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SCIENTIFIC LITERATURE · MED

Cerebral Amyloid-β Deposition, Axial Features, and Cognitive Alterations in Patients with Parkinson's Disease Treated with Bilateral STN-DBS: A Long-Term Cohort Study.

J Pers Med · 2024-12-10

DOI: 10.3390/jpm14121150PMID: 39728063

Open accessresearch-article; Journal ArticleOriginal source ↗

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Objectives: Our aim was to evaluate the possible long-term cerebral deposition of amyloid-β in patients with PD treated with subthalamic nucleus deep brain stimulation (STN-DBS) and its possible influence on axial and cognitive variables. Methods: Consecutive PD patients treated with bilateral STN-DBS with a long-term follow-up were included. The amyloid-β deposition was evaluated postoperatively through an 18F-flutemetamol positron emission tomography (PET) study. Axial symptoms were assessed using a standardized clinical-instrumental approach. The speech was assessed by perceptual and acoustic analysis, while gait was assessed by means of the instrumented Timed Up and Go test (iTUG). Motor severity was evaluated by applying the UPDRS part III score and subscores, while cognitive functions were assessed through a complete neuropsychological assessment. Different stimulation and drug conditions were assessed: on-stimulation/off-medication, off-stimulation/off-medication, and on-stimulation/on-medication conditions (single- and dual-task). Results: In total, 19 PD patients (male: 11; age: 63.52 years; on-stimulation/on-medication UPDRS-III: 17.05) with a five-year postoperative follow-up were included. The amyloid-β deposition was found in 21% of patients (4/19) with a prevalent involvement of prefrontal, limbic, and parietal areas. Compared with patients without amyloid-β deposition, PD patients with positive 18F-flutemetamol in the PET study showed a higher preoperative UPDRS-I (p = 0.037) score. Conclusions: Our results suggest that in the long term, after STN-DBS, a significant percentage of PD patients may present brain amyloid-β deposition. However, larger samples are needed to evaluate the possible role of amyloid-β deposition in the development of axial and cognitive alterations after surgery.

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