Striatal dopamine correlates to memory and attention in Parkinson's disease

• Published in: American journal of nuclear medicine and molecular imaging Vol. 11; no. 1; pp. 10 - 19
• Main Authors: Fornari, Luís Henrique Tieppo, da Silva Júnior, Neivo, Muratt Carpenedo, Camila, Hilbig, Arlete, Rieder, Carlos Roberto de Mello
• Format: Journal Article
• Language: English
• Published: United States e-Century Publishing Corporation 01.01.2021
• Subjects: Original; Parkinson disease; attention; memory; cognition; DATscan; radionuclide imaging
• ISSN: 2160-8407; 2160-8407

Parkinson's disease (PD) is clinically characterized by motor symptoms, however, specific cognitive impairments are common and poorly understood. This study was designed to assess whether cognitive performances are related to dopamine active transporter (DAT) availability in non-demented PD subjects. Fifty-four non-demented PD patients were enrolled. They underwent [ Tc] TRODAT-1 SPECT/CT and a comprehensive neuropsychological battery including attention/executive and memory tests. Multiple linear regression controlling the effect of age, disease duration and education was applied. The significance level was set at values of < 0.02. After controlling the effect of age, disease duration and education, lower scores in Rey's Auditory-Verbal Learning Test (RAVLT)/immediate recall were significantly related with lower uptake values in the less affected striatum and more affected caudate. Lower scores in RAVLT/short-term recall were also significantly associated with lower uptake values in the more affected caudate and reduced performance in Trail Making Test part B was related with reduced DAT values in the less affected anterior putamen. Our findings suggest that reduced DAT availability in both caudate and putamen is related to reduced performances in some memory and attention/executive tasks. Nigrocaudate dysfunction is related to lower memory performance while dopamine depletion in the anterior putamen is related to poorer attention performance. If the dopaminergic defects can mostly explain all the cognitive symptoms or this phenomenon just co-occur with other anatomical and biochemical changes remains unknown. Further studies in larger patient samples are required to clarify this issue.