Episodic memory deficit in HIV infection: common phenotype with Parkinson's disease, different neural substrates.
Episodic memory deficit in HIV infection: common phenotype with Parkinson's disease, different neural substrates.
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
US · Author affiliation · country only
Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 401 Quarry Rd, Stanford, CA, 94305, USA.Location evidence
Menlo Park, US · Author affiliation
Neuroscience Program, Center for Health Sciences, Bioscience Division, SRI International, 333 Ravenswood Ave, Menlo Park, CA, 94025, USA.Location evidence
Palo Alto, US · Author affiliation
Clinical Psychology, Palo Alto University, 1791 Arastradero Rd, Palo Alto, CA, 94304, USA.Location evidence
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Original abstract
Episodic memory deficits occur in people living with HIV (PLWH) and individuals with Parkinson's disease (PD). Given known effects of HIV and PD on frontolimbic systems, episodic memory deficits are often attributed to executive dysfunction. Although executive dysfunction, evidenced as retrieval deficits, is relevant to mnemonic deficits, learning deficits may also contribute. Here, the California Verbal Learning Test-II, administered to 42 PLWH, 41 PD participants, and 37 controls, assessed learning and retrieval using measures of free recall, cued recall, and recognition. Executive function was assessed with a composite score comprising Stroop Color-Word Reading and Backward Digit Spans. Neurostructural correlates were examined with MRI of frontal (precentral, superior, orbital, middle, inferior, supplemental motor, medial) and limbic (hippocampus, thalamus) volumes. HIV and PD groups were impaired relative to controls on learning and free and cued recall trials but did not differ on recognition or retention of learned material. In no case did executive functioning solely account for the observed mnemonic deficits or brain-performance relations. Critically, the shared learning and retrieval deficits in HIV and PD were related to different substrates of frontolimbic mnemonic neurocircuitry. Specifically, diminished learning and poorer free and cued recall were related to smaller orbitofrontal volume in PLWH but not PD, whereas diminished learning in PD but not PLWH was related to smaller frontal superior volume. In PD, poorer recognition correlated with smaller thalamic volume and poorer retention to hippocampal volume. Although memory deficits were similar, the neural correlates in HIV and PD suggest different pathogenic mechanisms.