Reduced Enhancement of Memory for Faces Encoded by Semantic and Socioemotional Processes in Patients with Parkinson’s Disease

2019 ◽  
Vol 26 (4) ◽  
pp. 418-429
Author(s):  
Paeksoon Park ◽  
Hodaka Yamakado ◽  
Ryosuke Takahashi ◽  
Shikiho Dote ◽  
Shiho Ubukata ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Office Worker ◽  
Long Term Memory ◽  
Retrieval Performance ◽  
Memory Enhancement ◽  
Semantic Judgment ◽  
Frontal Lobe Function ◽  
Individual Scores

AbstractObjectives:Patients with Parkinson’s disease (PD) exhibit impaired semantic and socioemotional processes, which are thought to be related to dysfunctions in the fronto-striatal circuit. However, little is known about how the memory enhancement by these processes was reduced in PD. The present study investigated this issue.Methods:The retrieval performance of face memories encoded by semantic and socioemotional processes was compared between 24 PD patients and 24 age-matched healthy controls (HC). During encoding, participants were presented with unfamiliar faces and made judgment about them in three encoding conditions of semantic judgment (Semantics), attractiveness judgment (Attractiveness), and form judgment (Form). In Semantics, participants rated to what degree each face looked like an office worker, whereas in Attractiveness, participants rated how attractive each face was. The Form condition as a control required participants to judge the shape of each face. During retrieval after encoding, participants made old or new judgment for target and distracter faces.Results:In HC, the retrieval of faces encoded by Semantics and Attractiveness was significantly more accurate than that encoded by Form, whereas this memory enhancement was not identified in PD. In addition, individual scores in frontal lobe function and long-term memory correlated with the retrieval performance of memories encoded in Semantics and Attractiveness but not Form.Conclusions:These findings suggest that the processing of semantic and socioemotional signals conveyed from faces could be impaired in PD and that the impairment of these processes could decrease the enhancement of face memories by semantic and socioemotional elaborations.

scholarly journals Correlation of EEG Slowing with Cognitive Domains in Nondemented Patients with Parkinson's Disease

2015 ◽  
Vol 39 (3-4) ◽  
pp. 207-214 ◽  
Author(s):  
Ronan Zimmermann ◽  
Ute Gschwandtner ◽  
Florian Hatz ◽  
Christian Schindler ◽  
Habib Bousleiman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Working Memory ◽  
Parkinson's Disease ◽  
Executive Function ◽  
Long Term Memory ◽  
Median Frequency ◽  
Term Memory ◽  
Cognitive Domains ◽  
Visuospatial Functions

Background: Cognitive deficits in Parkinson's disease (PD) are heterogeneous and can be classified into cognitive domains. Quantitative EEG is related to and predictive of cognitive status in PD. In this cross-sectional study, the relationship of cognitive domains and EEG slowing in PD patients without dementia is investigated. Methods: A total of 48 patients with idiopathic PD were neuropsychologically tested. Cognitive domain scores were calculated combining Z-scores of test variables. Slowing of EEG was measured with median EEG frequency. Linear regression was used for correlational analyses and to control for confounding factors. Results: EEG median frequency was significantly correlated to cognitive performance in most domains (episodic long-term memory, rho = 0.54; overall cognitive score, rho = 0.47; fluency, rho = 0.39; attention, rho = 0.37; executive function, rho = 0.34), but not to visuospatial functions and working memory. Conclusion: Global EEG slowing is a marker for overall cognitive impairment in PD and correlates with impairment in the domains attention, executive function, verbal fluency, and episodic long-term memory, but not with working memory and visuospatial functions. These disparate effects warrant further investigations.

scholarly journals Dopamine is associated with prioritization of reward-associated memories in Parkinson’s disease

Brain ◽  
2020 ◽  
Vol 143 (8) ◽  
pp. 2519-2531
Author(s):  
Madeleine E Sharp ◽  
Katherine Duncan ◽  
Karin Foerde ◽  
Daphna Shohamy
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Reinforcement Learning ◽  
Episodic Memory ◽  
Memory Capacity ◽  
Long Term Memory ◽  
Term Memory ◽  
Episodic Encoding ◽  
Stimulus Value

Abstract Patients with Parkinson’s disease have reduced reward sensitivity related to dopaminergic neuron loss, which is associated with impairments in reinforcement learning. Increasingly, however, dopamine-dependent reward signals are recognized to play an important role beyond reinforcement learning. In particular, it has been shown that reward signals mediated by dopamine help guide the prioritization of events for long-term memory consolidation. Meanwhile, studies of memory in patients with Parkinson’s disease have focused on overall memory capacity rather than what is versus what isn’t remembered, leaving open questions about the effect of dopamine replacement on the prioritization of memories by reward and the time-dependence of this effect. The current study sought to fill this gap by testing the effect of reward and dopamine on memory in patients with Parkinson’s disease. We tested the effect of dopamine modulation and reward on two forms of long-term memory: episodic memory for neutral objects and memory for stimulus-value associations. We measured both forms of memory in a single task, adapting a standard task of reinforcement learning with incidental episodic encoding events of trial-unique objects. Objects were presented on each trial at the time of feedback, which was either rewarding or not. Memory for the trial-unique images and for the stimulus-value associations, and the influence of reward on both, was tested immediately after learning and 2 days later. We measured performance in Parkinson’s disease patients tested either ON or OFF their dopaminergic medications and in healthy older control subjects. We found that dopamine was associated with a selective enhancement of memory for reward-associated images, but that it did not influence overall memory capacity. Contrary to predictions, this effect did not differ between the immediate and delayed memory tests. We also found that while dopamine had an effect on reward-modulated episodic memory, there was no effect of dopamine on memory for stimulus-value associations. Our results suggest that impaired prioritization of cognitive resource allocation may contribute to the early cognitive deficits of Parkinson’s disease.

Neurobehavioral Consequences Associated with Long Term Tramadol Utilization and Pathological Mechanisms

2020 ◽  
Vol 18 (10) ◽  
pp. 758-768 ◽  
Author(s):  
Khadga Raj ◽  
Pooja Chawla ◽  
Shamsher Singh
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Serotonin Reuptake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Serotonin Syndrome ◽  
Dopamine Synthesis ◽  
Synthetic Analog

: Tramadol is a synthetic analog of codeine used to treat pain of moderate to severe intensity and is reported to have neurotoxic potential. At therapeutic dose, tramadol does not cause major side effects in comparison to other opioid analgesics, and is useful for the management of neurological problems like anxiety and depression. Long term utilization of tramadol is associated with various neurological disorders like seizures, serotonin syndrome, Alzheimer’s disease and Parkinson’s disease. Tramadol produces seizures through inhibition of nitric oxide, serotonin reuptake and inhibitory effects on GABA receptors. Extensive tramadol intake alters redox balance through elevating lipid peroxidation and free radical leading to neurotoxicity and produces neurobehavioral deficits. During Alzheimer’s disease progression, low level of intracellular signalling molecules like cGMP, cAMP, PKC and PKA affect both learning and memory. Pharmacologically tramadol produces actions similar to Selective Serotonin Reuptake Inhibitors (SSRIs), increasing the concentration of serotonin, which causes serotonin syndrome. In addition, tramadol also inhibits GABAA receptors in the CNS has been evidenced to interfere with dopamine synthesis and release, responsible for motor symptoms. The reduced level of dopamine may produce bradykinesia and tremors which are chief motor abnormalities in Parkinson’s Disease (PD).

The mechanistic role of thymoquinone in Parkinson's disease: focus on neuroprotection in pre-clinical studies

2021 ◽  
Vol 14 ◽  
Author(s):  
Mohammad Najim Uddin ◽  
Mohammad Injamul Hoq ◽  
Israt Jahan ◽  
Shafayet Ahmed Siddiqui ◽  
Chayan Dhar Clinton ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Studies ◽  
Nigella Sativa ◽  
Biological Effects ◽  
Neuroprotective Activity ◽  
Substantia Nigra Pars Compacta ◽  
Movement Difficulties

: Thymoquinone (TQ) is one of the leading phytochemicals, which is abundantly found in Nigella sativa L. seeds. TQ exhibited various biological effects such as antioxidant, anti-inflammatory, antimicrobial, and anti-tumoral in several pre-clinical studies. Parkinson's disease (PD) is a long-term neurodegenerative disease with movement difficulties, and the common feature of neurodegeneration in PD patients is caused by dopaminergic neural damage in the substantia nigra pars compacta. The neuroprotective activity of TQ has been studied in various neurological disorders. TQ-mediated neuroprotection against PD yet to be reported in a single frame; therefore, this review is intended to narrate the potentiality of TQ in the therapy of PD. TQ has been shown to protect against neurotoxins via amelioration of neuroinflammation, oxidative stress, apoptosis, thereby protects neurodegeneration in PD models. TQ could be an emerging therapeutic intervention in PD management, but mechanistic studies have been remained to be investigated to clarify its neuroprotective role.

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