The ability to combine information from multiple sensory modalities into a single, unified percept is a key element in an organism's ability to interact with the external world. This process of perceptual fusion, the binding of multiple sensory inputs into a perceptual gestalt, is highly dependent on the temporal synchrony of the sensory inputs. Using fMRI, we identified two anatomically distinct brain regions in the superior temporal cortex, one involved with processing temporal-synchrony, and one with processing perceptual fusion of audiovisual speech. This dissociation suggests that the superior temporal cortex should be considered a "neuronal hub" composed of multiple discrete subregions that underlie an array of complementary low- and high-level multisensory integration processes. In this role, abnormalities in the structure and function of superior temporal cortex provide a possible common etiology for temporal-processing and perceptual-fusion deficits seen in a number of clinical populations, including individuals with autism spectrum disorder, dyslexia, and schizophrenia.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057325 | PMC |
http://dx.doi.org/10.1016/j.neuroimage.2010.12.063 | DOI Listing |
Background: Alzheimer's disease (AD) is a devastating neurodegenerative disorder with few therapies to treat, mitigate or prevent its onset. Understanding of this disease is predominantly based on research in non-Hispanic Whites (NHW) although AD disproportionately affects African Americans (AA) and Latin Americans (LA), underrepresented in AD research. To address this knowledge gap, the Accelerating Medicine Partnership for Alzheimer's Disease (AMP-AD) Diversity Working Group was launched to generate multi-omics data from post-mortem brain tissue from donors of predominantly AA and LA descent.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Mass General Institute for Neurodegenerative Disease, Charlestown, MA, USA.
Background: Some individuals can tolerate the presence of Alzheimer disease neuropathologic changes (ADNC) (e.g., plaques and tangles) without developing dementia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Yale School of Medicine, New Haven, CT, USA.
Background: While the apolipoprotein E (APOE) ε4 allele is a well-known risk factor for late-onset Alzheimer's disease (LOAD), not all carriers develop the condition, suggesting the presence of resilience and/or risk factors. The molecular signatures of resilience/risk in the brain, however, have not been thoroughly described, partly due to the scarcity of healthy APOEe4 carriers. This study addresses this gap using a novel multi-tissue, multi-omic dataset from the Religious Order Study and Memory and Aging Project cohorts highly enriched in APOEe4 carriers with and without LOAD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology, University of Sao Paulo Medical School, São Paulo, São Paulo, Brazil.
Background: Individuals meeting neuropathological criteria for Alzheimer's disease (AD) may manifest with atypical clinical syndromes. Past work showed that the neurobiological basis for these differences is related to specific neuronal vulnerabilities for tau pathology. For instance, amnestic cases have a higher burden of neurofibrillary changes in CA1.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is heterogeneous in both its clinical and neuropathologic course. Age at onset and distribution of corticolimbic tangles can vary widely among individuals. Genetic risk factors APOE ε4 and MAPT H1 increase AD risk.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!