ReviewFrontiers in neuroscience2018
Cognitive Decline, Dementia, Alzheimer's Disease and Presbycusis: Examination of the Possible Molecular Mechanism.
Review in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Hearing loss and dementia: radiologic and biomolecular basis of their shared characteristics. A systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Pooled it
- The ubiquitin-proteasome system and proteostasis in the cochlea and sensorineural hearing disorders.Molecular biomedicine · 2026Review
- Exploring the Relationship Between Hearing Loss and Cognitive Dysfunction from the Perspective of Molecular Mechanisms.Biomolecules · 2026Review
- Hearing Loss, Cognitive Decline, and Dementia: Clinical Intersections.Audiology research · 2026Review
- Hearing Loss as a Potentially Modifiable Marker of Dementia Risk: Neurological Evidence, Uncertainty, and Clinical Interpretation.Neuro-degenerative diseases · 2026Review
- A Global Burden Perspective on Obstructive Sleep Apnea, Hearing Loss, and Early-Onset Cognitive Decline.Neurology international · 2026Review
- Review
- Cryosectioning and Immunostaining Mouse Inner Ear Tissue: From Embryonic to Adult Stages.Journal of visualized experiments : JoVE · 2025Article
- Bioinformatics approach reveals the critical role of inflammation-related genes in age-related hearing loss.Scientific reports · 2025Article
- Hearing Loss and Alzheimer Disease.Current topics in behavioral neurosciences · 2025Review
- From genomic discovery to application in age-related hearing loss: a global bibliometric and cross-ethnic analysis.Frontiers in aging neuroscience · 2025Article
- Beyond the auditory system: cognitive implications of age-related hearing loss.Frontiers in aging neuroscience · 2025Review
- Article
- Article
- Intranasal delivery of NGF rescues hearing impairment in aged SAMP8 mice.Cell death & disease · 2023Article
- Is Hearing Loss a Risk Factor for Idiopathic Parkinson's Disease? An English Longitudinal Study of Ageing Analysis.Brain sciences · 2023Article
- D-Galactose and Hypoxia Induce the Early Onset of Age-Related Hearing Loss Deterioration in a Mouse Model.Tissue engineering and regenerative medicine · 2023Article
- CDK10, CDK11, FOXO1, and FOXO3 Gene Expression in Alzheimer's Disease Encephalic Samples.Cellular and molecular neurobiology · 2023Article
- Neurochemical and functional reorganization of the cognitive-ear link underlies cognitive impairment in presbycusis.NeuroImage · 2023Article
- Sex differences in hearing impairment due to diet-induced obesity in CBA/Ca mice.Biology of sex differences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidences of presbycusis and dementia are high among geriatric diseases. Presbycusis is the general term applied to age-related hearing loss and can be caused by many risk factors, such as noise exposure, smoking, medication, hypertension, family history, and other factors. Mutation of mitochondrial DNA in hair cells, spiral ganglion cells, and stria vascularis cells of the cochlea is the basic mechanism of presbycusis. Dementia is a clinical syndrome that includes the decline of cognitive and conscious states and is caused by many neurodegenerative diseases, of which Alzheimer's disease (AD) is the most common. The amyloid cascade hypothesis and tau hypothesis are the two major hypotheses that describe the AD pathogenic mechanism. Recent studies have shown that deposition of Aβ and hyperphosphorylation of the tau protein may cause mitochondrial dysfunction. An increasing number of papers have reported that, on one hand, the auditory system function in AD patients is damaged as their cognitive ability declines and that, on the other hand, hearing loss may be a risk factor for dementia and AD. However, the relationship between presbycusis and AD is still unknown. By reviewing the relevant literature, we found that the SIRT1-PGC1α pathway and LKB1 (or CaMKKβ)-AMPK pathway may play a role in the preservation of cerebral neuron function by taking part in the regulation of mitochondrial function. Then vascular endothelial growth factor signal pathway is activated to promote vascular angiogenesis and maintenance of the blood-brain barrier integrity. Recently, experiments have also shown that their expression levels are altered in both presbycusis and AD mouse models. Therefore, we propose that exploring the specific molecular link between presbycusis and AD may provide new ideas for their prevention and treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.