Objective: Previous studies have revealed that, compared with Parkinson's disease (PD) patients without freezing of gait (FoG), the ones with FoG showed greater prefrontal activation while doing lower-limb movements involving standing, walking and turning, which require both locomotor and balance control. However, the relation between FoG and pure locomotor control as well as its underlying mechanism remain unclear.
Methods: A total of 56 PD subjects were recruited and allocated to PD-FoG and PD-noFoG subgroups, and 34 age-matched heathy adults were included as heathy control (HC). Functional near-infrared spectroscopy was used to measure their prefrontal activation in a sitting lower-limb movement task, wherein subjects were asked to sit and tap their right toes as big and as fast as possible.
Results: Result of one-way ANOVA (Group: PD-FoG vs. PD-noFoG vs. HC) revealed greater activation in the right prefrontal cortex in the PD-FoG group than in the other 2 groups. Linear mixed-effects model showed consistent result. Furthermore, the right prefrontal activation positively correlated with the severity of FoG symptoms in PD-FoG patients.
Conclusion: These findings suggested that PD patients with FoG require additional cognitive resources to compensate their damaged automaticity in locomotor control, which is more pronounced in severe FoG patients than milder ones.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1093/cercor/bhac114 | DOI Listing |
Neurochem Res
January 2025
Precision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Air Force Medical University, Xi'an, 710038, China.
Depression is a common and complex neuropsychiatric disorder affecting people of all ages worldwide, associated with high rates of relapse and disability. Neohesperidin (NEO) is a dietary flavonoid with applications in therapeutics; however, its effects on depressive-like behavior remain unknown. Here, we evaluated the effects of NEO on depressive-like behavior induced by chronic and unpredictable mild stress (CUMS).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Korea University, Sejong, Sejong, Korea, Republic of (South).
Background: Amyloid-β accumulation is a pivotal factor in Alzheimer's disease (AD) progression. As treatment for AD has not been successful yet, the most effective approach lies in early diagnosis and the subsequent delay of disease progression. Hence, this study introduces a deep learning model to predict amyloid-β accumulation in the brain.
View Article and Find Full Text PDFNeurochem Res
January 2025
Laboratory of Chinese Medicine Brain Science, Innovative Institute of Chinese Medicine and Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, 250355, China.
Maintaining GABAergic inhibition within physiological limits in the medial prefrontal cortex (mPFC) is critical for working memory. While synaptic GABAR typically mediate the primary component of mPFC inhibition, the role of extrasynaptic δ-GABAR in working memory remains unclear. To investigate this, we used fiber photometry to examine the effects of δ-GABAR in freely moving mice.
View Article and Find Full Text PDFBackground: Single-nucleus RNA sequencing (snRNAseq) allows for the dissection of the cell type-specific transcriptional profiles of tissue specimens. In this study, we compared gene expression in multiple brain cell types in brain tissue from Alzheimer disease (AD) cases with no or other co-existing pathologies including Lewy body disease (LBD) and vascular disease (VaD).
Method: We evaluated differential gene expression measured from single nucleus RNA sequencing (snRNAseq) data generated from the hippocampus region tissue donated by 11 BU ADRC participants with neuropathologically confirmed AD with or without a co-existing pathology (AD-only = 3, AD+VaD = 6, AD+LBD = 2).
Alzheimers Dement
December 2024
Institut de l'Audition/Institut Pasteur, Paris, France.
Background: Memory consolidation is an essential process for our everyday lives that is severely disrupted in Alzheimer's Disease (AD). Memories are initially encoded in the hippocampus before being consolidated in the neocortex by synaptic plasticity processes that depend on protein synthesis. However, how molecular pathways affect synaptic signalling during memory consolidation in health and disease is unclear.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!