Abstract
Deficits in working memory (WM) in Parkinson’s disease (PD) are often considered to be secondary to dopaminergic depletion. However, the neurocognitive mechanisms by which dopamine causes these deficits remain highly contested, and PD is now also known to be associated with nondopaminergic pathology. Here, we examined how PD and dopaminergic medication modulate three components of WM: maintenance over time, updating contents with new information and making memories distracter-resistant. Compared with controls, patients were disproportionately impaired when retaining information for longer durations. By applying a probabilistic model, we were able to reveal that the source of this error was selectively due to precision of memory representations degrading over time. By contrast, replenishing dopamine levels in PD improved executive control over both the ability to ignore and update, but did not affect maintenance of information across time. This was due to a decrease in guess responses, consistent with the view that dopamine serves to prevent WM representations being corrupted by irrelevant information, but has no impact on information decay. Cumulatively, these results reveal a dissociation in the neural mechanisms underlying poor WM: whereas dopamine reduces interference, nondopaminergic systems in PD appear to modulate processes that prevent information decaying more quickly over time.
Highlights
Our understanding of the importance of dopamine in human brain function has been influenced greatly by observations on Parkinson’s disease (PD)
By contrast, replenishing dopamine levels in PD improved executive control over both the ability to ignore and update, but did not affect maintenance of information across time. This was due to a decrease in guess responses, consistent with the view that dopamine serves to prevent working memory (WM) representations being corrupted by irrelevant information, but has no impact on information decay
We examined the effect that dopaminergic medication has in PD patients on the ability to ignore and update information in WM
Summary
Our understanding of the importance of dopamine in human brain function has been influenced greatly by observations on Parkinson’s disease (PD). As well as the conspicuous motor deficits associated with the condition, cognitive impairment is well-established as a major feature (Kehagia et al 2012; Gratwicke et al 2015). Working memory (WM), the means by which information is retained and manipulated over short intervals, has been found to be impaired in PD (Lewis et al 2003, 2005; Sawamoto et al 2008). Our ability to effectively use PD as a model of dopamine depletion and to improve treatments for the associated cognitive symptoms has been hampered by a lack of understanding about the precise contribution of dopamine to patients’ cognitive impairment. While dopaminergic depletion has intuitively been considered to be the prime suspect underlying mnemonic impairments, this is not necessarily the case. PD is associated with other neurochemical disturbances to the serotonergic, noradrenergic and cholinergic systems (Dubois et al 1983; Zarow et al 2003; Kish et al 2008)
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