RESUMEN
The established role of disturbances in the microbiota-gut-brain axis in the development of diabetic cognitive impairment (DCI) has long been recognized. It has shown the potential of Akkermansia muciniphila (A. muciniphila) in improving metabolic disorders and exerting anti-inflammatory effects. However, there remains a lack of comprehensive understanding regarding the specific effects and mechanisms underlying the treatment of DCI with A. muciniphila. This study aimed to evaluate the potential of A. muciniphila in alleviating DCI in db/db mice. Eleven-week-old db/db mice were administered either live or pasteurized A. muciniphila (5 × 109 CFU/200 µL) for a duration of eight weeks. Administering live A. muciniphila significantly ameliorated cognitive impairments, improved the synaptic ultrastructure, and inhibited hippocampal neuron loss in the CA1 and CA3 subregions in db/db mice. Both live and pasteurized A. muciniphila effectively mitigated neuroinflammation. Moreover, live A. muciniphila increased the relative abundance of Lactococcus and Staphylococcus, whereas pasteurized A. muciniphila increased the relative abundance of Lactobacillus, Prevotellaceae_UCG_001, and Alistipes. Supplementation of A. muciniphila also induced alterations in serum and brain metabolites, with a particular enrichment observed in tryptophan metabolism, glyoxylate and dicarboxylate metabolism, nitrogen metabolism, and pentose and glucuronate interconversions. Correlation analysis further demonstrated a direct and substantial correlation between the altered gut microbiota and the metabolites in the serum and brain tissue. In conclusion, the results indicate that live A. muciniphila demonstrated greater efficacy compared to pasteurized A. muciniphila. The observed protective effects of A. muciniphila against DCI are likely mediated through the neuroinflammation and microbiota-metabolites-brain axis.
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Akkermansia , Disfunción Cognitiva , Microbioma Gastrointestinal , Probióticos , Animales , Microbioma Gastrointestinal/fisiología , Ratones , Disfunción Cognitiva/metabolismo , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/etiología , Masculino , Probióticos/farmacología , Probióticos/uso terapéutico , Verrucomicrobia , Ratones Endogámicos C57BL , PasteurizaciónRESUMEN
BACKGROUND: The incidence of exertional heat stroke (EHS) escalates during periods of elevated temperatures, potentially leading to persistent cognitive impairment postrecovery. Currently, effective prophylactic or therapeutic measures against EHS are nonexistent. METHODS: The selection of days 14 and 23 postinduction for detailed examination was guided by TEM of neuronal cells and HE staining of intestinal villi and the hippocampal regions. Fecal specimens from the ileum and cecum at these designated times were analyzed for changes in gut microbiota and metabolic products. Bioinformatic analyses facilitated the identification of pivotal microbial species and metabolites. The influence of supplementing these identified microorganisms on behavioral outcomes and the expression of functional proteins within the hippocampus was subsequently assessed. RESULTS: TEM analyses of neurons, coupled with HE staining of intestinal villi and the hippocampal region, indicated substantial recovery in intestinal morphology and neuronal injury on Day 14, indicating this time point for subsequent microbial and metabolomic analyses. Notably, a reduction in the Lactobacillaceae family, particularly Lactobacillus murinus, was observed. Functional annotation of 16S rDNA sequences suggested diminished lipid metabolism and glycan biosynthesis and metabolism in EHS models. Mice receiving this intervention (EHS + probiotics group) exhibited markedly reduced cognitive impairment and increased expression of BDNF/TrKB pathway molecules in the hippocampus during behavioral assessment on Day 28. CONCLUSION: Probiotic supplementation, specifically with Lactobacillus spp., appears to mitigate EHS-induced cognitive impairment, potentially through the modulation of the BDNF/TrKB signaling pathway within the hippocampus, illustrating the therapeutic potential of targeting the gut-brain axis.
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Disfunción Cognitiva , Microbioma Gastrointestinal , Golpe de Calor , Animales , Femenino , Masculino , Ratones , Eje Cerebro-Intestino , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/etiología , Disfunción Cognitiva/microbiología , Disfunción Cognitiva/psicología , Microbioma Gastrointestinal/fisiología , Golpe de Calor/complicaciones , Golpe de Calor/metabolismo , Golpe de Calor/fisiopatología , Hipocampo/citología , Hipocampo/fisiopatología , Lactobacillus/metabolismo , Neuronas/ultraestructura , Probióticos , Conducta Animal , Ácidos Grasos Volátiles/metabolismoRESUMEN
With the rising prevalence of diabetes and its association with cognitive impairment, interest in the use of dietary alkaloids and other natural products has grown significantly. Understanding how these compounds manage diabetic cognitive dysfunction (DCD) is crucial. This comprehensive review explores the etiology of DCD and the effects of alkaloids in foods and dietary supplements that have been investigated as DCD therapies. Data on how dietary alkaloids like berberine, trigonelline, caffeine, capsaicin, 1-deoxynojirimycin, nuciferine, neferine, aegeline, tetramethylpyrazine, piperine, and others regulate cognition in diabetic disorders were collected from PubMed, Research Gate, Web of Science, Science Direct, and other relevant databases. Dietary alkaloids could improve memory in behavioral models and modulate the mechanisms underlying the cognitive benefits of these compounds, including their effects on glucose metabolism, gut microbiota, vasculopathy, neuroinflammation, and oxidative stress. Evidence suggests that dietary alkaloids hold promise for improving cognition in diabetic patients and could open exciting avenues for future research in diabetes management.
Asunto(s)
Alcaloides , Cognición , Disfunción Cognitiva , Humanos , Alcaloides/uso terapéutico , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/metabolismo , Cognición/efectos de los fármacos , Suplementos Dietéticos , Animales , Berberina/uso terapéutico , Berberina/farmacología , Diabetes Mellitus/dietoterapia , Diabetes Mellitus/tratamiento farmacológico , Diabetes Mellitus/metabolismo , Estrés Oxidativo/efectos de los fármacos , Capsaicina/uso terapéutico , Cafeína/uso terapéutico , Cafeína/farmacología , Piperidinas/uso terapéutico , Piperidinas/farmacología , Microbioma Gastrointestinal/efectos de los fármacos , Benzodioxoles/uso terapéutico , Benzodioxoles/farmacología , Aporfinas , Alcamidas PoliinsaturadasRESUMEN
Dietary intervention could modulate age-related neurological disorders via the gut-brain axis. The potential roles of a probiotic and the dietary fiber complex (DFC) on brain and gut function in aged mice were investigated in this study. Lactobacillus casei LTL1361 and DFC were orally administrated for 12 weeks, and the learning and memory ability, as well as the oxidative parameters, inflammatory markers, gut barrier function and microbial metabolite short-chain fatty acids (SCFAs), were investigated. LTL1361 and DFC supplementation ameliorated cognitive ability, attenuated oxidative stress in brain and inflammation in serum and colon, ameliorated gut barrier function, and increased the SCFA concentrations and gene expression of SCFA receptors. The protective effect was more significantly enhanced in aged mice treated with the combination of LTL1361 and DFC than treated with LTL1361 or DFC alone. These results could be associated with the protected morphology of pyramidal nerve cells in hippocampus of mice brain and the downregulation of apoptosis marker caspase-3 in brain and upregulation of tight junction proteins in small intestine and colon. The results indicated that Lactobacillus casei LTL1361 and DFC alleviated age-related cognitive impairment, as well as protected brain and gut function. Lactobacillus casei LTL1361 and DFC might be used as novel and promising antiaging agents in human.
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Envejecimiento , Eje Cerebro-Intestino/efectos de los fármacos , Centenarios , Disfunción Cognitiva/prevención & control , Fibras de la Dieta/farmacología , Inflamación/prevención & control , Lacticaseibacillus casei/metabolismo , Animales , Disfunción Cognitiva/dietoterapia , Fibras de la Dieta/administración & dosificación , Modelos Animales de Enfermedad , Humanos , Inflamación/dietoterapia , Masculino , Ratones , Ratones Endogámicos C57BLRESUMEN
BACKGROUND: This narrative review presents the association between metabolic syndrome (MetS), along with its components, and cognition-related disorders, as well as the potential reversal role of diet against cognitive impairment by modulating MetS. METHODS: An electronic research in Medline (Pubmed) and Scopus was conducted. RESULTS: MetS and cognitive decline share common cardiometabolic pathways as MetS components can trigger cognitive impairment. On the other side, the risk factors for both MetS and cognitive impairment can be reduced by optimizing the nutritional intake. Clinical manifestations such as dyslipidemia, hypertension, diabetes and increased central body adiposity are nutrition-related risk factors present during the prodromal period before cognitive impairment. The Mediterranean dietary pattern stands among the most discussed predominantly plant-based diets in relation to cardiometabolic disorders that may prevent dementia, Alzheimer's disease and other cognition-related disorders. In addition, accumulating evidence suggests that the consumption of specific dietary food groups as a part of the overall diet can improve cognitive outcomes, maybe due to their involvement in cardiometabolic paths. CONCLUSIONS: Early MetS detection may be helpful to prevent or delay cognitive decline. Moreover, this review highlights the importance of healthy nutritional habits to reverse such conditions and the urgency of early lifestyle interventions.
Asunto(s)
Disfunción Cognitiva/dietoterapia , Dieta/métodos , Síndrome Metabólico/dietoterapia , Dieta Mediterránea , HumanosAsunto(s)
Antiinflamatorios/farmacología , Disfunción Cognitiva , Trastorno Depresivo , Fitosteroles/farmacología , Adulto , Animales , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/metabolismo , Trastorno Depresivo/dietoterapia , Trastorno Depresivo/tratamiento farmacológico , Trastorno Depresivo/metabolismo , Humanos , RatasRESUMEN
AIM: To investigate whether children with perinatal brain injury have impairments in specific components of visual attention, and whether early dietary supplementation can reduce any deficits. METHOD: Children participating in the Dolphin neonatal trial of dietary supplementation were tested at age 6 months with the Infant Fixation Shift Attention Test, and at 4 to 5 years with four subtests of the Early Childhood Attention Battery (ECAB) assessing different components of attention (selective, sustained, and executive function), and the Fluid Crystallized Intelligence Index of the Kaufman Assessment Battery for Children, Second Edition (KABC-II). From 59 children originally assigned to trial groups, 33 were available for testing at 4 to 5 years (18 treatment group of whom seven, six, and five showed mild, moderate, or severe neonatal brain injury; 15 controls with one, seven, and seven in the neonatal brain injury categories respectively). Given the imbalance in numbers with mild brain injury, analysis of trial group differences is restricted to moderate and severe brain injury severities (n=25). RESULTS: Children with perinatal brain injury showed poorer attention across all components relative to age norms (mean standard scores 75-87; p<0.001 for three of the four subtests), with the greatest impairment in sustained attention. These impairments remained when compared with cognitive age assessed using the Fluid Crystallized Intelligence Index. Impairment was reduced in the treatment compared to the control group (p=0.04 for flanker test, p=0.002 for counterpointing, and p=0.027 for the overall ECAB score). INTERPRETATION: Perinatal brain injury is associated with later impaired attention, beyond that predicted from any general cognitive disability. Impairment varies across attention components, being most severe for sustained attention. The effects on flanker and counterpointing suggest that dietary supplementation from 0 to 2 years of age may reduce attention problems. Measuring the different components of attention is important when considering assessment and interventions for children with perinatal brain injury.
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Atención/fisiología , Lesiones Encefálicas , Disfunción Cognitiva , Suplementos Dietéticos , Función Ejecutiva/fisiología , Enfermedades del Recién Nacido , Inteligencia/fisiología , Lesiones Encefálicas/complicaciones , Lesiones Encefálicas/fisiopatología , Preescolar , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/etiología , Disfunción Cognitiva/fisiopatología , Femenino , Humanos , Lactante , Recién Nacido , Enfermedades del Recién Nacido/fisiopatología , Estudios Longitudinales , Masculino , Gravedad del Paciente , Resultado del TratamientoRESUMEN
Dendritic spines are small, thin, hair-like protrusions found on the dendritic processes of neurons. They serve as independent compartments providing large amplitudes of Ca2+ signals to achieve synaptic plasticity, provide sites for newer synapses, facilitate learning and memory. One of the common and severe complication of neurodegenerative disease is cognitive impairment, which is said to be closely associated with spine pathologies viz., decreased in spine density, spine length, spine volume, spine size etc. Many treatments targeting neurological diseases have shown to improve the spine structure and distribution. However, concise data on the various modulators of dendritic spines are imperative and a need of the hour. Hence, in this review we made an attempt to consolidate the effects of various pharmacological (cholinergic, glutamatergic, GABAergic, serotonergic, adrenergic, and dopaminergic agents) and non-pharmacological modulators (dietary interventions, enriched environment, yoga and meditation) on dendritic spines structure and functions. These data suggest that both the pharmacological and non-pharmacological modulators produced significant improvement in dendritic spine structure and functions and in turn reversing the pathologies underlying neurodegeneration. Intriguingly, the non-pharmacological approaches have shown to improve intellectual performances both in preclinical and clinical platforms, but still more technology-based evidence needs to be studied. Thus, we conclude that a combination of pharmacological and non-pharmacological intervention may restore cognitive performance synergistically via improving dendritic spine number and functions in various neurological disorders.
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Espinas Dendríticas/efectos de los fármacos , Dieta , Enfermedades Neurodegenerativas/dietoterapia , Enfermedades Neurodegenerativas/tratamiento farmacológico , Colinérgicos/uso terapéutico , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/tratamiento farmacológico , Disfunción Cognitiva/epidemiología , Disfunción Cognitiva/psicología , Espinas Dendríticas/patología , Espinas Dendríticas/fisiología , Fármacos actuantes sobre Aminoácidos Excitadores/uso terapéutico , GABAérgicos/uso terapéutico , Humanos , Meditación/psicología , Enfermedades Neurodegenerativas/epidemiología , Enfermedades Neurodegenerativas/psicología , Neuronas/efectos de los fármacos , Neuronas/fisiología , Sinapsis/efectos de los fármacos , Sinapsis/metabolismo , Yoga/psicologíaRESUMEN
Traumatic brain injury (TBI) is a brain dysfunction without present treatment. Previous studies have shown that animals fed ketogenic diet (KD) perform better in learning tasks than those fed standard diet (SD) following brain injury. The goal of this study was to examine whether KD is a neuroprotective in TBI mouse model. We utilized a closed head injury model to induce TBI in mice, followed by up to 30 days of KD/SD. Elevated levels of ketone bodies were confirmed in the blood following KD. Cognitive and behavioral performance was assessed post injury and molecular and cellular changes were assessed within the temporal cortex and hippocampus. Y-maze and Novel Object Recognition tasks indicated that mTBI mice maintained on KD displayed better cognitive abilities than mTBI mice maintained on SD. Mice maintained on SD post-injury demonstrated SIRT1 reduction when compared with uninjured and KD groups. In addition, KD management attenuated mTBI-induced astrocyte reactivity in the dentate gyrus and decreased degeneration of neurons in the dentate gyrus and in the cortex. These results support accumulating evidence that KD may be an effective approach to increase the brain's resistance to damage and suggest a potential new therapeutic strategy for treating TBI.
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Lesiones Traumáticas del Encéfalo/dietoterapia , Dieta Cetogénica , Animales , Ansiedad , Astrocitos/patología , Lesiones Traumáticas del Encéfalo/sangre , Lesiones Traumáticas del Encéfalo/psicología , Corteza Cerebral/metabolismo , Corteza Cerebral/patología , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/psicología , Modelos Animales de Enfermedad , Traumatismos Cerrados de la Cabeza/sangre , Traumatismos Cerrados de la Cabeza/dietoterapia , Traumatismos Cerrados de la Cabeza/psicología , Hipocampo/metabolismo , Hipocampo/patología , Cuerpos Cetónicos/sangre , Masculino , Aprendizaje por Laberinto , Ratones , Ratones Endogámicos ICR , Neuronas/patología , Reconocimiento en Psicología , Sirtuina 1/metabolismoRESUMEN
BACKGROUND: Exploration of cerebrospinal fluid (CSF) amino acids and the impact of dietary intake on central levels may provide a comprehensive understanding of the metabolic component of Alzheimer's disease. OBJECTIVE: The objective of this exploratory study was to investigate the effects of two diets with varied nutrient compositions on change in CSF amino acids levels in adults with mild cognitive impairment (MCI) and normal cognition (NC). Secondary objectives were to assess the correlations between the change in CSF amino acids and change in Alzheimer's disease biomarkers. METHODS: In a randomized, parallel, controlled feeding trial, adults (NC, nâ=â20; MCI, nâ=â29) consumed a high saturated fat (SFA)/glycemic index (GI) diet [HIGH] or a low SFA/GI diet [LOW] for 4 weeks. Lumbar punctures were performed at baseline and 4 weeks. RESULTS: CSF valine increased and arginine decreased after the HIGH compared to the LOW diet in MCI (psâ=â0.03 and 0.04). This pattern was more prominent in MCI versus NC (diet by diagnosis interaction psâ=â0.05 and 0.09), as was an increase in isoleucine after the HIGH diet (pâ=â0.05). Changes in CSF amino acids were correlated with changes in Alzheimer's disease CSF biomarkers Aß42, total tau, and p-Tau 181, with distinct patterns in the relationships by diet intervention and cognitive status. CONCLUSION: Dietary intake affects CSF amino acid levels and the response to diet is differentially affected by cognitive status.
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Aminoácidos/líquido cefalorraquídeo , Biomarcadores/líquido cefalorraquídeo , Cognición/fisiología , Disfunción Cognitiva/dietoterapia , Dieta , Anciano , Arginina/líquido cefalorraquídeo , Ingestión de Alimentos , Femenino , Humanos , Masculino , Punción Espinal , Valina/líquido cefalorraquídeoRESUMEN
Our study aimed to evaluate whether the type of food products and the frequency of their consumption are associated with cognitive functioning in younger and older adults. The impact of diets that are high in added sugars and saturated fat on cognitive functioning, especially on memory, was at the center of our interest. Participants in the study were 204 healthy adults (aged 20-55) who performed a multitasking cognitive test and completed dietary and psychological questionnaires. Stepwise regression analysis with age and food consumption patterns as predictors, and the cognitive task performance as a dependent variable, revealed that cognitive task performance worsened with age. However, we found that the frequency of consuming different types of foods (healthy versus unhealthy dietary patterns) moderates the effects of age on cognitive functioning. Red meat and animal fat consumption were negatively correlated with cognitive performance, and this relation was dependent on the age of our participants. Conversely, white meat and fish consumption were positively related to memory. Different indices of dietary patterns (both positive and negative) were stronger predictors of cognitive performance in the older adult group. We interpret our results as evidence that diet may be a protective (or worsening) factor in age-related cognitive decline.
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Cognición , Envejecimiento Cognitivo/psicología , Disfunción Cognitiva/dietoterapia , Dieta/efectos adversos , Conducta Alimentaria , Memoria , Adulto , Factores de Edad , Disfunción Cognitiva/diagnóstico , Disfunción Cognitiva/psicología , Dieta Saludable , Femenino , Humanos , Masculino , Persona de Mediana Edad , Valor Nutritivo , Factores Protectores , Medición de Riesgo , Factores de Riesgo , Conducta de Reducción del Riesgo , Adulto JovenRESUMEN
BACKGROUND: Dietary advanced glycation end-products (AGEs) are linked to cognitive decline. However, clinical trials have not tested the effect of AGEs on cognition in older adults. OBJECTIVE: The aim of the current pilot trial was to examine the feasibility of an intervention to reduce dietary AGEs on cognition and on cerebral blood flow (CBF). METHODS: The design is a pilot randomized controlled trial of dietary AGEs reduction in older adults with type 2 diabetes. Seventy-five participants were randomized to two arms. The control arm received standard of care (SOC) guidelines for good glycemic control; the intervention arm, in addition to SOC guidelines, were instructed to reduce their dietary AGEs intake. Global cognition and CBF were assessed at baseline and after 6 months of intervention. RESULTS: At baseline, we found a reverse association between AGEs and cognitive functioning, possibly reflecting the long-term toxicity of AGEs on the brain. There was a significant improvement in global cognition at 6 months in both the intervention and SOC groups which was more prominent in participants with mild cognitive impairment. We also found that at baseline, higher AGEs were associated with increased CBF in the left inferior parietal cortex; however, 6 months of the AGEs lowering intervention did not affect CBF levels, despite lowering AGEs exposure in blood. CONCLUSION: The current pilot trial focused on the feasibility and methodology of intervening through diet to reduce AGEs in older adults with type 2 diabetes. Our results suggest that participants with mild cognitive impairment may benefit from an intensive dietary intervention.
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Cognición/efectos de los fármacos , Disfunción Cognitiva/dietoterapia , Diabetes Mellitus Tipo 2/dietoterapia , Ingestión de Alimentos , Productos Finales de Glicación Avanzada/metabolismo , Anciano , Circulación Cerebrovascular/efectos de los fármacos , Diabetes Mellitus Tipo 2/sangre , Femenino , Productos Finales de Glicación Avanzada/sangre , Humanos , Imagen por Resonancia Magnética , Masculino , Pruebas Neuropsicológicas/estadística & datos numéricos , Proyectos Piloto , Encuestas y CuestionariosRESUMEN
Alzheimer's disease (AD) and other dementias are now the seventh leading cause of death in the world and are projected to affect 115.4 million people by 2050. Delaying the onset of AD by just five years is estimated to reduce the cost and prevalence of the disease by half. There is no cure for AD nor any drug therapies to halt its progression once the disease begins. Lifestyle choices including diet are being seen as a viable complementary therapy to reduce cognitive decline, the hallmark of AD. Mediterranean, DASH (Dietary Approaches to Stop Hypertension), and MIND (Mediterranean-DASH Intervention for Neurodegenerative Delay) diets have biological mechanisms supporting their potential neuroprotective benefits, but the findings of study outcomes about these benefits have been inconsistent. This paper analyzed five Randomized Clinical Trials (RCTs) (from 2000 to 2021) and 27 observational studies (from 2010 to 2021) focused on the link between cognitive health and the Mediterranean/DASH/MIND diets to identify gaps and challenges that could lead to inconsistent results. These include a lack of accuracy in assessing food intake, multiple dietary pattern scoring systems, a shifting metric among studies focused on the Mediterranean diet, a lack of standards in the tools used to assess cognitive decline, and studies that were underpowered or had follow-up periods too short to detect cognitive change. Insights from these gaps and challenges are summarized in recommendations for future RCTs, including both pragmatic and explanatory RCTs.
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Disfunción Cognitiva/dietoterapia , Dieta , Neuroprotección , Dieta Mediterránea , Enfoques Dietéticos para Detener la Hipertensión , Humanos , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
BACKGROUND: Extra virgin olive oil (EVOO) constitutes a natural compound with high protection over cognitive function that could positively alter brain dynamics and the mixture of within and between-frequency connectivity. OBJECTIVE: The balance of cross-frequency coupling over within-frequency coupling can build a nonlinearity index (NI) that encapsulates the over-excitation of information flow between brain areas and across experimental time. The present study investigated for the very first time how the Greek High Phenolic Early Harvest Extra Virgin Olive Oil (HP-EH-EVOO) versus Moderate Phenolic (MP-EVOO) and Mediterranean Diet (MeDi) intervention in people with mild cognitive impairment (MCI) could affect their spontaneous EEG dynamic connectivity. METHODS: Forty-three subjects (14 in MeDi, 16 in MP-EVOO, and 13 in HP-EH-EVOO) followed an EEG resting-state recording session (eyes-open and closed) before and after the treatment. Following our dominant coupling mode model, we built a dynamic integrated dynamic functional connectivity graph that tabulates the functional strength and the dominant coupling mode model of every pair of brain areas. RESULTS: Signal spectrum within 1-13 Hz and theta/beta ratio have decreased in the HP-EH-EVOO group in the eyes-open condition. The intervention improved the FIDoCM across groups and conditions but was more prominent in the HP-EH-EVOO group (pâ<â0.001). Finally, we revealed a significant higher post-intervention reduction of NI (ΔNITotal and α) for the HP-EH-EVOO compared to the MP-EVOO and MeDi groups (pâ<â0.0001). CONCLUSION: Long-term intervention with HP-EH-EVOO reduced the over-excitation of information flow in spontaneous brain activity and altered the signal spectrum of EEG rhythms.
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Cognición , Disfunción Cognitiva/dietoterapia , Dieta Mediterránea , Electroencefalografía/estadística & datos numéricos , Aceite de Oliva , Anciano , Encéfalo , Femenino , Grecia , Humanos , Masculino , Pruebas Neuropsicológicas/estadística & datos numéricos , Fenoles , Sustancias ProtectorasRESUMEN
BACKGROUND: A growing awareness about non-pharmacological intervention for cognitively impaired individuals may represent an alternative therapeutic approach that is actively accepted by patients with very early stage of Alzheimer's disease. Understanding the neural basis of non-pharmacological intervention is a crucial step toward wide use for patients with cognitive disorders. OBJECTIVE: To investigate the underlying neural mechanism of shentai tea polyphenols in subjects with subjective cognitive decline (SCD) using functional near-infrared spectroscopy (fNIRS). METHODS: A total number of 36 patients with SCD participated in the study and received supplementation with shentai tea polyphenols for three months. All participants underwent a series of tests on neuropsychological function and fNIRS assessment during n-back tasks at baseline and follow-up. RESULTS: After intervention with shentai tea polyphenols in SCD, increased cerebral activity was observed in left dorsolateral prefrontal cortex (DLPFC), left premotor cortex (PMC), left primary somatosensory cortex (PSC), right inferior frontal gyrus (IFG), and premotor cortex (PMC). Moreover, shentai tea polyphenols intervention of three months significantly improved SCD subjects' cognitive functions (memory, language, and subjective cognitive ability) and depression condition. We further found that the improvement of Hamilton Depression Rating Scale and Auditory Verbal Learning Test-recognition scores had positive correlations with increased brain activity in right IFG and left DLPFC, respectively. CONCLUSION: This study provides new evidence that the frontal cortex was found to be specifically activated after non-pharmacological intervention of shentai tea polyphenols in SCD, which may be associated with cognitive enhancement and mental wellbeing. These findings provide important implications for the selection of shentai tea polyphenols interventions for SCD.
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Cognición/fisiología , Disfunción Cognitiva/dietoterapia , Disfunción Cognitiva/metabolismo , Autoevaluación Diagnóstica , Polifenoles/administración & dosificación , Té , Anciano , China/epidemiología , Disfunción Cognitiva/diagnóstico , Femenino , Humanos , Estudios Longitudinales , Masculino , Persona de Mediana Edad , Espectroscopía Infrarroja Corta/métodosRESUMEN
Disturbed deoxythymidine triphosphate biosynthesis due to the inhibition of thymidylate synthase (TS) can lead to uracil accumulation in DNA, eventually, lead to neurocytes apoptosis and cognitive decline. Folic acid supplementation delayed cognitive decline and neurodegeneration in senescence-accelerated mouse prone 8 (SAMP8). Whether folic acid, one of nutrition factor, the effect on the expression of TS is unknown. The study aimed to determine if folic acid supplementation could alleviate age-related cognitive decline and apoptosis of neurocytes by increasing TS expression in SAMP8 mice. According to folic acid concentration in diet, four-month-old male SAMP8 mice were randomly divided into three different diet groups by baseline body weight in equal numbers. Moreover, to evaluate the role of TS, a TS inhibitor was injected intraperitoneal. Cognitive test, apoptosis rates of neurocytes, expression of TS, relative uracil level in telomere, and telomere length in brain tissue were detected. The results showed that folic acid supplementation decreased deoxyuridine monophosphate accumulation, uracil misincorporation in telomere, alleviated telomere length shorting, increased expression of TS, then decreased apoptosis rates of neurocytes, and alleviated cognitive performance in SAMP8 mice. Moreover, at the same concentration of folic acid, TS inhibitor raltitrexed increased deoxyuridine monophosphate accumulation, uracil misincorporation in telomere, and exacerbated telomere length shorting, decreased expression of TS, then increased apoptosis rates of neurocytes, and decreased cognitive performance in SAMP8 mice. In conclusion, folic acid supplementation alleviated age-related cognitive decline and inhibited apoptosis of neurocytes by increasing TS expression in SAMP8 mice.
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Envejecimiento , Encéfalo/metabolismo , Disfunción Cognitiva/dietoterapia , Suplementos Dietéticos , Ácido Fólico/administración & dosificación , Neuronas/fisiología , Nucleótidos de Timina/biosíntesis , Animales , Apoptosis , Ácido Fólico/sangre , Ácido Fólico/metabolismo , Masculino , Memoria , Ratones , Prueba del Laberinto Acuático de Morris , Quinazolinas/farmacología , Acortamiento del Telómero , Tiofenos/farmacología , Timidilato Sintasa/antagonistas & inhibidores , Timidilato Sintasa/genética , Timidilato Sintasa/metabolismo , Uracilo/metabolismoRESUMEN
Prolonged high-fat diet (HFD) feeding impairs cognitive function in rodents. However, the mechanism of caloric restriction (CR) for remedying HFD-induced cognitive dysfunction remains elusive. In the present study, we investigated the effect of CR on HFD-induced cognitive dysfunction and its possible mechanism. BALB/c mice were fed with HFD for 16 weeks and subsequently subjected to CR for 12 weeks. After cognitive function was evaluated by behavioral tests such as Morris water maze and three-chamber paradigm tests, the mice were sacrificed. The prefrontal cortex and hippocampus were rapidly harvested and deposited at -80 °C. The neuroprotective mechanisms of CR on HFD-induced cognitive deficits were evaluated by histopathological and electron microscopy observations, western blotting and immunofluorescence. Compared with the normal control group, HFD mice exhibited obvious cognitive deficits, glucose tolerance impairment, neuronal degeneration and abnormalities of synaptic ultrastructure in the cortex and hippocampus. CR treatment improved cognitive dysfunction and histopathological changes as well as increased the cognition-related protein levels of PSD-95, synaptophysin and BDNF. Meanwhile, HFD increased the protein levels of pro-inflammatory factors including iNOS, COX-2 and IL-1ß but decreased the protein levels of anti-inflammatory factors such as CD206, TGF-ß, Ym-1 and Arg 1 in the prefrontal cortex and hippocampus, downregulated the protein levels of TREM2 and PI3K and decreased the phosphorylation level of AKT, which can be reversed by CR treatment. Therefore, our results indicated that CR ameliorated cognitive deficits of mice induced by a high-fat diet. The underlying mechanism is associated with the attenuation of the neuroinflammatory response mediated by the TREM2-PI3K/AKT signaling pathway.
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Restricción Calórica/métodos , Disfunción Cognitiva/dietoterapia , Glicoproteínas de Membrana/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Receptores Inmunológicos/metabolismo , Animales , Cognición , Disfunción Cognitiva/metabolismo , Dieta Alta en Grasa/efectos adversos , Hipocampo/metabolismo , Inflamación/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Prueba del Laberinto Acuático de Morris , Corteza Prefrontal/metabolismo , Transducción de Señal , Sinaptofisina/metabolismoRESUMEN
Consuming a balanced, nutritious diet is important for maintaining health, especially as individuals age. Several studies suggest that consuming a diet rich in antioxidants and anti-inflammatory components such as those found in fruits, nuts, vegetables, and fish may reduce age-related cognitive decline and the risk of developing various neurodegenerative diseases. Numerous studies have been published over the last decade focusing on nutrition and how this impacts health. The main objective of the current article is to review the data linking the role of diet and nutrition with aging and age-related cognitive decline. Specifically, we discuss the roles of micronutrients and macronutrients and provide an overview of how the gut microbiota-gut-brain axis and nutrition impact brain function in general and cognitive processes in particular during aging. We propose that dietary interventions designed to optimize the levels of macro and micronutrients and maximize the functioning of the microbiota-gut-brain axis can be of therapeutic value for improving cognitive functioning, particularly during aging.
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Antioxidantes/uso terapéutico , Encéfalo/metabolismo , Disfunción Cognitiva/dietoterapia , Envejecimiento Saludable/fisiología , Encéfalo/efectos de los fármacos , Disfunción Cognitiva/metabolismo , Disfunción Cognitiva/patología , Frutas , Microbioma Gastrointestinal/efectos de los fármacos , Envejecimiento Saludable/metabolismo , Humanos , Micronutrientes/uso terapéutico , Evaluación Nutricional , Estado Nutricional , Nueces , VerdurasRESUMEN
INTRODUCTION: Mild cognitive impairment (MCI) is often accompanied by metabolic abnormalities and inflammation that might play a role in the development of cognitive impairment. The use of ketogenic medium-chain triglycerides (kMCT) to improve cognition in this population has shown promising results but remains controversial because of the potentially detrimental effect of elevated intake of saturated fatty acids on cardiovascular (CV) health and perhaps inflammatory processes. The primary aim of this secondary data analysis report is to describe changes in cardiometabolic markers and peripheral inflammation during a 6-month kMCT intervention in MCI. METHODS: Thirty-nine participants with MCI completed the intervention of 30 g/day of either a kMCT drink or calorie-matched placebo (high-oleic acid) for 6 months. Plasma concentrations of cardiometabolic and inflammatory markers were collected before (fasting state) and after the intervention (2 h following the last drink). RESULTS: A mixed model ANOVA analysis revealed a time by group interaction for ketones (P < 0.001), plasma 8:0 and 10:0 acids (both P < 0.001) and IL-8 (P = 0.002) with follow up comparison revealing a significant increase in the kMCT group (+48%, P = 0.005), (+3,800 and +4,900%, both P < 0.001) and (+147%, P < 0.001) respectively. A main effect of time was observed for insulin (P = 0.004), triglycerides (P = 0.011) and non-esterified fatty acids (P = 0.036). CONCLUSION: Under these study conditions, 30 g/d of kMCT taken for six months and up to 2-hour before post-intervention testing had minimal effect on an extensive profile of circulating cardiometabolic and inflammatory markers as compared to a placebo calorie-matched drink. Our results support the safety kMCT supplementation in individuals with MCI. The clinical significance of the observed increase in circulating IL-8 levels is presently unknown and awaits future studies.
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Disfunción Cognitiva/dietoterapia , Ácidos Grasos/sangre , Insulina/sangre , Interleucina-8/sangre , Triglicéridos/administración & dosificación , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Disfunción Cognitiva/sangre , Dieta Cetogénica , Esquema de Medicación , Ayuno/sangre , Femenino , Humanos , Masculino , Resultado del Tratamiento , Triglicéridos/farmacocinéticaRESUMEN
Aging is inevitable and it is one of the major contributors to cognitive decline. However, the mechanisms underlying age-related cognitive decline are still the object of extensive research. At the biological level, it is unknown how the aging brain is subjected to progressive oxidative stress and neuroinflammation which determine, among others, mitochondrial dysfunction. The link between mitochondrial dysfunction and cognitive impairment is becoming ever more clear by the presence of significant neurological disturbances in human mitochondrial diseases. Possibly, the most important lifestyle factor determining mitochondrial functioning is nutrition. Therefore, with the present work, we review the latest findings disclosing a link between nutrition, mitochondrial functioning and cognition, and pave new ways to counteract cognitive decline in late adulthood through diet.