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06-11-2014 | Neurology | Article

Dopaminergic deficit link to Parkinson’s executive dysfunction boosted

Abstract

Free abstract

medwireNews: Research suggests that reduced striatal dopamine transporter (DAT) binding may underlie some of the cognitive dysfunction seen in patients with Parkinson’s disease (PD).

The findings from the Parkinson’s Progression Markers Initiative reveal associations between DAT binding and patients’ performances in the attention/executive domain, but not in other cognitive domains.

Although the associations were small, the researchers believe their findings “support the hypothesis that dopaminergic activity is related to executive functioning, but that visuospatial and memory dysfunctions in PD are related to other mechanisms.”

The analysis included 339 PD patients with complete imaging and cognitive data. They scored lower on most cognitive tests than 158 healthy controls. There were small, although statistically significant, associations between poorer performance for attention/executive function and reduced DAT binding in the left and right caudate and the right putamen.

There was also an association between memory and DAT binding, but only in the right caudate.

The researchers says this is in line with the theory that executive dysfunction in PD patients is related to dopaminergic frontostriatal deficits, and tends not to progress, whereas memory and visuospatial deficits are caused by nondopaminergic lesions, which progress and lead to dementia.

However, all these associations disappeared after accounting for age, report Françoise Siepel (Stavanger University Hospital, Norway) and study co-authors in Movement Disorders.

Of the individual executive function tests, the Symbol Digit Modalities Test was associated with DAT binding even after adjustment for age. But Siepel et al say: “We cannot exclude, however, that this association is, at least partly, the result of an influence of bradykinesia, which is much affected by dopaminergic depletion in the striatum.”

The team explored the effects of age further, on the basis that “dopaminergic loss dominates in younger PD patients, whereas other neuronal structures are more prominently affected in older patients.”

Consistent with this, they were unable to find a direct effect of PD on executive cognitive function; instead, the entire effect was indirect and mediated through DAT binding.

Furthermore, this effect was strongly influenced by age, with DAT binding explaining more of the difference in executive function between patients and controls for younger participants than for older patients. The indirect effect size ranged from –0.307 at age 47 years to –0.214 at age 72 years, but remained statistically significant at all ages.

medwireNews (www.medwirenews.com) is an independent clinical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2014

By Eleanor McDermid, Senior medwireNews Reporter

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