👤 Andrea Bonnin Márquez

Aging is traditionally characterized by progressive structural and cognitive decline; however, increasing evidence shows that the aging brain retains a remarkable capacity for reorganization. This adaptive neuroplasticity supports cognitive resilience-defined as the ability to maintain efficient cognitive performance despite age-related neural vulnerability. To synthesize current molecular, cellular, neuroimaging, and electrophysiological neuromarkers that characterize adaptive neuroplasticity and to examine how these mechanisms contribute to cognitive resilience across aging. This narrative review integrates findings from molecular neuroscience, multimodal neuroimaging (fMRI, DTI, PET), electrophysiology (EEG, MEG, TMS), and behavioral research to outline multiscale biomarkers associated with compensatory and efficient neural reorganization in older adults. Adaptive neuroplasticity emerges from the coordinated interaction of neurotrophic signaling (BDNF, CREB, IGF-1), glial modulation (astrocytic lactate metabolism, regulated microglial activity), synaptic remodeling, and neurovascular support (VEGF, nitric oxide). Multimodal neuromarkers-including preserved frontoparietal connectivity, DMN-FPCN coupling, synaptic density (SV2A-PET), theta-gamma coherence, and LTP-like excitability-consistently correlate with resilience in executive functions, memory, and processing speed. Behavioral enrichment, physical activity, and cognitive training further enhance these biomarkers, creating a bidirectional loop between experience and neural adaptability. Adaptive neuroplasticity represents a fundamental mechanism through which older adults maintain cognitive function despite biological aging. Integrating molecular, imaging, electrophysiological, and behavioral neuromarkers provides a comprehensive framework to identify resilience trajectories and to guide personalized interventions aimed at preserving cognition. Understanding these multilevel adaptive mechanisms reframes aging not as passive decline but as a dynamic continuum of biological compensation and cognitive preservation. Show less

Type 2 diabetes has been linked to oxidative stress, inflammation, and an imbalance in the gut microbiota, all of which contribute to neuroinflammation and cognitive decline. Gut microbiota influence inflammation and produce various substances, including butyrate, a short-chain fatty acid that promotes brain-derived neurotrophic factor (BDNF), which is essential for memory. This study investigated whether prebiotics, probiotics, or a combination of both (symbiotics) could improve memory in diabetic rats. Male Wistar rats were divided into five groups: control; diabetic and obese (induced by a high-fat diet and streptozotocin); diabetic and obese with prebiotics (inulin); diabetic and obese with probiotics (Lactobacillus acidophilus); and diabetic and obese with symbiotics (inulin + L. acidophilus). Treatments lasted 42 d. Memory performance was evaluated using the Morris water maze (spatial memory) and the Eight-arm radial maze (working memory). After testing, hippocampal tissue was analyzed for inflammatory markers (TNF-α, IL-10), BDNF, and butyric acid. Diabetes impaired memory and increased neuroinflammatory markers. All supplemented groups showed improved memory. The symbiotic group exhibited the most pronounced benefits, with higher levels of BDNF, IL-10, and butyric acid, and reduced TNF-α. Electrophysiological recordings revealed that diabetes reduced the firing frequency of CA1 pyramidal cells and decreased the synaptic strength in the hippocampus. Symbiotic supplementation preserved these neuronal and synaptic functions. Symbiotic treatment effectively countered diabetes-induced cognitive deficits by reducing neuroinflammation, increasing neurotrophic support, and maintaining synaptic plasticity. These results imply that altering the gut microbiota through symbiotic supplementation may be an effective approach to prevent or mitigate diabetes-associated cognitive decline. Show less

Apolipoprotein E (APOE) alleles are well-established genetic risk factors for Alzheimer's disease (AD), but their effects on AD biomarkers (amyloid beta [Aβ]42/40, phosphorylated tau [p-tau]181, neurofilament light chain [NfL], and glial fibrillary acidic protein [GFAP]) may vary across populations due to ancestry-, age-, and sex-related differences. We hypothesized that these effects vary across Hispanic/Latino background groups with distinct ancestral admixture. We analyzed ε2 and ε4 allele associations with AD biomarkers using survey-weighted linear regression models, adjusting for demographic covariates. Secondary analyses examined genetic analysis group- and ancestry-specific effects. ε4 was associated with lower Aβ42/40 and higher p-tau181and GFAP levels, but not with NfL, suggesting its role in Aβ and tau deposition and neuroinflammation. ε4 associations were stronger in those with higher European and lower African ancestry. These findings expand on prior studies suggesting that genetic ancestry modifies APOE-associated AD risk in Hispanic/Latino populations and highlight the importance of capturing ancestry-based heterogeneity in AD biomarker research. Show less

Blood-based biomarkers hold promise as a minimally invasive tool for identifying early signs of Alzheimer's disease pathology and neurodegeneration. We investigated associations between plasma biomarkers of amyloid-beta, tau, neuroaxonal injury, and glial activation with cognitive performance among community-dwelling Hispanic/Latino adults in the United States. We analyzed cross-sectional data from 5730 adults aged 50 years and older (unweighted; mean [SD], 63.5 [8.2] years) in the Study of Latinos-Investigation of Neurocognitive Aging (SOL-INCA; 2016-2018). Plasma concentrations of amyloid-beta (Aβ Here we show higher ln(pTau-181) and ln(NfL) are associated with lower global cognitive performance (b Plasma biomarkers related to Alzheimer's disease pathophysiology and broader neurodegenerative processes are associated with cognitive performance among Hispanic/Latino adults. These findings highlight the potential utility of blood-based biomarkers for identifying early cognitive vulnerability in this population. Show less

High-density lipoprotein (HDL) is well-known for its cardioprotective effects, as it possesses anti-inflammatory, anti-oxidative, anti-thrombotic, and cytoprotective properties. Traditionally, studies and therapeutic approaches have focused on raising HDL cholesterol levels. Recently, it became evident that, not HDL cholesterol, but HDL composition and functionality, is probably a more fruitful target. In disorders, such as chronic kidney disease or cardiovascular diseases, it has been observed that HDL is modified and becomes dysfunctional. There are different modification that can occur, such as serum amyloid, an enrichment and oxidation, carbamylation, and glycation of key proteins. Additionally, the composition of HDL can be affected by changes to enzymes such as cholesterol ester transfer protein (CETP), lecithin-cholesterol acyltransferase (LCAT), and phospholipid transfer protein (PLTP) or by modification to other important components. This review will highlight some main modifications to HDL and discuss whether these modifications are purely a consequential result of pathology or are actually involved in the pathology itself and have a causal role. Therefore, HDL composition may present a molecular target for the amelioration of certain diseases, but more information is needed to determine to what extent HDL modifications play a causal role in disease development. Show less