scholarly journals Visual short-term memory deficits associated with GBA mutation and Parkinson’s disease

Brain ◽  
2014 ◽  
Vol 137 (8) ◽  
pp. 2303-2311 ◽  
Author(s):  
Nahid Zokaei ◽  
Alisdair McNeill ◽  
Christos Proukakis ◽  
Michelle Beavan ◽  
Paul Jarman ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Short Term Memory ◽  
Memory Deficits ◽  
Short Term ◽  
Term Memory ◽  
Visual Short Term Memory

TEMPORAL ORDERING AND SHORT-TERM MEMORY DEFICITS IN PARKINSON'S DISEASE

Brain ◽  
1988 ◽  
Vol 111 (3) ◽  
pp. 525-539 ◽  
Author(s):  
H. J. SAGAR ◽  
E. V. SULLIVAN ◽  
J. D. E. GABRIELI ◽  
S. CORKIN ◽  
J. H. GROWDON
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Short Term Memory ◽  
Memory Deficits ◽  
Short Term ◽  
Term Memory ◽  
Temporal Ordering

scholarly journals Visual short-term memory deficits in REM sleep behaviour disorder mirror those in Parkinson’s disease

Brain ◽  
2015 ◽  
Vol 139 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Michal Rolinski ◽  
Nahid Zokaei ◽  
Fahd Baig ◽  
Kathrin Giehl ◽  
Timothy Quinnell ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Rem Sleep ◽  
Short Term Memory ◽  
Memory Deficits ◽  
Behaviour Disorder ◽  
Short Term ◽  
Term Memory ◽  
Visual Short Term Memory ◽  
Sleep Behaviour ◽  
Rem Sleep Behaviour Disorder

scholarly journals Dopamine affects short-term memory corruption over time in Parkinson’s disease

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Sean James Fallon ◽  
Matthew Gowell ◽  
Maria Raquel Maio ◽  
Masud Husain
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Short Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Over Time

scholarly journals Ketamine reversed short-term memory impairment and depressive-like behavior in animal model of Parkinson's disease

2021 ◽  
Vol 168 ◽  
pp. 63-73
Author(s):  
Débora Dalla Vecchia ◽  
Luiz Kae Sales Kanazawa ◽  
Etiéli Wendler ◽  
Palloma de Almeida Soares Hocayen ◽  
Maria Aparecida Barbato Frazão Vital ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Memory Impairment ◽  
Short Term Memory ◽  
Short Term ◽  
Term Memory

scholarly journals Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

2020 ◽  
Author(s):  
Dina Monir ◽  
Motamed Mahmoud ◽  
Omyma Galal ◽  
Ibrahim Rehan ◽  
Amany Abdelrahman
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Neurodegenerative Disorder ◽  
Short Term ◽  
Term Memory ◽  
Nrf2 Pathway

Abstract Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism.This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of NRF2-ARE pathway as a mechanism involved in exercise associated improvement in rotenone rat model of PD.Method: Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination) groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks.Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone model of PD. When treadmill exercise introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor co-ordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to NRF2 pathways such as TFAM, NRF2, Noq.1 mRNA expression.Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating NRF2 pathway.

scholarly journals Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Dina M. Monir ◽  
Motamed E. Mahmoud ◽  
Omyma G. Ahmed ◽  
Ibrahim F. Rehan ◽  
Amany Abdelrahman
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Motor Coordination ◽  
Short Term Memory ◽  
Treadmill Exercise ◽  
Short Term ◽  
Term Memory ◽  
Nrf2 Pathway

Abstract Background Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions, and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism. This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of the Nrf2- ARE pathway as a mechanism involved in exercise-associated improvement in rotenone-induced PD in rats. Method Animals were divided into 5 groups, (Control, rotenone, rotenone\exercise, rotenone\L-dopa, and rotenone\exercise\L-dopa (combination)groups). After the PD induction, rats in the rotenone\exercise and combination groups were daily treadmill exercised for 4 weeks. Results Treadmill exercise significantly improved behavioral and motor aspects of rotenone-induced PD. When treadmill exercise was introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor coordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to Nrf2 pathways such as TFAM, Nrf2 and NQO.1 mRNA expression. Conclusion This study suggests that forced exercise improved parkinsonian like features by activating the Nrf2 pathway.

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