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Posterior Parietal Cortex Dysfunction Is Central to Working Memory Storage and Broad Cognitive Deficits in
Britta Hahn1, Benjamin M Robinson2, Carly J Leonard3
1Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, Maryland 21228, bhahn@som.umaryland.edu.
Summary
Working memory storage deficits in schizophrenia are linked to posterior parietal cortex (PPC) dysfunction, not just prefrontal cortex issues. Reduced PPC activity modulation explains significant cognitive impairments in people with schizophrenia (PSZ).
Area of Science:
- Neuroscience
- Cognitive Psychology
- Psychiatry
Background:
- Working memory (WM) deficits are prominent in people with schizophrenia (PSZ), often attributed to prefrontal cortex (PFC) dysfunction.
- However, WM storage capacity, distinct from manipulation, is increasingly linked to posterior parietal cortex (PPC) activity.
- This suggests PPC dysfunction may underlie WM storage deficits in PSZ, contributing to broader cognitive impairments.
Purpose of the Study:
- To investigate the neural correlates of WM storage capacity in PSZ using functional magnetic resonance imaging (fMRI).
- To determine if reduced WM storage capacity in PSZ is associated with abnormal activity in the PPC.
- To examine the relationship between PPC activity, WM storage, and overall cognitive function in PSZ.
Main Methods:
- 37 people with schizophrenia (PSZ) and 37 healthy controls underwent fMRI while performing a change detection task designed to isolate WM storage.
- Task performance was used to derive working memory capacity (K) at varying set sizes.
- Whole-brain analysis identified brain regions where BOLD activity covaried with K, and interaction analyses compared PSZ and controls.
Main Results:
- Across both groups, working memory capacity (K) predicted BOLD activity in the PPC (including superior/inferior parietal lobules, intraparietal sulcus) and middle occipital gyrus.
- People with schizophrenia (PSZ) showed significantly less K-dependent signal modulation in the left PPC compared to healthy controls.
- The relationship between K and PPC activation statistically accounted for a substantial portion (43.4%) of the cognitive differences between groups.
Conclusions:
- Posterior parietal cortex (PPC) dysfunction is central to working memory storage deficits in people with schizophrenia (PSZ).
- The failure to flexibly modulate PPC activity based on WM load contributes significantly to the broad cognitive deficits observed in schizophrenia.
- These findings highlight the importance of the PPC in understanding the neurobiology of schizophrenia and suggest potential therapeutic targets beyond the PFC.
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