A neurocomputational account of cognitive deficits in Parkinson's disease

Abstract

Parkinson’s disease (PD) is caused by the accelerated death of dopamine (DA) producing neurons. Numerous studies documenting cognitive deficits of PD patients have revealed impairments in a variety of tasks related to memory, learning, visuospatial skills, and attention. While there have been several studies documenting cognitive deficits of PD patients, very few computational models have been proposed. In this article, we use the COVIS model of category learning to simulate DA depletion and show that the model suffers from cognitive symptoms similar to those of human participants affected by PD. Specifically, DA depletion in COVIS produced deficits in rule-based categorization, non-linear information-integration categorization, probabilistic classification, rule maintenance, and rule switching. These were observed by simulating results from younger controls, older controls, PD patients, and severe PD patients in five well-known tasks. Differential performance among the different age groups and clinical populations was modeled simply by changing the amount of DA available in the model. This suggests that COVIS may not only be an adequate model of the simulated tasks and phenomena but also more generally of the role of DA in these tasks and phenomena.

Dissociating the Cognitive Effects of Levodopa versus Dopamine Agonists in a Neurocomputational Model of Learning in Parkinson’s Disease

“…Experimental data, however, point to an essential role for both D 1 and D 2 receptors in PFC for working memory [18,69]. Like our model, a prior model by Helie et al [70] also assumes that PD affects prefrontal dopamine. Our model simulates the functional contribution of D 1 and D 2 receptors in both the BG and PFC in learning and working memory.…”

Learning robust cortico-cortical associations with the basal ganglia: An integrative review

“…The BG are recruited to facilitate the entry of new information into WM and/or to switch attention between different WM items (e.g., Ashby, Alfonso-Reese, Turken, & Waldron, 1998;Frank, Loughry, & O'Reilly, 2001;Monchi, Taylor, & Dagher, 2000;. This is because cortical DA is thought to stabilize representations, whereas BG DA is used to quickly update the representations in a task-relevant manner (Cools et al, 2007;H elie, Paul, & Ashby, 2012a, 2012b. In addition, there is mounting evidence that the BG may also help mediate WM maintenancednot just manipulation.…”

Effect of black mulberry (Morus nigra) extract treatment on cognitive impairment and oxidative stress status of d-galactose-induced aging mice

“…Brain is the most sensitive organ that gets affected by oxidative damage because of its high metabolic rate, high oxygen need and relatively low antioxidative defence mechanism. Brain aging has an important role in cognitive dysfunction, which is usually related with neurodegenerative diseases (Hélie et al 2012;O'Neill 2013). D-Galactose is a reducing sugar which can be metabolized at the normal level.…”