While cognitive dysfunction in Parkinson's disease (PD) is increasingly recognized as a progressive symptom of the underlying neurodegenerative disease, our understanding of the functional and structural anatomic changes underlying these cognitive changes remains incomplete. Like the motor system, research point to a complex interplay between multiple parallel yet interconnected networks or circuits that are affected in PD and give rise to cognitive symptomatology. These circuits are most often studied in the context of disorders of executive function, and tightly linke to frontal lobe dysfunction. While the tasks employed vary across studies and it is often unclear whether differences in anatomy and function are causal or compensatory, the literature points to several key circuits that seem to be uniquely impaired in PD patients with cognitive dysfunction. This chapter reviews four of these circuits including the frontostriatal, frontoparietal, mesocortical, and noradrenergic circuits. By gaining a better understanding of the functional neuroanatomy of these circuits, we begin to develop a more comprehensive and unifed picture of how they to account for the pathophysiology of cognitive dysfunction in PD.
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http://dx.doi.org/10.1016/bs.pbr.2022.01.007 | DOI Listing |
J Racial Ethn Health Disparities
January 2025
Department of Biobehavioral Health, The Pennsylvania State University, 219 Biobehavioral Health Bldg, University Park, PA, 16802, USA.
Racialized stress disproportionately impacts Black individuals and confers increased risk for psychological distress and executive dysfunction. However, there is little evidence on psychological distress' association with cognitive flexibility (CF), an executive function theorized to be a neurocognitive resilience factor, as it is shown to reflect the ability to adapt thoughts/behaviors to changing environmental stimuli. As such, we aimed to examine the relation between racialized stress and psychological distress and the potential buffering effects of CF.
View Article and Find Full Text PDFAging Clin Exp Res
January 2025
Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Oviedo, 33003, Spain.
Background: The presence of frailty is common in people with Parkinson's disease, as is cognitive dysfunction. Previous research on frailty has focused on the physical aspects of the pathology.
Aims: To analyze the relationship between frailty and cognitive impairment in patients with Parkinson's disease and to know which disease characteristics are associated with frailty.
Neurochem 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 PDFNeurochem Res
January 2025
Diagnostic Radiology Department, National Cancer Institute, Misrata, Libya.
Huntington's disease (HD) is a progressive neurodegenerative disease resulting from a mutation in the huntingtin (HTT) gene and characterized by progressive motor dysfunction, cognitive decline, and psychiatric disturbances. Currently, no disease-modifying treatments are available. Recent research has developed therapeutic agents that may have the potential to directly target the disease pathology, such as gene silencing or clearing the mutant protein.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Center of Excellence in Cardiac Electrophysiology Research, Chiang Mai University, Chiang Mai, Thailand.
Background: Our previous studies reported that D-galactose (D-gal) administration for four to eight weeks caused metabolic disturbance, brain mitochondrial dysfunction, and brain aging, leading to cognitive dysfunction in similar with natural aging condition. Spermidine is a polyamine that can be found naturally. Spermidine has been showed the beneficial effects on various models, such as attenuating metabolic/gut impairments in obesity, and ameliorating memory loss in aged model.
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