Among neurodegenerative diseases, Alzheimer’s disease (AD) is a leading cause of death in elderly individuals. AD is characterized, among other clinical findings, by unexplained weight loss, cachexia and altered immune function. To explore whether any relationship between gender and circulating levels of several eating-controlling metabolites exist, we evaluated leptin, tumor necrosis factor (TNF)-α, triiodothyronine (T₃), free (F) thyroxine (T₄), TSH, PRL, insulin (INS), and cortisol in 15 AD-treated patients (age range 55–82 years): 9 postmenopausal females (without hormone replacement therapy) and 6 males. The results (mean ± SEM) indicated that circulating leptin levels were significantly (p < 0.05) higher in female AD (40.34 ± 11.1 ng/ml) than in male AD (6.07 ± 1.39 ng/ml) patients. The difference found in circulating leptin levels was noticed regardless of BMI (26.75 ± 1.77 and 24.55 ± 1.93 kg/m², in females and males, respectively) and waist:hip ratios (0.91 ± 0.03 and 0.94 ± 0.02, in females and males, respectively). Moreover, serum TNF-α concentrations were also significantly (p < 0.02) higher in AD females (12.24 ± 1.47 pg/ml) than in AD males (6.62 ± 1.44 pg/ml), regardless of TNF-α:BMI ratios (0.50 ± 0.09 and 0.28 ± 0.08, in females and males, respectively; p > 0.05). Finally, no differences were observed between gender (in female and male AD patients, respectively) in circulating levels of T₃ (151.33 ± 9.91 vs. 116 ± 17.04 ng/dl), FT₄ (1.26 ± 0.08 vs. 1.24 ± 0.06 ng/dl), TSH (1.28 ± 0.16 vs. 2.46 ± 0.67 µIU/ml), PRL (10.53 ± 2.47 vs. 12.61 ± 2.37 ng/ml), INS (11.76 ± 1.95 vs. 8.59 ± 1.34 µIU/ml) and cortisol (15.71 ± 1.23 vs. 12.63 ± 1.47 µg/dl). These results indicate that our AD group of patients, with normal corticoadrenal and thyroid functions and normoprolactinemia, displayed a gender-related characteristic in the circulating levels of two very important anorectic signals, leptin and TNF-α, being both higher in female than in male AD patients, regardless of BMI. Our study suggests that increased circulating levels of both anorexigenic adipokines may contribute to the metabolic changes observed in AD females.

Background The pandemic of SARS‐CoV‐2 is focusing all energies on the impact on survival of affected individuals, treatment and prevention, but increasingly attention is focusing on its enduring consequences. We established a global consortium to study a longitudinal representative cohort of individuals, to characterize neurological and neuropsychiatric sequalae from direct viral, immune‐, vascular‐ or accelerated neurodegenerative injury to the central nervous system (CNS). Method We propose to characterize the neurobehavioral phenomenology associated with SARS‐CoV‐2 in a large, multinational, longitudinal cohort of post COVID‐19 infection patients following three sampling strategies: 1) Opportunity sample of patients discharged after hospital admission for COVID‐19 related symptoms. 2) A stratified random sample from COVID‐19 testing registries (including asymptomatic and negative participants). 3) Ascertaining COVID‐19 exposure (antibody) status in ongoing longitudinal, community‐based cohort studies that are already collecting biosamples, cognitive, behavioral and neuroimaging data. We will obtain core data within 6 months of discharge or testing. Core characterization will include interviews with the Schedules of Clinical Assessment in Neuropsychiatry (SCAN), neurological exams, emotional reactivity scales and a neurocognitive assessment. Wherever feasible, we will also collect neuroimaging, biosamples and genetic data. Longitudinal follow up will be conducted at 9 and 18 months of the initial evaluation. An mHealth keeping‐in‐touch process will be set up to minimize attrition rates. The population cohorts provide a large, unbiased, normative and validation sample, albeit with more heterogenous outcome ascertainment. They also permit examination of pre‐ and post‐COVID trends in symptoms and biomarkers. Since some ethnic groups, as well as in individuals with blood type A, are at higher risk of COVID‐19 infection and death, a role of genetics in determining susceptibility to infection and poor outcomes seems well supported. We will collect genome‐wide genotypes from our cohort individuals to address the role of ancestry and genetic variation on susceptibility to neuropsychiatric sequelae. High rates of mutation in COVID‐19 strongly suggest that viral infectivity, including neurotropism, may not be uniform across countries affected by the pandemic. Results Pending. Conclusion Our consortium is in a unique position to address the interaction between genetics (including ancestral DNA), and viral strain variation on CNS sequelae of SARS‐CoV‐2.

No abstract

ArtículoMaterial original autorizado para la publicación en la revista Psicodebate. Facultad de Ciencias Sociales. Universidad de Palermo.Recibido 22-11-2013 | Aceptado 25-02-2014 ResumenEl objetivo de este trabajo es describir, desde la neuropsicología, el proceso de Toma de Decisiones (TD) en sujetos que padecen la Enfermedad de Alzheimer (EA). Para ello, se estableció una comparación del desempeño en TD de 40 sujetos con diagnóstico de enfermedad de Alzheimer con el desempeño de un grupo control de 40 sujetos sin diagnóstico de enfermedad neurológica y /o psiquiátrica, pareados por NSEC. El desempeño en la TD se evaluó con la tarea de Game Dice Task (GDT) -Tarea del Juego de los Dados de Brand-. También se aplicaron otras pruebas y tareas de evaluación cognitiva para determinar la relación de la TD con otras Funciones Ejecutivas (FE). Los resultados permitieron establecer que el proceso de TD se deteriora desde los comienzos de la enfermedad, evidenciando que el de los tiempos de respuesta. También se observó deterioro en todas las funciones ejecutivas evaluadas. El trabajo provee evidencia empírica que soporta la idea de que la TD se encuentra estrechamente relacionada a las demás FE.Palabras Clave: Toma de decisiones (TD) -Enfermedad de Alzheimer (EA) -Game Dice Task (GDT) -Neuropsicología.

No abstract