Objectives: Sensorineural hearing loss (presbycusis) affects up to half of the adults, is associated with cognitive decline. Whether this association reflects the cause, the consequence, or parallel processes driven by other factors remains unclear. Both presbycusis and cognition are linked to elevated metabolic risk, which in turn raises with age.
Method: In a multioccasion longitudinal design, we used latent change score models with strong factorial invariance to assess the change in pure-tone threshold auditory function, fluid intelligence, metabolic risk, variability therein, and the dynamic relationships among the 3 domains. We examined, up to 4 times over more than 7 years, a sample of relatively healthy 687 adults (aged 18.17-83.25 years).
Results: We found that levels of auditory and cognitive functioning at time t-1 influence each other's subsequent change between times t-1 and t, even when controlling for the reciprocal effects of metabolic risk on both. Thus, auditory and cognitive functioning do not only decline in parallel in healthy adults, but also affect each other's trajectories. To the best of our knowledge, this is the first long-term study with such evidence.
Discussion: Our results are in accord with extant hypotheses about auditory-cognitive associations in old age (e.g., social isolation, cognitive load, increased inflammation, reduced gene expression, and other microvascular or neuropathological factors). They also echo previous reports underscoring the need for improving access to hearing aids and other rehabilitative services aimed at reducing hearing loss. If applied early in the aging process, such interventions may mitigate cognitive decline.
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http://dx.doi.org/10.1093/geronb/gbac148 | DOI Listing |
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Department of Endocrinology and Metabolism, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
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January 2025
Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Road, Tainan, 70401, Taiwan.
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J Gastrointest Cancer
January 2025
Colorectal Research Center, Imam Khomeini Hospital complex, Tehran University of Medical Sciences, Keshavarz Blvd, Tehran, Iran.
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Division of Cardiology, Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.
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January 2025
Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Multiple endocrine neoplasia type 1 (MEN1) syndrome is an autosomal dominant disorder caused by a germline pathogenic variant in the MEN1 tumor suppressor gene. Patients with MEN1 have a high risk for primary hyperparathyroidism (PHPT) with a penetrance of nearly 100%, pituitary adenomas (PitAd) in 40% of patients, and neuroendocrine neoplasms (NEN) of the pancreas (40% of patients), duodenum, lung, and thymus. Increased MEN1-related mortality is mainly related to duodenal-pancreatic and thymic NEN.
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