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Odor perception plays a critical role in early human development, but the underlying neural mechanisms are not fully understood. To investigate these, we presented appetitive and aversive odors to infants of both sexes at 1 month of age while recording functional magnetic resonance imaging (fMRI) and nasal airflow data. Infants slept during odor presentation to allow MRI scanning. We found that odors evoke robust fMRI activity in the bilateral olfactory cortex and thalamus and that fMRI response magnitudes in the olfactory cortex differ across odors. However, in contrast to prior work in adults, we did not find compelling evidence that odor stimuli evoke discriminable fMRI activity patterns in the olfactory cortex or thalamus using two different multivariate pattern analysis techniques. Finally, the average inhale airflow rate was higher for appetitive odors than aversive odors, which tentatively suggests that infants could modulate their respiration to reflect odor valence. Overall, these results show strong neural responses to odors at this early developmental stage and highlight nasal airflow as a behavioral metric for assessing odor preference in infants.
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http://dx.doi.org/10.1523/JNEUROSCI.1780-24.2025 | DOI Listing |
Heterozygous loss-of-function mutations are one established cause of isolated dystonia and hyposmia. Homozygous mutations have been reported in siblings with generalized dystonia and intellectual disability. encodes major [NM_001369387.
View Article and Find Full Text PDFNeurology
September 2025
Department of Statistical Science, Hangzhou Shansier Medical Technologies Co., Ltd., China.
Background And Objectives: β-Amyloid (Aβ) likely triggers the spread of pathologic tau from the entorhinal cortex (EC) to the neocortex, but whether distinct Aβ levels exert differential influences on tau propagation beyond the EC remains unclear. We aimed to investigate the modifying effect of Aβ on the association of initial tau deposition with successive tau accumulation.
Methods: A retrospective analysis was performed using data from 2 longitudinal observational cohort studies, the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the Harvard Aging Brain Study (HABS), both conducted in the United States.
CNS Neurosci Ther
September 2025
Biomedical Science Graduate Program (BMSGP), Chonnam National University, Hwasun, Republic of Korea.
Objectives: Hepatic encephalopathy (HE) is a neuropsychiatric disorder associated with cirrhosis and chronic liver disease primarily driven by ammonia (NH3) toxicity, which leads to neuroinflammation and cognitive deficits. Recent studies have identified olfactory dysfunction as a potential early indicator of HE, linked to ammonia-induced neurotoxicity in the brain.
Methods: After confirming physiological alterations in olfactory cells induced by ammonia, we assessed gene expression changes in olfactory bulbs of bile duct ligation (BDL) mice as an HE mouse model.
Sci Adv
September 2025
Aging, Cognition & Technology Group, German Center for Neurodegenerative Diseases (DZNE), Magdeburg 39120, Germany.
Path integration, the ability to track one's position using self-motion cues, is critically dependent on the grid cell network in the entorhinal cortex, a region vulnerable to early Alzheimer's disease pathology. In this study, we examined path integration performance in individuals with subjective cognitive decline (SCD), a group at increased risk for Alzheimer's disease, and healthy controls using an immersive virtual reality task. We developed a Bayesian computational model to decompose path integration errors into distinct components.
View Article and Find Full Text PDFFront Cell Neurosci
August 2025
Physiologisches Institut, Justus-Liebig-Universität, Giessen, Germany.
Attention-deficit hyperactivity disorder (ADHD) is the most prevalent neurodevelopmental disorder worldwide. To improve treatment strategies against ADHD a better understanding of underlying pathophysiology is required. Spontaneously hypertensive rats (SHR) from the strain SHR/NCrl are a suitable rodent model of ADHD.
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