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A decline in neuronal plasticity during the adult life span has been proposed to be associated with a reduced level of the effectors of plasticity responses (e.g., BDNF). Alteration of plasticity is also correlated with age-related hearing loss (presbycusis), but to date no detailed studies of BDNF expression have been performed in the young or aging mature cochlea. We have used rat and gerbil animal models for presbycusis, which displayed hearing loss in the final third of the animals' natural life span. We demonstrate for the first time a co-localization of BDNF protein, transcripts III and IV in cochlear neurons with a declining distribution towards low-frequency processing cochlear turns. BDNF protein was also found within the neuronal projections of the cochlea. A significant reduction of BDNF transcripts in high-frequency processing cochlear neurons was observed during aging, though this did not coincide with a major reduction of BDNF protein. In contrast, BDNF protein in peripheral and central projections was drastically reduced. Our results suggest that reduced BDNF protein levels in auditory nerves over age may be a crucial factor in the altered brainstem plasticity observed during presbycusis.
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http://dx.doi.org/10.1016/j.neurobiolaging.2006.02.008 | DOI Listing |
Sci Adv
September 2025
School of Electrical and Electronic Engineering, Yonsei University, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea.
Brain-computer interfaces (BCIs) enable direct communication between the brain and computers. However, their long-term functionality remains limited due to signal degradation caused by acute insertion trauma, chronic foreign body reaction (FBR), and biofouling at the device-tissue interface. To address these challenges, we introduce a multifunctional surface modification strategy called targeting-specific interaction and blocking nonspecific adhesion (TAB) coating for flexible fiber, achieving a synergistic integration of mechanical compliance and biochemical stability.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Phytoveda Pvt. Ltd, Mumbai, 400022, India.
Background: The dysregulation of long-chain noncoding RNAs (lncRNAs) causes several complex human diseases including neurodegenerative disorders across the globe.
Methods And Results: This study aimed to investigate lncRNA expression profiles of Withania somnifera (WS)-treated human neuroblastoma SK-N-SH cells at different timepoints (3 & 9 h) and concentrations (50 & 100 µg/mL) using RNA sequencing. Differential gene expression analysis showed a total of 4772 differentially expressed lncRNAs, out of which 3971 were upregulated and 801 were downregulated compared to controls.
J Mol Neurosci
September 2025
Department of Physiology, School of Medicine, Dokuz Eylul University, Izmir, Turkey.
The ketogenic diet (KD), a high-fat, low-carbohydrate regimen, has been shown to exert neuroprotective effects in various neurological models. This study explored how KD-alone or combined with antibiotic-induced gut microbiota depletion-affects cognition and neuroinflammation in aging. Thirty-two male rats (22 months old) were assigned to four groups (n = 8): control diet (CD), ketogenic diet (KD), antibiotics with control diet (AB), and antibiotics with KD (KDAB).
View Article and Find Full Text PDFPharmacol Biochem Behav
September 2025
Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Universidad de Málaga (UMA), Málaga, 29010, Spain; Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina (IBIMA Plataforma BIONAND), Málaga, Spain. Electronic address:
Adolescence is a period of heightened neuroplasticity and vulnerability to environmental insults, including drug exposure. In this study, we investigated the short- and long-term behavioral effects, as well as the long-term hippocampal effects, of chronic cocaine administration during adolescence, along with the potential neuroprotective role of insulin-like growth factor 2 (IGF2) in male C57BL/6J mice. Over 21 days, mice received daily intraperitoneal injections of saline, cocaine, IGF2, or a combination of cocaine and IGF2.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37240.
Major depressive disorder affects millions worldwide, yet current treatments require prolonged administration. In contrast, ketamine produces rapid antidepressant effects by blocking spontaneous N-Methyl-D-Aspartate (NMDA) receptor signaling, which lifts the suppression of protein synthesis and triggers homeostatic synaptic plasticity. Here, we identify a parallel signaling pathway involving metabotropic glutamate receptor 5 (mGluR5) that promotes rapid antidepressant-like effects.
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