Congenital cytomegalovirus (CMV) infection is the main cause of non-hereditary sensorineural hearing loss (SNHL). In order to shed light on SNHL pathophysiology, we examined the auditory pathway in CMV-infected fetuses; the temporal lobe, in particular the auditory cortex, and the inner ear. We investigated both inner ears and temporal lobes of 20 human CMV-infected fetuses at 21 weeks of gestation. As a negative group, five fetuses from spontaneous miscarriages without CMV infection were studied. Inner ears and temporal lobes were histologically examined, immunohistochemistry for CMV and CMV-PCR were performed. On the auditory cortex, we evaluated the local microglial reaction to the infection. CMV-positive cells were found in 14/20 brains and the damage was classified as severe, moderate, or mild, according to histological features. Fetuses with severe brain damage had a statistically higher temporal lobe viral load and a higher number of activated microglial cells in the auditory cortex compared to fetuses with mild brain damage (: 0.01; : 0.01). In the inner ears, the marginal cells of the stria vascularis were the most CMV positive. In our study, CMV affected the auditory pathway, suggesting a tropism for this route. In addition, in the auditory cortex, microglial activation may favor further tissue damage contributing to hearing loss.
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http://dx.doi.org/10.3390/ijms25052636 | DOI Listing |
Eur Arch Psychiatry Clin Neurosci
January 2025
Department of Psychiatry, National Clinical Research Center for Mental Disorders, and National Center for Mental Disorders, The Second Xiangya Hospital of Central South University, Changsha, 310016, Hunan, China.
Auditory verbal hallucinations (AVHs) in schizophrenia are hypothesized to involve alterations in hemispheric lateralization, but the specific neural mechanisms remain unclear. This study investigated functional intra- and inter-hemispheric connectivity to identify lateralization patterns unique to AVHs. Resting-state fMRI data were collected from 60 schizophrenia patients with persistent AVHs (p-AVH group), 39 patients without AVHs (n-AVH group), and 59 healthy controls (HC group).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Miami, Miami, FL, USA.
Background: Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Johns Hopkins University, Baltimore, MD, USA.
Background: Alzheimer's disease is a progressive form of dementia where cognitive capacities deteriorate due to neurodegeneration. Interestingly, Alzheimer's patients exhibit cognitive fluctuations during all stages of the disease. Though it is thought that contextual factors are critical for unlocking these hidden memories, understanding the neural basis of cognitive fluctuations has been hampered due to the lack of behavioral approaches to dissociate memories from contextual-performance.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Background: Prior longitudinal studies among older adults have documented associations between hearing loss and changes in brain morphology. Whether interventions involving hearing aids can reduce age-related atrophy is unknown. A substudy within the Aging and Cognitive Health Evaluation in Elders (ACHIEVE, Clinicaltrials.
View Article and Find Full Text PDFMol Ther
January 2025
Institute of Experimental Medicine CAS, Department of Neuroregeneration, Videnska 1083, 142 20, Prague, Czech Republic. Electronic address:
Neurons in the central nervous system (CNS) lose regenerative potential with maturity, leading to minimal corticospinal tract (CST) axon regrowth after spinal cord injury (SCI). In young rodents, knockdown of PTEN, which antagonises PI3K signalling by hydrolysing PIP3, promotes axon regeneration following SCI. However, this effect diminishes in adults, potentially due to lower PI3K activation leading to reduced PIP3.
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