Plasma biomarkers are promising tools for the screening and diagnosis of dementia in clinical settings. We analyzed plasma levels of Alzheimer’s core biomarkers, neurofilament light chain (NfL) and glial fibrillary acid protein (GFAP), through single-molecule Array in 108 patients with Alzheimer’s (AD, cerebrospinal fluid with an amyloid+ tau+ neurodegeneration+ profile), 73 patients with frontotemporal dementia (FTD, 24 with genetic diagnosis), and 54 controls. The best area under the curve (AUC) was used to assess the discriminative power. Patients with AD had lower Aß42/40 ratios and NfL levels, along with higher levels of p-tau181 and GFAP, compared with FTD patients. Single biomarkers discriminated well between dementia patients and controls: the Aß42/40 ratio (AUC:0.86) or GFAP (AUC:0.83) was found for AD, and the NfL (AUC:0.84) was found for FTD patients. However, a combination of two (NfL with p-tau181, or the GFAP/NfL ratio, AUCs ~0.87) or three biomarkers (NfL, P-tau181, and Aß42/40 ratio, AUC: 0.90) was required to distinguish between AD and FTD. Biomarker profiles were similar across different FTD phenotypes, except for carriers of PGRN mutations, who had higher levels of NfL than C9orf72 expansion carriers. In our series, NfL alone provided the best distinction between FTD and controls, while a combination of two or three biomarkers was required to obtain good discrimination between AD and FTD.

Background: Obesity, mainly visceral obesity, causes a low-grade of chronic inflammation (meta-inflammation), associated with comorbidities such as type 2 diabetes, cardiovascular diseases, and certain cancers. Precision Nutrition aims to understand the bidirectional crosstalk between the genome and diet to improve human health. Additionally, by leveraging individual data, Precision Nutrition seeks to predict how people will respond to specific foods or dietary patterns, with the ultimate goal of providing personalized nutritional recommendations tailored to their unique needs and lifestyle factors, including poor dietary habits (e.g., high intake of sugar or saturated fatty acids, alcohol consumption, etc.) and sedentary habits, exacerbate obesity in genetically predisposed individuals. Genetic, metabolic, and environmental factors can play a crucial role during obesity. Objective: To investigate the effects of genetic variability in sweet taste receptors and their downstream signaling pathways in the gut–brain axis on anthropometry, biochemistry, and lifestyle variables. Methods: A sample of 676 volunteers (mean age of 42.22 ± 12 years, ranging from 18 to 73 years) from the database of the GENYAL platform for nutritional trials at the IMDEA Food Institute were included in this study. We present a first-in-class genetic chip, Glucosensing, designed to interrogate 25 single-nucleotide polymorphisms (SNPs) located in genes encoding sweet taste receptors and components of downstream signaling pathways. These include elements of the gut–brain axis and its associated metabolic networks, enabling a comprehensive analysis of individual variability in sweet taste perception and metabolic responses. Results: Several significant associations were found after correction for multiple comparisons, representing potential targets for personalized interventions.

Toxic oil syndrome (TOS) is a multisystemic disease that emerged in Spain in 1981 due to the ingestion of aniline-adulterated rapeseed oil fraudulently sold as olive oil. Although neurological sequelae, including cognitive deficits, have been documented in long-term survivors, it remains unclear whether TOS leads to chronic or progressive neurodegeneration. In this case-control study, we measured blood concentrations of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and phosphorylated tau 217 (pTau217) in 50 individuals with clinically confirmed TOS and 50 matched healthy controls. Biomarkers were quantified using ultrasensitive immunoassay platforms (Quanterix SIMOA SR-X and Fujirebio Lumipulse G600II). Group differences were evaluated using non-parametric tests, and multiple linear regression was applied to assess associations between biomarkers and clinical variables. While NfL levels were slightly higher in TOS patients (p = 0.025), no significant group differences were observed for pTau217 or GFAP. Age was a consistent predictor of biomarker levels, particularly for GFAP and pTau217, and female sex was independently associated with higher GFAP concentrations. Lower educational attainment was linked to increased NfL levels. Clinical status (TOS vs. control) did not significantly predict biomarker concentrations in any model. These findings suggest no evidence of overt or ongoing neurodegeneration in long-term TOS survivors as detected by current blood biomarkers. However, the possibility of subtle, compartmentalized, or slowly evolving neurotoxic processes cannot be excluded. Future longitudinal studies incorporating serial biomarker assessments, advanced neuroimaging, and oxidative stress markers are warranted to clarify the long-term neurological consequences of TOS and to detect subclinical trajectories of delayed neurotoxicity in this population.

Toxic Oil Syndrome (TOS) was a multisystemic disease that emerged in Spain in 1981 due to the ingestion of aniline-contaminated rapeseed oil. Although neurological sequelae, including cognitive deficits, have been documented in long-term survivors, it remains unclear whether TOS leads to chronic or progressive neurodegeneration. In this case-control study, we measured blood concentrations of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and phosphorylated tau 217 (pTau217) in 50 individuals with clinically confirmed TOS and 50 matched healthy controls. Biomarkers were quantified using ultrasensitive immunoassay platforms (Quanterix SIMOA SR-X and Fujirebio Lumipulse G600II). Group differences were evaluated using non-parametric tests, and multiple linear regression was applied to assess associations between biomarkers and clinical variables. While NfL levels were slightly higher in TOS patients, the difference was not statistically significant. Similarly, no significant group differences were observed for pTau217 or GFAP. Age was a consistent predictor of biomarker levels, particularly for GFAP and pTau217, and female sex was independently associated with higher GFAP concentrations. Lower educational attainment was linked to increased NfL levels. Clinical status (TOS vs. control) did not significantly predict biomarker concentrations in any model. These findings suggest no evidence of overt or ongoing neurodegeneration in long-term TOS survivors as detected by current blood biomarkers. However, the possibility of subtle or slowly evolving neurotoxic processes cannot be excluded. Longitudinal studies incorporating neuroimaging are warranted to clarify the long-term neurological impact of TOS and to identify potential subclinical trajectories of neurodegeneration in this population.