophysiological properties of auditory neurons, using patch-clamp electrophysiology, but transduction channel activity decreased. To further test for a causative role of the metabolic rate in auditory decline, we manipulated metabolism of the auditory organ through diet and cold-rearing but found no difference in sound-evoked nerve activity. We found that although metabolism correlates with age-related auditory decline, it is not causative. Finally, we performed RNA-Seq on the auditory organs of young and old locusts, and whilst we found enrichment for Gene Ontology terms associated with metabolism, we also found enrichment for a number of additional aging GO terms. We hypothesize that age-related hearing loss is dominated by accumulative damage in multiple cell types and multiple processes which outweighs its metabolic decline.

Sensory capability of young, middle-aged and elderly Irish assessors to identify beef steaks of varying texture.

This study assessed the capability of various Irish assessor age cohorts to identify beef steaks of varying texture. Varying steak textures Moderately Tough (MTH), Moderately Tender (MTR) and Tender (TR) were achieved by aging beef longissimus thoracis et lumborum (LTL) muscle for 2, 7 and 21days respectively. Warner Bratzler Shear Force (WBSF) was measured to standardise the samples. Sensory evaluation was carried using 428 participants; 18-30yrs (years) (n=143), 31-60yrs (n=80), 61-75yrs (n=99) and 76-85yrs old (n=106). Within 6 age cohort categories (18-70), significant positive and negative correlations were observed for TR and MTH tenderness categories respectively. Poor identification of tenderness classification was found in the 71-85 age cohort groupings. Consequently more research is required in this area so that guidelines could be presented for industrial uptake. This study supports the hypothesis that changes in textural perception occur with age in humans.

Hand tactile discrimination, social touch and frailty criteria in elderly people: A cross sectional observational study.

Frailty is a common syndrome among elderly and sensory decline may exacerbate functional decline. The hand function, the manual dexterity, the performance of the daily living skills and the social interactions are determined, in a large degree, by sensory integrity. However, hand tactile sensory deterioration has been little explored in frailty. We performed a cross sectional observational study with 181 of institutionalized elders. From the initial sample we selected 50 subjects (68-99 years) who met the inclusion/exclusion criteria. Our goals were (1) to analyse the relationship between tactile discrimination (TD) of the hand, avoidance behaviours and attitudes towards social touch (BATST) and phenotype frailty criteria (unintentional weight loss, self-perception of exhaustion, decrease grip strength - GS, slow walking speed, low level of physical activity), (2) to explore whether other variables can contribute to explain the differences between pre-frail and frail elders. The results showed that increasing age is related to decline of TD of the hand (p=0.021) and to decrease in GS (p=0.025); women have significantly lower level of GS (p=0.001); TD decrease is correlated with higher avoidance BATST (p=0.000) and with lower GS (p=0.000); Lower GS corresponds to more avoidance BATST (p=0.003). Hand TD also can differentiate frail and pre-frail elderly subjects in this sample (p=0.037). Decreased TD of the hand may have implications on the functionality and on interpersonal relationships. TD of the hand also explains frailty levels in this sample. Hand TD should be used in assessment and intervention protocols in pre-frail and frail elders.

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer's Disease.

Sporadic Alzheimer's disease (AD) is a devastating neurodegenerative disorder. It is essential to unravel its etiology and pathogenesis. This should enable us to study the presymptomatic stages of the disease and to analyze and reverse the antemortem behavioral, memory, and cognitive dysfunction. Prima facie, an ongoing chronic vulnerability involving neural insult may lead normal elderly to mild cognitive impairment (MCI) and then to AD. Development of effective preventive and therapeutic strategies to thwart the disease pathology obviously requires a thorough delineation of underlying disruptive neuropathological processes. Our sensory capacity for touch, smell, taste, hearing, and vision declines with advancing age. Declines in different sensory attributes are considered here to be the primary "first-tier pathologies." Olfactory loss is among the first clinical signs of neurodegenerative diseases including AD and Parkinson's disease (PD). Sensory dysfunction in the aged promotes pathological disturbances in the locus coeruleus, basal forebrain, entorhinal cortex, hippocampus, and several key areas of neocortex and brainstem. Hence, sensory dysfunction is the pivotal factor that may upregulate cognitive and memory dysfunction. The age-related constellation of comorbid pathological factors may include apolipoprotein E (APOE) genotype, obesity, diabetes, hypertension, alcohol abuse, head trauma, and obstructive sleep apnea. The concepts and trajectories delineated here are the dynamic pillars of the current hypothesis presented-it postulates that the sensory decline, in conjunction with the above pathologies, is crucial in triggering neurodegeneration and promoting cognitive/memory dysfunction in aging and AD. The application of this thesis can be important in formulating new multifactorial preventive and treatment strategies (suggested here) in order to attenuate cognitive and memory decline and ameliorate pathological dysfunction in aging, MCI, and AD.

A review of causal mechanisms underlying the link between age-related hearing loss and cognitive decline.

Accumulating evidence points to a link between age-related hearing loss and cognitive decline, but their relationship is not clear. Does one cause the other, or does some third factor produce both? The answer has critical implications for prevention, rehabilitation, and health policy but has been difficult to establish for several reasons. First, determining a causal relationship in natural, correlational samples is problematic, and hearing and cognition are difficult to measure independently. Here, we critically review the evidence for a link between hearing loss and cognitive decline. We conclude that the evidence is convincing, but that the effects are small when hearing is measured audiometrically. We review four different directional hypotheses that have been offered as explanations for such a link, and conclude that no single hypothesis is sufficient. We introduce a framework that highlights that hearing and cognition rely on shared neurocognitive resources, and relate to each other in several different ways. We also discuss interventions for sensory and cognitive decline that may permit more causal inferences.