Parkinson’s disease (PD) is an irreversible neurodegenerative disorder clinically manifesting in uncontrolled motor symptoms. There are two primary hallmark features of Parkinson’s disease—an irreversible loss of dopaminergic neurons of the substantia nigra pars compacta and formation of intracellular insoluble aggregates called Lewy bodies mostly composed of alpha-synuclein. Using a clinical improvements-first approach, we identified several clinical trials involving consumption of a specific diet or nutritional supplementation that improved motor and nonmotor functions. Here, we aimed to investigate if and how pyrroloquinoline quinone (PQQ) compound disrupts preformed alpha-synuclein deposits using SH-SY5Y cells, widely used Parkinson’s disease cellular model. SH-SY5Y neuroblastoma cells, incubated in presence of potassium chloride (KCl) to induce alpha-synuclein protein aggregation, were treated with PQQ for up to 48 hr. Resulting aggregates were examined and quantified using confocal microscopy. Overall, nutritional compound PQQ reduced the average number and overall size of intracellular cytoplasmic alpha-synuclein aggregates in a PD cellular model.

Background: Capgras syndrome is characterized by the recurrent, transient belief that a person has been replaced by an identical imposter. We reviewed clinical characteristics of Dementia with Lewy Bodies (DLB) patients with Capgras syndrome compared to those without Capgras.

Methods: We identified 55 consecutive DLB patients (11 cases with Capgras syndrome (DLB-C) and 44 cases without evidence of Capgras (DLB). Semi-structured interviews with the patient and an informant, neurological exams, and neuropsychological testing were performed. Caregivers were assessed for caregiver burden and depression. Primary comparisons were made between DLB-C and DLB. Exploratory analyses using stepwise logistic regression and bootstrap analyses were performed to determine clinical features associated with Capgras.

Results: DLB-C patients experienced more visual hallucinations and self-reported anxiety, had higher scores on the Neuropsychiatric Inventory, and were less likely to be treated with cholinesterase inhibitors at time of initial evaluation. Extrapyramidal symptoms and depression were not associated with Capgras. Caregivers of DLB-C patients had higher caregiver burden. DLB-C was associated with self-reported anxiety (OR = 10.9; 95% CI = 2.6–47.6). In a bootstrap analysis, clinical findings that were predictors of Capgras included visual hallucinations (log(OR) = 18.3; 95% CI = 17.9–19.3) and anxiety (log(OR) = 2.9; 95% CI = 0.31–20.2).

Conclusions: Our study suggests that Capgras syndrome is common in DLB and usually occurs in the presence of anxiety and visual hallucinations, suggesting related etiopathogenesis. Early appreciation of Capgras syndrome may afford the opportunity to alleviate caregiver burden and improve patient and caregiver outcomes.

Background: Mild cognitive impairment (MCI) may be accompanied by extra pyramidal signs (EPS), which are related to the severity and type of cognitive impairment. We aimed to elucidate further the relationship between MCI and EPS, analyzing the correlation between the severity of EPS and cognitive functions, and the presence of EPS and neuro-psychiatric features.

Methods: Data were obtained from a longitudinal study of 150 MCI outpatients. Participants underwent a clinical assessment including the Unified Parkinson Disease Rating Scale, the Neuropsychiatric Inventory, the Tinetti Scale, and a standardized neuropsychological battery. Mild EPS could be defined as being present (MCI with mild EPS) using a subscale of UPDRS, based on three specific symptoms: bradykinesia, rigidity and tremor.

Results: The two groups, one with mild EPS (24%) and one without EPS (76%), differed in gait abnormalities and presence of extrapyramidal symptoms. Groups did not differ in terms of general cognitive functions evaluated using the Mini-mental State Examination, while subjects with MCI with mild EPS performed significantly worse than those with MCI without EPS in total global score and in non-memory items of the Alzheimer's Disease Assessment Scale. Moreover, severity of EPS was significantly correlated with low performance on executive functions and with high performance on episodic memory. The group with MCI with mild EPS were observed to have a greater prevalence of patients with anxiety, depression, apathy and sleep disturbances than in MCI without EPS.

Conclusion: MCI may be associated with mild parkinsonian signs, the severity of which are related to the severity of cognitive impairment, in particular of non-memory functions, and to a differential pattern of psycho-behavioral symptoms.

There is always hope—even now that immunization with beta-amyloid has not busted international psychogeriatrics; now that a term once so popular in European neuropsychiatry—“Parkinson plus”—has been de-constructed with the tools of a smart modern neurology (and that dementia with Lewy bodies has been reinvented); now that molecular biology has left some temporary responsibility for clinicians dealing with demented patients themselves, would it not be thrilling to attempt a fundamental reconsideration of some basic concepts of great—albeit temporary—practical relevance?