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With the aging of the global population, neurodegenerative diseases are emerging as a major public health issue. The adoption of a less sedentary lifestyle has been shown to have a beneficial effect on cognitive decline, but the molecular mechanisms responsible are less clear. Here we provide a detailed analysis of the complex molecular, cellular, and systemic mechanisms underlying age-related cognitive decline and how lifestyle choices influence these processes. A review of the evidence from animal models, human studies, and postmortem analyses emphasizes the importance of integrating physical exercise with cognitive, multisensory, and motor stimulation as part of a multifaceted approach to mitigating cognitive decline. We highlight the potential of these non-pharmacological interventions to address key aging hallmarks, such as genomic instability, telomere attrition, and neuroinflammation, and underscore the need for comprehensive and personalized strategies to promote cognitive resilience and healthy aging.

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Aging is a multifaceted biological process characterized by progressive molecular and cellular damage accumulation. The brain hippocampus undergoes functional deterioration with age, caused by cellular deficits, decreased synaptic communication, and neuronal death, ultimately leading to memory impairment. One of the factors contributing to this dysfunction is the loss of mitochondrial function. In neurons, mitochondria are categorized into synaptic and non-synaptic pools based on their location. Synaptic mitochondria, situated at the synapses, play a crucial role in maintaining neuronal function and synaptic plasticity, whereas non-synaptic mitochondria are distributed throughout other neuronal compartments, supporting overall cellular metabolism and energy supply. The proper function of synaptic mitochondria is essential for synaptic transmission as they provide the energy required and regulate calcium homeostasis at the communication sites between neurons. Maintaining the structure and functionality of synaptic mitochondria involves intricate processes, including mitochondrial dynamics such as fission, fusion, transport, and quality control mechanisms. These processes ensure that mitochondria remain functional, replace damaged organelles, and sustain cellular homeostasis at synapses. Notably, deficiencies in these mechanisms have been increasingly associated with aging and the onset of age-related neurodegenerative diseases. Synaptic mitochondria from the hippocampus are particularly vulnerable to age-related changes, including alterations in morphology and a decline in functionality, which significantly contribute to decreased synaptic activity during aging. This review comprehensively explores the critical roles that mitochondrial dynamics and quality control mechanisms play in preserving synaptic activity and neuronal function. It emphasizes the emerging evidence linking the deterioration of synaptic mitochondria to the aging process and the development of neurodegenerative diseases, highlighting the importance of these organelles from hippocampal neurons as potential therapeutic targets for mitigating cognitive decline and synaptic degeneration associated with aging. The novelty of this review lies in its focus on the unique vulnerability of hippocampal synaptic mitochondria to aging, underscoring their importance in maintaining brain function across the lifespan.

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OBJECTIVES: Mild cognitive impairment (MCI) is a unique indicator of underlying distress that may be strongly associated with suicide risk. Despite this, to date, no study has examined the association between MCI and suicidal ideation. Therefore, the present study aimed to examine the association between MCI and suicidal ideation among adults aged ≥65 years from 6 low- and middle-income countries (LMICs; China, Ghana, India, Mexico, Russia, and South Africa). METHODS: Cross-sectional, nationally representative data from the World Health Organization's Study on Global Ageing and Adult Health were analyzed. MCI was defined using the National Institute on Aging-Alzheimer's Association criteria. Self-reported information on past 12-month suicidal ideation was collected. Multivariable logistic regression and meta-analysis were conducted to assess associations. RESULTS: Data on 13,623 individuals aged ≥65 years were analyzed. The prevalence of suicidal ideation ranged from 0.5% in China to 6.0% in India, whereas the range of the prevalence of MCI was 9.7% (Ghana) to 26.4% (China). After adjustment for potential confounders, MCI was significantly associated with 1.66 (95% confidence interval [95% CI] = 1.12-2.46) times higher odds for suicidal ideation. DISCUSSION: Mild cognitive impairment was significantly associated with higher odds for suicidal ideation among older adults in LMICs. Future longitudinal studies from LMICs are necessary to assess whether MCI is a risk factor for suicidal ideation.

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BACKGROUND: Subjective cognitive decline (SCD), considered a preclinical dementia stage, is less understood in Hispanics, a high-risk group for dementia. We investigated SCD to mild cognitive impairment (MCI) progression risk, as well as baseline and longitudinal features of depressive symptoms, SCD complaints, and objective cognitive performance among Hispanics compared to non-Hispanic Whites (NHW). METHODS: Hispanic (n = 23) and NHW (n = 165) SCD participants were evaluated at baseline and 2-year follow-up. Evaluations assessed function, depressive symptoms, SCD, and objective cognitive performance. RESULTS: Hispanics were at increased risk of progression to MCI (OR: 6.10, 95% CI 1.09-34.20, P = .040). Hispanic participants endorsed more depressive symptoms at baseline (P = .048) that worsened more longitudinally (OR: 3.16, 95% CI 1.18-8.51, P = .023). Hispanic participants had increased SCD complaints on the Brief Cognitive Rating Scale (BCRS) (ß = .40 SE: .17, P = .023), and in specific BCRS domains: concentration (ß = .13, SE: .07, P = .047), past memory (ß = .13, SE: .06, P = .039) and functional abilities (ß = .10, SE: .05, P = .037). In objective cognitive performance, Hispanic ethnicity associated with decline in MMSE (ß = -.27, SE: .13, P = .039), MoCA (ß = -.80 SE: .34, P = .032), Trails A (ß = 2.75, SE: .89, P = .002), Trails B (ß = 9.18, SE: 2.71, P = .001) and Guild Paragraph Recall Delayed (ß = -.80 SE: .28, P = .005). Conclusions: Hispanic ethnicity associated with a significantly increased risk of 2-year progression of SCD to MCI compared to NHW. This increased risk associated with increased depressive symptoms, distinctive SCD features, and elevated amnestic and non-amnestic objective cognitive decline. This supports further research to refine the assessment of preclinical dementia in this high-risk group.

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Alzheimer's disease (AD) is a complex neurodegenerative process, also considered a metabolic condition due to alterations in glucose metabolism and insulin signaling pathways in the brain, which share similarities with diabetes. This study aimed to investigate the therapeutic effects of benfotiamine (BFT), a vitamin B1 analog, in the early stages of the neurodegenerative process in a sporadic model of Alzheimer's-like disease induced by intracerebroventricular injection of streptozotocin (STZ). Supplementation with 150 mg/kg of BFT for 7 days reversed the cognitive impairment in short- and long-term memories caused by STZ in rodents. We attribute these effects to BFT's ability to modulate glucose transporters type 1 and 3 (GLUT1 and GLUT3) in the hippocampus, inhibit GSK3 activity in the hippocampus, and modulate the insulin signaling in the hippocampus and entorhinal cortex, as well as reduce the activation of apoptotic pathways (BAX) in the hippocampus. Therefore, BFT emerges as a promising and accessible intervention in the initial treatment of conditions similar to AD.

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BACKGROUND: Alzheimer's disease (AD) is the most common cause of dementia worldwide. Omega-3 fatty acids (n-3-PUFA) are essential to normal neural development and function. Souvenaid®, a medical supplement that contains n-3-PUFA's: eicosatetraenoic acid (EPA) and docosahexaenoic acid (DHA), has emerged as an alternative, slowing cognitive decline in AD patients. In this study, we investigated the effect of dietary supplementation with n-3-PUFA, EPA, DHA, and Souvenaid® in AD patients. AIM: This systematic review and meta-analysis aim to establish the relationship between n-3-PUFA, EPA, DHA, and Souvenaid® with cognitive effects, ventricular volume and adverse events in AD patients. METHODS: A systematic search of randomized control trials (RCT), cohorts, and case-control studies was done in PubMed, Scopus, Web of Science, Cochrane, and Embase for AD adult patients with dietary supplementation with n-3-PUFA, EPA, DHA, or Souvenaid® between 2003 and 2024. RESULTS: We identified 14 studies with 2766 subjects aligned with our criteria. Most publications described positive cognitive outcomes from supplements (58%). The most common adverse events reported were gastrointestinal symptoms. CDR scale showed reduced progression of cognitive decline (SMD = -0.4127, 95% CI: [-0.5926; -0.2327]), without subgroup differences between different dietary supplement interventions. ADCS-ADL, MMSE, ADAS-cog, adverse events, and ventricular volume did not demonstrate significant differences. However, Souvenaid® showed a significant negative effect (SMD = -0.3593, 95% CI: -0.5834 to -0.1352) in ventricular volumes. CONCLUSIONS: The CDR scale showed reduced progression of cognitive decline among patients with n-3-PUFA supplemental interventions, with no differences between different n-3-PUFA supplements.

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Cognitive decline, particularly in dementia, presents complex challenges in early detection and diagnosis. While Item Response Theory (IRT) has been instrumental in identifying patterns of cognitive impairment through psychometric tests, its parametric models often require large sample sizes and strict assumptions. This creates a need for more adaptable, less demanding analytical methods. This study aimed to evaluate the effectiveness of Mokken scale analysis (MSA), a nonparametric IRT model, in identifying hierarchical patterns of cognitive impairment from psychometric tests. Using data from 1164 adults over 60 years old, we applied MSA to the orientation subscale of ACE-III. Our analysis involved calculating scalability, monotone homogeneity, invariant item ordering (IIO) and response functions. The MSA effectively retrieved the hierarchical order of cognitive impairment patterns. Most items showed strong scalability and consistent patterns of cognitive performance. However, challenges with IIO were observed, particularly with items having adjacent difficulty parameters. The findings highlight MSA's potential as a practical alternative to parametric IRT models in cognitive impairment research. Its ability to provide valuable insights into patterns of cognitive deterioration, coupled with less stringent requirements, makes it a useful tool for clinicians and researchers.

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Epilepsy, characterized by recurrent seizures, impacts 70-80% of patients, leading to cognitive deficits. The intricate relationship between seizure control and cognitive impairment remains complex. Epileptic encephalopathy (EE), an intensified form often rooted in genetic factors, is detectable through next-generation sequencing, aiding in precise diagnoses, family counseling, and potential treatment strategies. We present a case involving two sisters with refractory generalized seizures evolving into dysarthria, dysphagia, ataxia, and cognitive decline. Despite normal physical exams, abnormal electroencephalogram results consistent with epilepsy were noted. Whole Exome Sequencing identified heterozygous variants in the alanyl-tRNA synthetase (AARS) and Calcium Voltage-Gated Channel Subunit Alpha 1 (CACNA1A) genes. The AARS variant (c.C2083T, p.R695*) was maternal, while the CACNA1A variant (c.G7400C, p.R2467P) was paternal. Patients A and B exhibited a unique blend of neurological and psychiatric conditions, distinct from common disorders that begin adolescence, like Juvenile Myoclonic Epilepsy. Whole Exome Sequencing uncovered an AARS gene and CACNA1A gene, linked to various autosomal dominant phenotypes. Presence in both parents, coupled with familial reports of migraines and seizures, provides insight into accelerated symptom progression. This study underscores the importance of genetic testing in decoding complex phenotypes and emphasizes the value of documenting family history for anticipating related symptoms and future health risks.

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Background: Recent studies have identified plasma metabolites associated with cognitive decline and Alzheimer's disease; however, little research on this topic has been conducted in Latinos, especially Puerto Ricans. Objective: This study aims to add to the growing body of metabolomics research in Latinos to better understand and improve the health of this population. Methods: We assessed the association between plasma metabolites and global cognition over 12 years of follow-up in 736 participants of the Boston Puerto Rican Health Study (BPRHS). Metabolites were measured with untargeted metabolomic profiling (Metabolon, Inc) at baseline. We used covariable adjusted linear mixed models (LMM) with a metabolite * time interaction term to identify metabolites (of 621 measured) associated with ∼12 years cognitive trajectory. Results: We observed strong inverse associations between medium-chain fatty acids, caproic acid, and the dicarboxylic acids, azelaic and sebacic acid, and global cognition. N-formylphenylalanine, a tyrosine pathway metabolite, was associated with improvement in cognitive trajectory. Conclusions: The metabolites identified in this study are generally consistent with prior literature and highlight a role medium chain fatty acid and tyrosine metabolism in cognitive decline.

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Background: Cognitive deficits are commonly reported after COVID-19 recovery, but little is known in the older population. This study aims to investigate possible cognitive damage in older adults 6 months after contracting COVID-19, as well as individual risk factors. Methods: This cross-sectional study involved 70 participants aged 60-78 with COVID-19 6 months prior and 153 healthy controls. Montreal Cognitive Assessment-Basic (MoCA-B) screened for cognitive impairment; Geriatric Depression Scale and Geriatric Anxiety Inventory screened for depression and anxiety. Data were collected on demographics and self-reports of comorbid conditions. Results: The mean age of participants was 66.97 ± 4.64 years. A higher proportion of individuals in the COVID group complained about cognitive deficits (χ2 = 3.574; p = 0.029) and presented with deficient MoCA-B scores (χ2 = 6.098, p = 0.014) compared to controls. After controlling for multiple variables, all the following factors resulted in greater odds of a deficient MoCA-B: COVID-19 6-months prior (OR, 2.44; p = 0.018), age (OR, 1.15; p < 0.001), lower income (OR, 0.36; p = 0.070), and overweight (OR, 2.83; p = 0.013). Further analysis pointed to individual characteristics in COVID-19-affected patients that could explain the severity of the cognitive decline: age (p = 0.015), lower income (p < 0.001), anxiety (p = 0.049), ageusia (p = 0.054), overweight (p < 0.001), and absence of cognitively stimulating activities (p = 0.062). Conclusion: Our study highlights a profile of cognitive risk aggravation over aging after COVID-19 infection, which is likely mitigated by wealth but worsened in the presence of overweight. Ageusia at the time of acute COVID-19, anxiety, being overweight, and absence of routine intellectual activities are risk factors for more prominent cognitive decline among those infected by COVID-19.

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Cognitive decline is common among older individuals, and although the underlying brain mechanisms are not entirely understood, researchers have suggested using EEG frontal alpha activity during general anaesthesia as a potential biomarker for cognitive decline. This is because frontal alpha activity associated with GABAergic general anaesthetics has been linked to cognitive function. However, oscillatory-specific alpha power has also been linked with chronological age. We hypothesize that cognitive function mediates the association between chronological age and (oscillatory-specific) alpha power. We analysed data from 380 participants (aged over 60) with baseline screening assessments and intraoperative EEG. We utilized the telephonic Montreal Cognitive Assessment to assess cognitive function. We computed total band power, oscillatory-specific alpha power, and aperiodics to measure anaesthesia-induced alpha activity. To test our mediation hypotheses, we employed structural equation modelling. Pairwise correlations between age, cognitive function and alpha activity were significant. Cognitive function mediated the association between age and classical alpha power [age → cognitive function → classical alpha; ß = -0.0168 (95% confidence interval: -0.0313 to -0.00521); P = 0.0016] as well as the association between age and oscillatory-specific alpha power [age → cognitive function → oscillatory-specific alpha power; ß = -0.00711 (95% confidence interval: -0.0154 to -0.000842); P = 0.028]. However, cognitive function did not mediate the association between age and aperiodic activity (1/f slope, P = 0.43; offset, P = 0.0996). This study is expected to provide valuable insights for anaesthesiologists, enabling them to make informed inferences about a patient's age and cognitive function from an analysis of anaesthetic-induced EEG signals in the operating room. To ensure generalizability, further studies across different populations are needed.

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BACKGROUND: Life's Simple 7, a lifestyle and cardiovascular index associated with cognition, has been updated to Life's Essential 8 (LE8) to include sleep. LE8 has been related to cardiovascular outcomes but its association with cognition is unclear. METHODS: In this longitudinal analysis of the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), LE8 score was based on health behaviors (diet, physical activity, nicotine exposure, and sleep health) as well as health-related factors (body mass index, blood lipids, blood glucose, and blood pressure). Cognition was assessed in three waves, 4 years apart, using the Consortium to Establish a Registry for Alzheimer's Disease - Word List, semantic and phonemic verbal fluency, the Trail-Making Test B (TMT-B), and a global composite score. We used linear mixed-model analysis, inverse probability weighting, and interaction analysis. RESULTS: At baseline, the mean age of the study cohort was 51.4 ± 8.9 years, 56% were women, and 53% were White. Higher baseline LE8 scores were associated with slower decline in global cognition (ß = 0.001, 95% confidence interval [CI] 0.001, 0.002; p < 0.001), memory (ß = 0.001, 95% CI 0.000, 0.002; p = 0.013), verbal fluency (ß = 0.001, 95% CI 0.000, 0.002; p = 0.003), and TMT-B (ß = 0.004, 95% CI 0.003, 0.005; p < 0.001). This association was mainly driven by LE8 health factors, particularly blood glucose and blood pressure. Age, sex, and race were modifiers of the association between LE8 and global cognitive decline (p < 0.001), suggesting it was more pronounced in older, male, and Black participants. CONCLUSIONS: Higher baseline LE8 scores were associated with slower global and domain-specific cognitive decline during 8 years of follow-up, mainly due to health factors such as blood glucose and blood pressure. Sociodemographic factors were modifiers of this association.

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BACKGROUND: Increased interindividual variability in cognitive performance during aging has been proposed as an indicator of cognitive reserve. OBJECTIVE: To determine if interindividual variability performance in episodic memory (PAL), working memory (SWM), reaction time (RTI), and sustained attention (RVP) could differentiate clusters of differential cognitive performance in healthy young and older adults and search for cognitive tests that most contribute to these differential performances. METHODS: We employed hierarchical cluster and canonical discriminant function analyses of cognitive scores using the Cambridge Neuropsychological Test Automated Battery (CANTAB) to identify cognitive variability in older and young adults using the coefficient of variability of cognitive performances between and within groups. We also analyzed potential influences of age, education, and physical activity. RESULTS: Cluster analysis distinguished groups with differential cognitive performance and correlation analysis revealed coefficient of variability and cognitive performance associations. The greater the coefficient of variability the poorer was cognitive performance in RTI but not in PAL and SWM. Older adults showed diverse trajectories of cognitive decline, and better education or higher percentage of physically active individuals exhibited better cognitive performance in both older and young adults. CONCLUSION: PAL and SWM are the most sensitive tests to investigate the wide age range encompassing older and young adults. In older adults' intragroup analysis PAL showed greater discriminatory capacity, indicating its potential for clinical applications late in life. Our data underscore the importance of studying variability as a tool for early detection of subtle cognitive declines and for interpreting results that deviate from normality.

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Introduction: Arterial hypertrophy and remodeling are adaptive responses present in systemic arterial hypertension that can result in silent ischemia and neurodegeneration, compromising brain connections and cognitive performance (CP). However, CP is affected differently over time, so traditional screening methods may become less sensitive in assessing certain cognitive domains. The study aimed to evaluate whether cerebrovascular hemodynamic parameters can serve as a tool for cognitive screening in hypertensive without clinically manifest cognitive decline. Methods: Participants were allocated into groups: non-hypertensive (n = 30) [group 1], hypertensive with systolic blood pressure (SBP) < 140 and diastolic blood pressure (DBP) < 90 mmHg (n = 54) [group 2] and hypertensive with SBP ≥ 140 or DBP ≥ 90 (n = 31) [group 3]. Measurements of blood pressure and middle cerebral artery blood flow velocity were obtained from digital plethysmography and transcranial Doppler. For the cognitive assessment, the Mini Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) and a broad neuropsychological battery were applied. Results: Patients in groups 2 and 3 show no significant differences in most of the clinical-epidemiological variables or pulsatility index (p = 0.361), however compared to group 1 and 2, patients in group 3 had greater resistance-area product [RAP] (1.7 [±0.7] vs. 1.2 [±0.2], p < 0.001). There was a negative correlation between RAP, episodic memory (r = -0.277, p = 0.004) and cognitive processing speed (r = -0.319, p = 0.001). Conclusion: RAP reflects the real cerebrovascular resistance, regardless of the direct action of antihypertensive on the microcirculation, and seems to be a potential alternative tool for cognitive screening in hypertensive.

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This narrative review addresses the complex relationship between neurological diseases and artistic expression, which can have a profound impact on a painter´s works. This exploration highlights the dynamic and ever-evolving connection between neuroscience and art, offering insights into the extraordinary ways in which the human brain and artistic expression intersect and evolve. Following brain damage, there may be the emergence of sudden artistic talents, intriguing changes in the styles of established artists, the paradoxical facilitation of artistic abilities despite the cognitive decline consequent to these injuries, besides coping strategies that artists adopt in response to the challenges of health. Therefore, this article investigates different scenarios where brain injuries and disorders have had a profound impact on artists, leading to the emergence of new talents, changes in artistic styles, and unexpected improvements in their work, as well as adaptations in their artistic practices, as represented by some painters such as Tommy McHugh (1949 -2012), Francisco Goya (1746-1828), Otto Dix (1891-1969), Willem de Kooning (1904-1997), William Charles Utermohlen (1933-2007) and Charles Meryon (1821-1868). Consequently, works of art can be valuable but understudied tools for understanding brain dysfunction, although they must be interpreted with great care.

Esta revisão narrativa aborda a complexa relação entre doenças neurológicas e expressão artística, que pode ter um impacto profundo na obra de um pintor. Esta exploração destaca a conexão dinâmica e em constante evolução entre a neurociência e a arte, oferecendo insights sobre as formas extraordinárias pelas quais o cérebro humano e a expressão artística se cruzam e evoluem. Após danos cerebrais, pode haver o surgimento de talentos artísticos repentinos, mudanças intrigantes nos estilos de artistas estabelecidos, a facilitação paradoxal de habilidades artísticas, apesar do declínio cognitivo consequente a essas lesões, além de estratégias de enfrentamento que os artistas adotam em resposta aos desafios de saúde. Portanto, este artigo investiga diferentes cenários onde lesões e distúrbios cerebrais tiveram um impacto profundo nos artistas, levando ao surgimento de novos talentos, mudanças nos estilos artísticos e melhorias inesperadas em seu trabalho, bem como adaptações em suas práticas artísticas, bem como representado por alguns pintores como Tommy McHugh (1949 -2012), Francisco Goya (1746-1828), Otto Dix (1891-1969), Willem de Kooning (1904-1997), William Charles Utermohlen (1933-2007) e Charles Meryon (1821-1868). Consequentemente, as obras de arte podem ser ferramentas valiosas, mas pouco estudadas, para a compreensão da disfunção cerebral, embora devam ser interpretadas com muito cuidado.

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ABSTRACT Introduction: Mild Cognitive Impairment (MCI) is common in Parkinson's Disease (PD). Few studies have compared the Health-Related Quality of Life (HRQoL) in patients with and without MCI due to PD (PD-MCI), and its correlation to patients' subjective cognitive and communicative difficulties has not been explored. Objective: We aimed to compare HRQoL in PD-MCI and PD without MCI (PD-nMCI), and explore its possible relationship to subjective cognitive and communicative complaints. Methods: We included 29 PD-nMCI and 11 PD-MCI patients. The HRQoL was assessed with the Parkinson's Disease Questionnaire-39 (PDQ-39): its Cognition dimension was used as a measure of subjective cognitive complaints, its Communication dimension for subjective communicative complaints, and the summary index (PDQ-39 SI) as an indicator of HRQoL. Non-parametric partial correlations between the Cognition and Communication dimensions, and the adjusted PDQ-39 SI were conducted. Results: PD-MCI patients had greater subjective cognitive and communicative complaints and worse HRQoL than PD-nMCI patients. In the PD-MCI group, both subjective cognitive and communicative complaints exhibited significant direct correlations with the adjusted HRQoL scores. Conclusions: HRQoL seems to be affected in PD-MCI, and it might be influenced by greater subjective cognitive and communicative complaints. Including patient-reported outcome measures of HRQoL, and providing cognitive and speech rehabilitation, as well as psy-chotherapeutic strategies to face these deficits can enhance the patient-centred approach in PD.

RESUMEN Introducción: El deterioro cognitivo leve (DCL) es frecuente en la enfermedad de Parkinson (EP). Pocos estudios han comparado la calidad de vida relacionada con la salud (CVRS) en pacientes con DCL debido a EP (EP-DCL) sin explorar la relación entre la CVRS y las quejas subjetivas cognitivas y comunicativas de los pacientes. Objetivo: Comparar la CVRS en EP-DCL y EP sin DCL (EP-nDCL) explorando sus posibles relaciones con las quejas subjetivas cognitivas y comunicativas. Métodos: Se incluyó a 29 EP-DCL y 11 EP-nDCL. La CVRS se evaluó con el cuestionario PDQ-39: su dimensión Cognición se usó como medida de las quejas subjetivas cognitivas; su dimensión Comunicación, como medida de las quejas subjetivas comunicativas y su puntuación resumen (PDQ-39 SI), como indicador de CVRS. Se realizaron correlaciones parciales no paramétricas entre el PDQ-39 SI ajustado y las dimensiones Cognición y Comunicación. Resultados: Los pacientes EP-DCL presentaron una peor CVRS y mayores quejas subjetivas cognitivas y comunicativas. En el grupo EP-DCL, tanto las quejas subjetivas cognitivas como las comunicativas mostraron correlaciones directas significativas con la puntuación de CVRS ajustada. Conclusiones: La CVRS de los pacientes con EP-DCL parece estar afectada e influida por las quejas subjetivas en cognición y comunicación. Incluir los resultados de CVRS reportados por los pacientes, proveer rehabilitación cognitiva y del lenguaje y estrategias de psicoterapia para afrontar dicho déficit podrían mejorar el abordaje centrado en el paciente en la EP.

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Cognitive decline usually begins after individuals reach maturity, which is more evident in late adulthood. Rapid and constant cognitive screenings allow early detection of cognitive decline and motivate individuals to participate in prevention interventions. Due to accelerated technological advances, cognitive screening and training are now available to the layperson using electronic devices connected to the internet. Large datasets generated by these platforms provide a unique opportunity to explore cognitive development throughout life and across multiple naturalistic environments. However, such data collection mechanisms must be validated. This study aimed to determine whether the data gathered by commercial visuospatial and phonological working memory tests (CogniFit Inc., San Francisco, USA) confirm the well-established argument that age predicts cognitive decline. Data from 3,212 participants (2,238 females) who were 45 years old or older were analyzed. A linear regression analysis explored the relationship between age and working memory while controlling for gender, sleep quality, and physical activity (variables that are known to affect working memory). We found that age negatively predicts working memory. Furthermore, there was an interaction between age and gender for visuospatial working memory, indicating that although male participants significantly outperformed females, the relationship between age and working memory differs for females and males. Our results suggest that the computerized assessment of visuospatial and phonological working memory is sensible enough to predict cognitive functions in aging. Suggestions for improving the sensitivity of self-reports are discussed. Further studies must explore the nature of gender effects on cognitive aging.

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Emerging evidence suggests that immune receptors may participate in many aging-related processes such as energy metabolism, inflammation, and cognitive decline. CD300f, a TREM2-like lipid-sensing immune receptor, is an exceptional receptor as it integrates activating and inhibitory cell-signaling pathways that modulate inflammation, efferocytosis, and microglial metabolic fitness. We hypothesize that CD300f can regulate systemic aging-related processes and ultimately healthy lifespan. We closely followed several cohorts of two strains of CD300f-/- and WT mice of both sexes for 30 months and observed an important reduction in lifespan and healthspan in knockout mice. This was associated with systemic inflammaging, increased cognitive decline, reduced brain glucose uptake observed by 18FDG PET scans, enrichment in microglial aging/neurodegeneration phenotypes, proteostasis alterations, senescence, increased frailty, and sex-dependent systemic metabolic changes. Moreover, the absence of CD300f altered macrophage immunometabolic phenotype. Taken together, we provide strong evidence suggesting that myeloid cell CD300f immune receptor contributes to healthy aging.

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As the life expectancy and growth of the aging population increase globally, efforts to promote healthy longevity become more important. Holistic policy guidelines and actions have been designed to advocate and fortify healthy aging at multiple levels. Oral health, a fundamental contributor of overall health and well-being, forms a core part of the noncommunicable disease agenda within the sustainable development goals set by the World Health Organization. Aging significantly heightens the risk of myriad oral disorders and other noncommunicable diseases. As of 2019, oral disorders accounted for 8.9 million disability-adjusted life-years in individuals older than 60 y. In addition to the development of multidisciplinary aging-friendly policies to promote healthy aging, basic biology and translational research has been encouraged that focuses on deciphering the underlying mechanisms involved in age-related physical and cognitive decline or dysregulation of oral tissues. Given the relevance of oral health aging as a critical component of the One Health Initiative, this special issue encompasses a collection of articles dedicated to recent advances in the behavioral and social implications of age-related oral diseases and tooth loss on several aspects of the quality of life of adults as they age. Furthermore, it includes articles detailing molecular mechanisms associated with cellular aging and their implications for oral tissue health, periodontal disease severity, and the regenerative potential of stem cells.

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INTRODUCTION: Subjective Cognitive Decline (SCD) refers to a self-perceived experience of decreased cognitive function without objective signs of cognitive impairment in neuropsychological tests or daily living activities. Despite the abundance of instruments addressing SCD, there is no consensus on the methods to be used. Our study is founded on 11 questions selected due to their recurrence in most instruments. The objective was to determine which one of these questions could be used as a simple screening tool. METHODS: 189 participants aged 65 and over selected from Primary Care centers in Santiago de Chile responded to these 11 questions and were evaluated with the MiniMental State Examination (MMSE), the Free and Cued Selective Reminding Test (FCSRT), the Pfeffer functional scale, and the Geriatric Depression Scale (GDS). An Item ResponseTheory (IRT) method was performed to assess the contribution of each of the 11 questions to the SCD latent trait and its discrimination ability. RESULTS: Based on the results of the exploratory factor analysis showing very high/low saturation of several questions on the factors, and the high residual correlation between some questions, the IRT methods led to select one question ("Do you feel like your memory has become worse?") which revealed to be the most contributive and discriminant. Participants who answered yes had a higher GDS score. There was no association with MMSE, FCSRT, and Pfeffer scores. CONCLUSION: The question "Do you feel like your memory has become worse?" may be a good proxy of SCD and could be included in routine medical checkups.

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