The aim of this study was to determine the diagnostic value and agreement analyses between Clinical Dementia Rating (CDR) and dementia diagnostic criteria (gold standard), Blessed Dementia Rating scale (BDRS), and Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised (DSM III-R) criteria for severity. In a sample of 343 Southern Brazilian participants, CDR was consecutively assessed in 295 dementia patients (Alzheimer disease, vascular dementia, and questionable) and 48 healthy elderly. The National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for probable Alzheimer disease and the National Institute of Neurological Disorders and Stroke and Association Internationale pour la Recherché et l'Enseignement en Neurosciences (NINDS-AIREN) for probable vascular dementia were the gold standard. A battery of cognitive tests and the Mini Mental State Examination (as a screening test at study entry) were also applied. Sensitivity and specificity were obtained through contingency tables. Validity and reliability were measured through κ coefficient, Kendall b, and percent agreement. CDR agreement among raters was demonstrated by percent agreement. Agreement to gold standard was good (κ=0.75), as well as to the Blessed scale (κ=0.73), and excellent to the DSM III-R (κ=0.78). CDR detection of dementia among healthy elderly or questionable dementia was 86% and 80% sensitive, respectively, and 100% specific for both settings. In conclusion, agreement of CDR global score with the gold standard was good, and diagnostic values were high.

Parkinson's disease (PD) is characterized by progressive motor impairment attributed to progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta. In addition to an accumulation of iron, there is also an increased production of reactive oxygen/nitrogen species (ROS/RNS) and inflammatory markers. These observations suggest that iron dyshomeostasis may be playing a key role in neurodegeneration. However, the mechanisms underlying this metal-associated oxidative stress and neuronal damage have not been fully elucidated. To determine peripheral levels of iron, ferritin, and transferrin in PD patients and its possible relation with oxidative/nitrosative parameters, whilst attempting to identify a profile of peripheral biomarkers in this neurological condition. Forty PD patients and 46 controls were recruited to compare serum levels of iron, ferritin, transferrin, oxidative stress markers (superoxide dismutase (SOD), catalase (CAT), nitrosative stress marker (NOx), thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP) and vitamin C) as well as inflammatory markers (NTPDases, ecto-5’-nucleotidase, adenosine deaminase (ADA), ischemic-modified albumin (IMA) and myeloperoxidase). Iron levels were lower in PD patients, whereas there was no difference in ferritin and transferrin. Oxidative stress (TBARS and AOPP) and inflammatory markers (NTPDases, IMA, and myeloperoxidase) were significantly higher in PD, while antioxidants FRAP, vitamin C, and non-protein thiols were significantly lower in PD. The enzymes SOD, CAT, and ecto-5’-nucleotidase were not different among the groups, although NOx and ADA levels were significantly higher in the controls. Our data corroborate the idea that ROS/RNS production and neuroinflammation may dysregulate iron homeostasis and collaborate to reduce the periphery levels of this ion, contributing to alterations observed in the pathophysiology of PD.

Background: Human genetics research lacks diversity; over 80% of genome‐wide association studies have been conducted on individuals of European ancestry. In addition to limiting insights regarding disease mechanisms, disproportionate representation can create disparities preventing equitable implementation of personalized medicine.Objective: This systematic review provides an overview of research involving Parkinson's disease (PD) genetics in underrepresented populations (URP) and sets a baseline to measure the future impact of current efforts in those populations.Methods: We searched PubMed and EMBASE until October 2021 using search strings for “PD,” “genetics,” the main “URP,” and and the countries in Latin America, Caribbean, Africa, Asia, and Oceania (excluding Australia and New Zealand). Inclusion criteria were original studies, written in English, reporting genetic results on PD from non‐European populations. Two levels of independent reviewers identified and extracted information.Results: We observed imbalances in PD genetic studies among URPs. Asian participants from Greater China were described in the majority of the articles published (57%), but other populations were less well studied; for example, Blacks were represented in just 4.0% of the publications. Also, although idiopathic PD was more studied than monogenic forms of the disease, most studies analyzed a limited number of genetic variants. We identified just nine studies using a genome‐wide approach published up to 2021, including URPs.Conclusion: This review provides insight into the significant lack of population diversity in PD research highlighting the immediate need for better representation. The Global Parkinson's Genetics Program (GP2) and similar initiatives aim to impact research in URPs, and the early metrics presented here can be used to measure progress in the field of PD genetics in the future. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Several lines of evidence suggest that neuroimmune mechanisms may be involved in the neurodegenerative process of Parkinson’s disease (PD). Interleukin-6 (IL-6) is increased in the nigrostriatal region and in the cerebrospinal fluid of patients with PD. IL-6 serum level was evaluated in PD patients. The effects of levodopa treatment and disease severity on IL-6 were also studied. The IL-6 levels were similar between PD patients (treated and not treated) and controls. However, there was a negative correlation of IL-6 levels and the activities of daily living scale (P < 0.05), indicating that patients with more severe disease have higher levels of this cytokine. No correlation involving levodopa treatment and IL-6 serum level was found. The results suggest that only marginal effects of IL-6 occur on the peripheral immune system, and that the role of IL-6 and others neuroimmune factors needs to be well elucidated on PD.

OBJETIVO: Avaliar a concordância da escala CDR com critérios diagnósticos e mini exame do estado mental (MEEM), e correlação com escala de Blessed, numa amostra de pacientes do sul do Brasil. MÉTODO: A escala foi avaliada em 269 pacientes com doença de Alzheimer (DA), demência vascular e demência questionável num desenho transversal. Os critérios do NINCDS-ADRDA para provável DA e NINDS-AIREN para provável demência vascular foram os padrões-ouro. O MEEM, a escala Blessed para gravidade da demência, o escore isquêmico de Hachinski, e uma bateria de testes cognitivos também foram aplicados. RESULTADOS: A concordância com o padrão-ouro foi boa (kappa=0,73), e com o MEEM em categorias foi moderada (kappa= 0,53). Observou-se correlação significativa da escala CDR com Blessed (r=0,96; p=0,001). Não se observou diferença de escolaridade ou de idade entre as categorias da escala CDR. CONCLUSÃO: A concordância da CDR foi boa para os critérios diagnósticos e moderada para o MEEM. A escala mostrou validade de construto para gravidade de demência. Não se observou impacto da escolaridade sobre este instrumento.

The age‐standardized prevalence of Parkinson's disease (PD) has increased substantially over the years and is expected to increase further. This emphasizes the need to identify modifiable risk factors of PD, which could form a logical entry point for the prevention of PD. The World Health Organization (WHO) has recommended reducing exposure to specific environmental factors that have been reported to be associated with PD, in particular pesticides, trichloroethylene (TCE), and air pollution. In this review we critically evaluate the epidemiological and biological evidence on the associations of these factors with PD and review evidence on whether these putative associations are causal. We conclude that when considered in isolation, it is difficult to determine whether these associations are causal, in large part because of the decades‐long lag between relevant exposures and the incidence of manifest PD. However, when considered in tandem with evidence from complementary research lines (such as animal models), it is increasingly likely that these associations reflect harmful causal effects. Fundamentally, whilst we highlight some evidence gaps that require further attention, we believe the current evidence base is sufficiently strong enough to support our call for stronger policy action. © 2024 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.