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Objective: in patients with Parkinson's Disease (PD), oral health can be affected by motor and non-motor symptoms and/or medication use. Therefore, the aim was to systematically review the literature on oral health and associated factors of oral health in PD patients. Design: a literature search was performed from inception up to April 5th, 2023. Original studies that assessed oral health-related factors in PD patients and were written in English or Dutch, were included. Results: 11276 articles were identified, of which 43 met the inclusion criteria (quality range poor-good). A higher prevalence of dental biofilm, bleeding/gingivitis, pocket depth (≥4 mm), tooth mobility, caries, and number of decayed missing filled teeth/surfaces was found in PD patients than in controls. However, no difference between both groups was found when analysing edentulism and wearing dentures. Poor oral health of PD patients was associated with a longer disease duration, higher disease severity, and more prescribed medications. Conclusions: oral health of PD patients is worse than that of healthy individuals. It is associated with the duration and severity of PD and medication use. Therefore, we advise regular appointments with oral health care professionals, with an important focus on prevention.

Background: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is an effective treatment for disabling fluctuations in motor symptoms in Parkinson's disease (PD) patients. However, iterative exploration of all individual contact points (four in each STN) by the clinician for optimal clinical effects may take months. Objective: In this proof of concept study we explored whether magnetoencephalography (MEG) has the potential to noninvasively measure the effects of changing the active contact point of STN-DBS on spectral power and functional connectivity in PD patients, with the ultimate aim to aid in the process of selecting the optimal contact point, and perhaps reduce the time to achieve optimal stimulation settings. Methods: The study included 30 PD patients who had undergone bilateral DBS of the STN. MEG was recorded during stimulation of each of the eight contact points separately (four on each side). Each stimulation position was projected on a vector running through the longitudinal axis of the STN, leading to one scalar value indicating a more dorsolateral or ventromedial contact point position. Using linear mixed models, the stimulation positions were correlated with band-specific absolute spectral power and functional connectivity of i) the motor cortex ipsilateral tot the stimulated side, ii) the whole brain. Results: At group level, more dorsolateral stimulation was associated with lower low-beta absolute band power in the ipsilateral motor cortex (p =.019). More ventromedial stimulation was associated with higher whole-brain absolute delta (p =.001) and theta (p =.005) power, as well as higher whole-brain theta band functional connectivity (p =.040). At the level of the individual patient, switching the active contact point caused significant changes in spectral power, but the results were highly variable. Conclusions: We demonstrate for the first time that stimulation of the dorsolateral (motor) STN in PD patients is associated with lower low-beta power values in the motor cortex. Furthermore, our group-level data show that the location of the active contact point correlates with whole-brain brain activity and connectivity. As results in individual patients were quite variable, it remains unclear if MEG is useful in the selection of the optimal DBS contact point.

Background: Motor and cognitive impairment in Parkinson's disease (PD) is associated with dopaminergic dysfunction that stems from substantia nigra (SN) degeneration and concomitant α-synuclein accumulation. Diffusion magnetic resonance imaging (MRI) can detect microstructural alterations of the SN and its tracts to (sub)cortical regions, but their pathological sensitivity is still poorly understood. Objective: To unravel the pathological substrate(s) underlying microstructural alterations of SN, and its tracts to the dorsal striatum and dorsolateral prefrontal cortex (DLPFC) in PD. Methods: Combining post-mortem in situ MRI and histopathology, T1-weighted and diffusion MRI, and neuropathological samples of nine PD, six PD with dementia (PDD), five dementia with Lewy bodies (DLB), and 10 control donors were collected. From diffusion MRI, mean diffusivity (MD) and fractional anisotropy (FA) were derived from the SN, and tracts between the SN and caudate nucleus, putamen, and DLPFC. Phosphorylated-Ser129-α-synuclein and tyrosine hydroxylase immunohistochemistry was included to quantify nigral Lewy pathology and dopaminergic degeneration, respectively. Results: Compared to controls, PD and PDD/DLB showed increased MD of the SN and SN-DLPFC tract, as well as increased FA of the SN-caudate nucleus tract. Both PD and PDD/DLB showed nigral Lewy pathology and dopaminergic loss compared to controls. Increased MD of the SN and FA of SN-caudate nucleus tract were associated with SN dopaminergic loss. Whereas increased MD of the SN-DLPFC tract was associated with increased SN Lewy neurite load. Conclusions: In PD and PDD/DLB, diffusion MRI captures microstructural alterations of the SN and tracts to the dorsal striatum and DLPFC, which differentially associates with SN dopaminergic degeneration and Lewy neurite pathology.

Background: Computerized cognitive training may be promising to improve cognitive impairment in Parkinson's disease and has even been suggested to delay cognitive decline. However, evidence to date is limited. The aim of this study was to assess the durability of eight-week cognitive training effects at up to two years follow-up. Methods: One hundred and thirty-six (1 3 6) individuals with Parkinson's disease, subjective cognitive complaints but without severe cognitive impairment (Montreal Cognitive Assessment ≥ 22) participated in this double-blind RCT. Participants underwent an eight-week home-based intervention of either adaptive, computerized cognitive training with BrainGymmer (n = 68) or an active control (n = 68). They underwent extensive neuropsychological assessment, psychiatric questionnaires and motor symptom assessment at baseline and one and two years after the intervention. We used mixed-model analyses to assess changes in cognitive function at follow-up and performed Fisher's exact tests to assess conversion of cognitive status. Results: There were no group differences on any neuropsychological assessment outcome at one- and two-year follow-up. Groups were equally likely to show conversion of cognitive status at follow-up. A considerable amount of assessments was missed (1y: n = 27; 2y: n = 33), most notably due to COVID-19 regulations. Conclusions: Eight-week cognitive training did not affect long-term cognitive function in Parkinson's disease. Future studies may focus on one cognitive subgroup to enhance reliability of study results. Intervention improvements are needed to work towards effective, lasting treatment options.

The authors apologize for an error in the published version of the above article. In the visualization of deep brain stimulation contact point positions (Figure 1 and Supplementary Figure E), left and right were swapped. As a result, we wrongly stated that left-sided stimulation positions were correlated with the occurrence of post-operative apathy. Instead, this statement should have been made regarding right-sided stimulation positions. Since we did not elaborate on the lateralization of our results, the error did not affect the main conclusions of the article. Furthermore, the p-value displayed in Figure 1B did not match the p-value in the main text and the figure legend, which we have now corrected. We have now included the corrected versions of Figure 1 and Supplementary Figure E, as well as the corrections we have made to the main text:[Formula presented] Corrigendum Fig. 1 Stimulation locations of contact points in relation to change in apathy severityA) Stimulation locations in MNI-space (viewed from respectively dorsolateral left, posterior and dorsolateral right). The subthalamic nucleus (blue) and red nucleus (red) were added for reference purposes. Increases in apathy severity are color-coded, ranging from no increase (green/yellow) to strong increase (dark red). MNI, Montreal Neurological Institute; L, left; R, right.B) Stimulation locations were projected on a vector through the longitudinal axis of the STN, where negative values indicated more ventromedial stimulation positions. There was a significant correlation between stimulation position and increase in apathy severity for the right side (r(24) = 0.498, p = 0.010), but not for the left side (r(24) = 0.141, p = 0.491). [Formula presented] Corrigendum Supplementary Fig. E Stimulation locations of contact points in relation to improvement in motor score. Stimulation locations in MNI-space (viewed from respectively dorsolateral left, posterior and dorsolateral right). The subthalamic nucleus (blue) and red nucleus (red) were added for reference purposes. Improvements in motor score (% UPDRS-III, contrasting pre- versus post-DBS scores) are color-coded, ranging from no improvement (green/yellow) to strong improvement (dark red). Next, stimulation locations were projected on a vector through the longitudinal axis of the STN, where negative values indicated more ventromedial stimulation positions. There were no significant correlations between stimulation position and improvement in motor performance; left side (r(24) = 0.055, p = 0.788); right side (r(24) = −0.197, p = 0.335). MNI, Montreal Neurological Institute; L, left; R, right; UPDRS-III, Unified Parkinson's disease Rating Scale, motor part. Correction to abstract. The paragraph describing the results was changed into: “Results: …For the right hemisphere, increase in apathy was associated with a more dorsolateral stimulation location (p = 0.010) …” Correction to results. Apathy and DBS localization. This paragraph was changed into: “. There was a significant correlation between a more dorsolateral stimulation position (along a vector) and increase in apathy severity post-DBS for the right side (p = 0.010), but not for the left side (p = 0.491; Fig.1B). In contrast, there was no relationship between stimulation position (along the same vector) and the degree of improvement in total motor score (UPDRS-III; Supplementary Fig E). Next, we performed a hierarchical linear regression model using A backward elimination method to study the relationship between stimulation location and change in apathy score, including the following covariates: pre-to post-operative change in executive functioning, depression score, anxiety score, LEDD total, LEDD of dopamine agonist, and motor function. For the right side this resulted in the following model: R2 = 0.465; change in depression score, b(standardized) = 0.587, p = 0.039; stimulation position, b(standardized) = 0.727, p = 0.015. For the left side no statistically significant model could be fitted. Correction to discussion. The first paragraph of the discussion section was changed into: “.The pre-to-post-DBS increase in apathy severity was associated with a more dorsolateral position of the stimulation for the right hemisphere, …” The fourth paragraph of the discussion section was changed into: “. In addition, we observed a significant correlation between increase in pre-to-post DBS apathy score and a more dorsolateral stimulation location relative to the STN for the right hemisphere, but not for the left hemisphere. As the occurrence of apathy has previously not been related to laterality of DBS [45,46], we refrain from drawing any conclusions from this left-right difference.” The sixth paragraph of the discussion section was changed into: “… In our study increases in apathy severity were not associated with changes in executive functioning, whereas in the multiple regression model there was a relation between improvement in depression scores and better apathy scores after surgery (in the context of right-sided stimulation). It remains to be determined whether the occurrence of apathy after DBS has a cognitive or emotional-affective basis.” The final paragraph of the discussion section was changed into: “In conclusion, we found that increase in apathy severity after STN-DBS might well be an effect of the stimulation itself. Increased apathy severity scores correlated with a more dorsolateral stimulation location (right hemisphere) and with …”