Ralph N. Martins

Vision impairment is common among older adults and affects dementia screening assessments, which include visually presented items. We developed and validated a version of the Montreal Cognitive Assessment (MoCA) for people with vision impairment that includes all the cognitive domains included in the standard MoCA. Visual components of the MoCA were adapted by developing alternative spoken forms. We used both individual item analysis and item substitution to identify the optimal set of alternative items for inclusion in the Montreal Cognitive Assessment for People With Vision Impairment (MoCA-VI) in place of the original items to maximize sensitivity and specificity for dementia. We evaluated the performance and reliability of the final tool, including adjustments for demographic factors. One hundred twenty-eight participants with vision impairment (presenting distance visual acuity worse than 6/12), 79 cognitively healthy and 49 with dementia, completed the adapted MoCA. An additional 86 participants with normal vision completed the standard MoCA and alternative items to assess score equivalence and independence from vision impairment. Twenty-six participants were retested 2-4 weeks after initial testing. With the optimal item set, the final MoCA-VI had an area under the curve of 0.96 (95% CI [0.93, 0.99]). At a cut point of 24 points or less, sensitivity was 95.9%, with a specificity of 92.4%. The intraclass correlation for test-retest reliability was 0.84 (95% CI [0.81, 0.96]). The MoCA-VI is a specific and reliable test for possible dementia among adults with vision impairment. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

BackgroundGlobally, coffee and tea are consumed extensively, potentially providing neuroprotection through anti-inflammatory and antioxidative stress effects.ObjectiveThis study aimed to investigate associations between coffee and tea intake and cognitive function.MethodsIn a longitudinal prospective cohort study, dementia-free (n = 8715; age range 60.0-85.2 years) older adults from the UK Biobank self-reported coffee and tea intake over the previous year; 'never', 'moderate' (1-3 cups/day), or 'high' (≥4 cups/day). Participants completed cognitive assessments at ≥2 timepoints (mean of 9.11 years).ResultsThose 'never' consuming coffee and 'moderate' coffee consumers (β = 0.06, p = 0.005; β = 0.07, p < 0.001, respectively), as well as 'moderate' tea consumers and 'high' tea consumers (β = 0.06, p = 0.009; β = 0.06, p = 0.003, respectively) had slower fluid intelligence decline. Additionally, those 'never' consuming coffee and 'moderate' coffee consumers had a slower increase in pairs matching errors (β = -0.05, p = 0.022; β = 0.05, p = 0.013) compared to 'high' consumers.Conclusions'Moderate' coffee, and 'moderate' and 'high' tea intake may be a protective factor against cognitive decline. Randomized controlled trials are required to establish causal relationships leading to evidence-based recommendations regarding benefits of coffee and tea intake.

BackgroundEvidence suggests that plant-based diets (PBDs) may be protective against neurodegenerative diseases such as Alzheimer's disease (AD).ObjectiveThis study examined associations between blood-based AD biomarkers in individuals 30-75 years without current or diagnosed cardiovascular disease following different PBDs versus regular meat-eating diets (RMEs).MethodsThis secondary analysis of the Plant-based Diets study measured Aβ1-42/Aβ1-40, p-tau181, NFL, and GFAP in 237 plasma samples using SIMOA from individuals following vegan, pesco-vegetarian (PVs), lacto-ovo vegetarian (LOVs), semi-vegetarian (SVs), or RME diets. Multivariable regression adjusted for age and sex.ResultsFollowing adjustments for age and sex, plasma Aβ1-42/Aβ1-40 ratio was significantly higher in PVs 0.011 (CI: 0.006, 0.016, p < 0.01), LOVs 0.011 (CI: 0.007, 0.016, p < 0.01) and SVs 0.015 (0.009-0.020, p < 0.01) groups compared to RMEs. Plasma p-tau181 was significantly higher in PVs 3.4 (CI: 0.4-6.4, p < 0.05) and LOVs 7.1 (CI: 2.5, 11.8, p < 0.01), NFL higher in PVs 5.2 (CI: 1.6, 8.7, p < 0.01) and LOVs 4.0 (CI: 1.6, 6.5, p = 0.01), and GFAP higher in PVs 26 (CI: 6, 47, p < 0.05) and LOVs 21 (5, 367, p = 0.01), all compared to RMEs.ConclusionsThis analysis suggests that PBDs may be associated with blood-based AD biomarkers. Higher Aβ1-42/Aβ1-40 levels in PV, LOV and SV dietary patterns compared to RMEs could indicate lesser amyloid burden, but elevated levels of other AD biomarkers in some PBDs warrant further investigation into nutrient-specific roles in AD pathology.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β plaque accumulation, tau tangles, and extensive neuroinflammation. Neuroinflammation, driven by glial cells like microglia and astrocytes, plays a critical role in AD progression. Initially, these cells provide protective functions, such as debris clearance and neurotrophic support. However, as AD progresses, chronic activation of these cells exacerbates inflammation, contributing to synaptic dysfunction, neuronal loss, and cognitive decline. Microglia release pro-inflammatory cytokines and reactive oxygen species (ROS), while astrocytes undergo reactive astrogliosis, further impairing neuronal health. This maladaptive response from glial cells significantly accelerates disease pathology. Current AD treatments primarily aim at symptomatic relief, with limited success in disease modification. While amyloid-targeting therapies like Aducanumab and Lecanemab show some promise, their efficacy remains limited. In this context, natural compounds have gained attention for their potential to modulate neuroinflammation and promote neuroprotection. Among these, butyrate and lauric acid are particularly notable. Butyrate, produced by a healthy gut microbiome, acts as a histone deacetylase (HDAC) inhibitor, reducing pro-inflammatory cytokines and supporting neuronal health. Lauric acid, on the other hand, enhances mitochondrial function, reduces oxidative stress, and modulates inflammatory pathways, thereby supporting glial and neuronal health. Both compounds have been shown to decrease amyloid-β deposition, reduce neuroinflammation, and promote neuroprotection in AD models. This review explores the mechanisms through which butyrate and lauric acid modulate glial and neuronal activity, highlighting their potential as therapeutic agents for mitigating neuroinflammation and slowing AD progression.

Alzheimer's disease (AD) is a neurodegenerative disease characterised by neuropathological hallmarks, including extracellular amyloid plaques and neurofibrillary tangles. The disease is clinically defined by cognitive dysfunction, including learning, memory deficits, and behavioural changes. With the rising global prevalence of AD, early diagnosis is critical for implementing effective interventions before irreversible neuronal damage occurs. Biomarkers correlating amyloid deposition, tau pathology, neuroinflammation, and neurodegeneration are currently being investigated using cerebrospinal fluid analysis and positron emission tomography imaging. These methods are invasive or costly, limiting their widespread clinical utility. Blood-based biomarkers offer a promising alternative due to accessibility, cost-effectiveness, and feasibility for large-scale screening. Among blood-based biomarkers, plasma glial fibrillary acidic protein (GFAP) levels have gained interest in identifying individuals at risk of AD at preclinical stages. However, significant challenges remain, including methodological inconsistencies, analytical variability, and the need for standardisation across immunoassay platforms to ensure the clinical applicability of plasma GFAP measurement in AD diagnosis. Additionally, the specificity of GFAP for AD needs further evaluation, as increased plasma levels are also observed in other diseases. Similar issues are found with p-tau 217, the blood biomarker candidate for AD that has received the most attention. This review summarises the role of GFAP in the neuropathology of AD, provides evidence on plasma GFAP as an early blood biomarker for AD and identifies key knowledge gaps that need to be addressed. Future advancements in assay development and large-scale longitudinal studies are essential to validate its diagnostic and prognostic potential for community-based AD screening.