The Impact of Socioeconomic Status on Visual Acuity Changes in Schoolchildren: A One-Year Follow-Up.

(1) Background: Visual acuity (VA) is essential for children's quality of life, and its relationship with socioeconomic status (SES) highlights disparities in healthcare. This study investigated the influence of SES on changes in schoolchildren's VA over one year. (2) Methods: Initial examinations were conducted on 1822 children (8-10 years).

Precision and agreement of axial length in paediatric population measured with MYAH and AL-Scan biometers.

Clinical Relevance: Measuring axial length is key in the field of myopia development and control. Hence, the precision and agreement of commercially available biometers is of vital interest to understand their variability and interchangeability in the paediatric population.

Background: Different biometers are available to measure axial length and monitor myopia progression in clinical practice.

Children's visual impairment and visual care related to socioeconomic status in Catalonia (Spain).

Background: The objective of this study is to assess the prevalence of visual impairment and visual care practices and its association with socioeconomic conditions in the infant population in Catalonia.

Methods: The Catalan Institute of Statistics provided a random sample of 0 to 14-year-old non-institutionalized children whose parents were interviewed in a continuous health survey from 2011 to 2015 in Catalonia. A multistage stratified and random sampling procedure considering age, sex, county and town was followed.

Why are there gender inequalities in visual impairment?

Background: In high-income countries, the prevalence of blindness and visual impairment is higher among women, regardless of age although the mechanisms that produce these gender inequalities are not well understood. The objectives of this study were to analyse gender inequalities in the prevalence of blindness and visual impairment, age of onset, diagnosed and undiagnosed status and related eye diseases among visually impaired individuals.

Methods: Data were obtained from the 2008 Spanish Survey on 'Disability, Personal Autonomy and Dependency Situations' (n = 213 626) participants 360 blind (160 men and 200 women), and 5560 with some visual impairment (2025 men and 3535 women).

Prevalence of visual impairment in El Salvador: inequalities in educational level and occupational status.

Objective: To examine the prevalence of blindness, visual impairment, and related eye diseases and conditions among adults in El Salvador, and to explore socioeconomic inequalities in their prevalence by education level and occupational status, stratified by sex.

Methods: Based upon the Rapid Assessment of Avoidable Blindness (RAAB) methodology, this nationwide sample comprised 3 800 participants (3 399 examined) ≥ 50 years old from 76 randomly selected clusters of 50 persons each. The prevalence of blindness, visual impairment and related eye diseases and conditions, including uncorrected refractive error (URE), was calculated for categories of education level and occupational status.

Visual correction and occupational social class.

Purpose: To determine whether types of optical correction for refractive error are associated with sex, social class, and occupational group in the working population.

Methods: A cross-sectional study was carried out among employees in Catalonia (Spain) aged 16 to 65 years who underwent the Asepeyo Prevention Society health examination in 2009 (86,831 participants: 59,397 men and 27,421 women). The type and purpose of refractive correction used were self-reported, as were sociodemographic variables; visual acuity with habitual correction was also measured.

Visual impairment and blindness in spanish adults: geographic inequalities are not explained by age or education.

Objectives: The objectives of this study were to examine for the first time the prevalence of visual impairment and blindness among adults in Spain, to explore regional differences, and to assess whether they may vary as a function of sex or be explained by age and individual or regional socioeconomic position.

Design: Data were obtained from the 2008 Spanish Survey on Disability, Personal Autonomy, and Dependency Situations, a cross-sectional survey based on a representative sample of the noninstitutionalized population of Spain.

Participants: The sample was composed of 213 626 participants aged ≥15 years (103 093 men and 110 533 women); 360 were blind (160 men and 200 women), 4048 had near visual impairment (1397 men and 2651 women), and 4034 had distance visual impairment (1445 men and 2589 women).

[Prevalence and burden of visual impairment in Catalonia, Spain].

The aim of this work is to determine the prevalence of visual impairment in Catalonia and analyze inequalities in vision. Cross sectional study in the population having ≥ 15 years of age (7,881 men and 8,045 women) based on data from the Encuesta de Salud de Cataluña 2006. Logistic regression models were used to calculate the adjusted odds ratio by age, civil state, level of studies, income and working situation with a confidence interval (CI) of 95%.

Mutational screening of the mortalin gene (HSPA9) in Parkinson's disease.

Mortalin is a mitochondrial chaperone of the heat shock protein 70 family. Mortalin plays a central role in mitochondrial biogenesis through its capacity to direct the import of nuclear-encoded proteins into the mitochondria. As mitochondrial dysfunction has been involved in Parkinson's disease (PD), changes in mortalin function and expression could manifest as a higher risk of developing PD.

Lrrk2 R1441G-related Parkinson's disease: evidence of a common founding event in the seventh century in Northern Spain.

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene together represent the most common genetic determinant of Parkinson's disease (PD) identified to date. The vast majority of patients with LRRK2-related PD reported in the literature carry one of three pathogenic substitutions: G2019S, R1441C, or R1441G. While G2019S and R1441C are geographically widespread, R1441G is most prevalent in the Basque Country and is rare outside of Northern Spain.

Mutational screening of the mitochondrial transcription factors B1 and B2 (TFB1M and TFB2M) in Parkinson's disease.

Mitochondrial dysfunction has been implicated in Parkinson's disease (PD). The nuclear encoded transcription factors A, B1 and B2 are essential for mitochondrial DNA replication. Sequence variants at the genes encoding TFAM, TFB1M and TFB2M could contribute to the risk of developing PD.

Mitochondrial transcription factor A (TFAM) gene variation in Parkinson's disease.

Mitochondrial function is necessary to supply the energy required for cell metabolism. Mutations/polymorphisms in mitochondrial DNA (mtDNA) have been implicated in Parkinson's disease (PD). The mitochondrial transcription factor A (TFAM) controls the transcription of mtDNA and regulates the mtDNA-copy number, thus being important for maintaining ATP production.

No association between Parkinson's disease and three polymorphisms in the eNOS, nNOS, and iNOS genes.

Nitric oxide synthases (NOS) and mitochondrial DNA-polymorphisms have been associated with the risk of developing Parkinson's disease (PD). In this report, we genotyped 450 PD-patients and 200 controls for three polymorphisms in the endothelial, inducible and neuronal NOS-genes, and for the T4336C and A10398G mitochondrial DNA-polymorphisms. None of the eNOS (intron 4 VNTR), iNOS (exon 22 A/G), or nNOS (exon 29T/C) were significantly associated with PD.

LRRK2 mutations are a common cause of Parkinson's disease in Spain.

Pathogenic mutations in the leucine-rich repeat kinase 2 gene (LRRK2; PARK8) have been implicated in autosomal dominant, late-onset parkinsonism. The LRRK2 6055G > A (G2019S) mutation is the most common reported to date, and has been observed in a number of different European populations. So far, only the LRRK2 4321C > G (R1441G) mutation has been identified in the Spanish population.

Mitochondrial DNA polymorphisms and risk of Parkinson's disease in Spanish population.

Mutations in mitochondrial DNA (mtDNA) have been implicated in the development of Parkinson's disease (PD). Mitochondrial function is necessary to supply the energy required for cell metabolism, and mutations in mitochondrial genes should have a deleterious effect in neuronal function. An association between several common mtDNA-polymorphisms and the risk of PD has been described.

LRRK2 R1441G in Spanish patients with Parkinson's disease.

Pathogenic mutations in leucine-rich repeat kinase 2 (LRRK2; PARK8) have been implicated in autosomal dominant, late-onset Parkinson's disease (PD). The LRRK2 4321C>G (R1441G) mutation was originally identified in Spanish families originating from the Basque region. Within this ethnicity, Lrrk2 R1441G substitutions have been suggested as a frequent cause of disease.

Homozygous partial genomic triplication of the parkin gene in early-onset parkinsonism.

Autosomal recessive mutations in the parkin gene are the predominant cause of familial, early-onset parkinsonism; missense mutations involving one or a few nucleotides, exonic deletions and duplications have been described. Here we report a family with two affected brothers. Direct sequencing of parkin did not detect mutations, but semi-quantitative analysis identified a novel exonic rearrangement of exons 2-4.

Chemokines (RANTES and MCP-1) and chemokine-receptors (CCR2 and CCR5) gene polymorphisms in Alzheimer's and Parkinson's disease.

Parkinson's disease (PD) is a complex disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. Late-onset Alzheimer's disease (LOAD) is the most common cause of dementia in the elderly, affecting about 5% of the population older than 65 years. Several works have demonstrated the involvement of inflammation in the pathogenesis of both, PD and LOAD.

Single-nucleotide polymorphisms in the promoter region of the PARKIN gene and Parkinson's disease.

Mutations in the PARKIN gene have been identified in families with recessively inherited Parkinson disease (PD). Common DNA-polymorphisms at the PARKIN gene could contribute to the risk for PD in the general population. Here we searched for DNA-polymorphisms in the PARKIN promoter.

Association between the TNFalpha-308 A/G polymorphism and the onset-age of Alzheimer disease.

Local inflammatory processes associated with amyloid plaques would contribute to the progression of late-onset Alzheimer disease (LOAD). Tumor necrosis factors alpha (TNF(alpha)) and beta (LT(alpha)) are inflammatory cytokines involved in the local immune response occurring in the central nervous system of LOAD patients. Genetic variation at these genes could contribute to the risk of developing AD or influence the age at the onset of the disease.

Early-onset Parkinson's disease associated with a new parkin mutation in a Spanish family.

Mutations in the PARKIN gene are associated with early-onset (juvenile) Parkinson's disease. We analyzed the coding sequence of this gene (exons 1-12) in patients from a family with three affected siblings, born to first-degree consanguineous parents, with an onset before 23 years and foot dystonia as the initial clinical symptom. The three patients were alive without cognitive impairment at ages of 70, 69, and 65 years, showing a marked response to levodopa treatment.

Angiotensin converting enzyme and endothelial nitric oxide synthase DNA polymorphisms and late onset Alzheimer's disease.

Objectives: Several lines of evidence suggest that the endothelial constitutive nitric oxide synthase (ecNOS) and angiotensin converting enzyme (ACE) may have a role in Alzheimer's disease. ACE is widely expressed in the brain, and a DNA polymorphism at the ACE gene has been linked to the risk for late onset Alzheimer's disease. Nitric oxide (NO) production by microglial cells, astrocytes, and brain microvessels is enhanced in patients with Alzheimer's disease.

Association between an alpha(2) macroglobulin DNA polymorphism and late-onset Alzheimer's disease.

An association between a five-base-pair deletion/insertion DNA polymorphism at the alpha(2) macroglobulin gene (A2M) and late-onset Alzheimer's disease (LOAD) has been recently described. We developed a PCR assay to analyze this polymorphism in 190 LOAD patients (older than 65 years) and 400 controls from Spain. Controls were stratified into three groups: <65 years (n = 200), 65 to 80 years (n = 100), and 81 years or older (n = 100).