Previous research suggests that different aspects of tool knowledge are mediated by different memory systems. It is believed that tool attributes (e.g., function, color) are represented as declarative memory while skill learning is supported by procedural memory. It has been proposed that other aspects (e.g., skilled tool use) may rely on an interaction of both declarative and procedural memory. However, the specific form of procedural memory underlying skilled tool use and the nature of interaction between declarative and procedural memory systems remain unclear. In the current study, individuals with Parkinson's disease (PD) and healthy controls were trained over 2 sessions, 3 weeks apart, to use a set of novel complex tools. They were also tested on their ability to recall tool attributes as well as their ability to demonstrate grasp and use of the tools to command. Results showed that, compared to controls, participants with PD showed intact motor skill acquisition and tool use to command within sessions, but failed to retain performance across sessions. In contrast, people with PD showed equivalent recall of tool attributes and tool grasping relative to controls, both within and across sessions. Current findings demonstrate that the frontal-striatal network, compromised in PD, mediates long-term retention of motor skills. Intact initial skill learning raises the possibility of compensation from declarative memory for frontal-striatal dysfunction. Lastly, skilled tool use appears to rely on both memory systems which may reflect a cooperative interaction between the two systems. Current findings regarding memory representations of tool knowledge and skill learning may have important implications for delivery of rehabilitation programs for individuals with PD.
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http://dx.doi.org/10.1016/j.neuropsychologia.2014.11.005 | DOI Listing |
Chaos
January 2025
AIMdyn, Inc., Santa Barbara, California 93101, USA.
Koopman operator theory has found significant success in learning models of complex, real-world dynamical systems, enabling prediction and control. The greater interpretability and lower computational costs of these models, compared to traditional machine learning methodologies, make Koopman learning an especially appealing approach. Despite this, little work has been performed on endowing Koopman learning with the ability to leverage its own failures.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Neurology, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Alzheimer's disease (AD) is a central nervous system degenerative disease with a stealthy onset and a progressive course characterized by memory loss, cognitive dysfunction, and abnormal psychological and behavioral symptoms. However, the pathogenesis of AD remains elusive. An increasing number of studies have shown that oligodendrocyte progenitor cells (OPCs) and oligodendroglial lineage cells (OLGs), especially OPCs and mature oligodendrocytes (OLGs), which are derived from OPCs, play important roles in the pathogenesis of AD.
View Article and Find Full Text PDFCancer Immunol Immunother
January 2025
Public Center of Experimental Technology, The School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuan Province, China.
Although immune checkpoint inhibitors have changed the treatment paradigm for non-small cell lung cancer (NSCLC), not all patients benefit from them. Therefore, there is an urgent need to explore novel immune checkpoint inhibitors. Neuropilin-1 (Nrp-1) is a unique immune checkpoint capable of exerting antitumor effects through CD8 T cells.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Background: Alzheimer's disease (AD) is the most common tauopathy and characterized by the progressive accumulation of Aß and tau. Tau is expressed in two major isoforms containing either 3 or 4 c-terminal repeats labeled as 3R and 4R tau. While these two isoforms occur in roughly equimolar ratios in AD, most research focus and mouse models of tau center only the 4Rtau protein and not 3Rtau.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Inhibitory interneurons normally regulate neural networks underlying memory and cognition, but are disrupted in Alzheimer's disease. Proper interneuron activity reduces amyloid-beta, whereas hyperexcitability elevates amyloid levels. Still, the underlying pathologic processes mediating interneuron dysfunction remain unknown.
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