Metabolic brain disease最新文献

{"title":"Exosomes and non-coding RNAs: bridging the gap in Alzheimer's pathogenesis and therapeutics.","authors":"Guo Chunhui, You Yanqiu, Chen Jibing, Luo Ning, Li Fujun","doi":"10.1007/s11011-024-01520-7","DOIUrl":"10.1007/s11011-024-01520-7","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disease that primarily affects the elderly population and is the leading cause of dementia. Meanwhile, the vascular hypothesis suggests that vascular damage occurs in the early stages of the disease, leading to neurodegeneration and hindered waste clearance, which in turn triggers a series of events including the accumulation of amyloid plaques and Tau protein tangles. Non-coding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been found to be involved in the regulation of AD. Furthermore, lncRNAs and circRNAs can act as competitive endogenous RNAs to inhibit miRNAs, and their interactions can form a complex regulatory network. Exosomes, which are extracellular vesicles (EVs), are believed to be able to transfer ncRNAs between cells, thus playing a regulatory role in the brain by crossing the blood-brain barrier (BBB). Exosomes are part of the intercellular carrier system; therefore, utilizing exosomes to deliver drugs to recipient cells might not activate the immune system, making it a potential strategy to treat central nervous system diseases. In this review, we review that AD is a multifactorial neurological disease and that ncRNAs can regulate its multiple pathogenic mechanisms to improve our understanding of the etiology of AD and to simultaneously regulate multiple pathogenic mechanisms of AD through the binding of ncRNAs to exosomes to improve the treatment of AD.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"84"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring SERPINA3 as a neuroinflammatory modulator in Alzheimer's disease with sex and regional brain variations.","authors":"Cristina Sanfilippo, Paola Castrogiovanni, Rosa Imbesi, Michele Vecchio, Martina Sortino, Giuseppe Musumeci, Manlio Vinciguerra, Michelino Di Rosa","doi":"10.1007/s11011-024-01523-4","DOIUrl":"10.1007/s11011-024-01523-4","url":null,"abstract":"<p><p>SERPINA3, a serine protease inhibitor, is strongly associated with neuroinflammation, a typical condition of AD. Its expression is linked to microglial and astrocytic markers, suggesting it plays a significant role in modulating neuroinflammatory responses. In this study, we examined the SERPINA3 expression levels, along with CHI3L1, in various brain regions of AD patients and non-demented healthy controls (NDHC). Nineteen microarray datasets were analyzed, with brain samples stratified by sex and age from areas including the prefrontal cortex, occipital lobe, and cerebellum. Results showed that SERPINA3 was significantly highly expressed in AD patients compared to NDHCs only in males. Sex-specific differences were observed only in NDHCs, where females had higher SERPINA3 levels than males. ROC analysis suggested that SERPINA3 could be a strong marker for distinguishing AD in males but not females. In NDHCs, SERPINA3 expression correlated more strongly with age than in AD patients. In brain regions, SERPINA3 expression in NDHC females was higher across multiple areas, while in AD patients, this difference was limited to the prefrontal cortex. The most significant differences between NDHC and AD patients were found in the occipital and prefrontal regions. Furthermore, we identified a potential nuclear localization for SERPINA3, supported by immunohistochemistry analysis from The Human Protein Atlas. Correlation with neuropathological traits, including Clinical Dementia Rating (CDR) and Braak Neurofibrillary Tangle Score, showed positive significant associations between SERPINA3 and CDR in AD patients. Performing a docking analysis, we revealed an interaction region between SERPINA3 and CHI3L1 proteins, suggesting a potential role in AD. Tissue transcriptomic deconvolution analysis indicated a significant overlap between SERPINA3 expression and microglial/astrocytic signatures, suggesting that SERPINA3 plays a key role in modulating neuroinflammation in AD.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"83"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chitosan lactate improves repeated closed head injury-generated motor and neurological dysfunctions in mice by impacting microbiota gut-brain axis.","authors":"Mohd Rabi Bazaz, Hara Prasad Padhy, Manoj P Dandekar","doi":"10.1007/s11011-024-01517-2","DOIUrl":"10.1007/s11011-024-01517-2","url":null,"abstract":"<p><p>The negative impact of repeated-mild traumatic brain injury (rmTBI) is profoundly seen in circadian-disrupted individuals. The unrelenting inflammation, glial activation, and gut dysbiosis are key neuropathological aberrations in the aftermath of rmTBI. In this study, we examined the impact of chitosan lactate (CL) on circadian disturbance (CD) + rmTBI-generated neurological dysfunctions and its prebiotic response on the gut-brain axis. Adult C57BL/6 mice were exposed to circadian disruption (CD) prior to rmTBI insults. The neurobehavioral changes were assessed by rotarod, open-field test (OFT), elevated zero maze (EZM), forced-swim test (FST), Y-maze, and novel object recognition test (NORT). The inflammatory, neuronal, and synaptic markers in the frontal cortex and hippocampus, and cecal gut microbiota phylum were examined using RT-PCR and western blotting. The goblet cells, tight junction proteins (occludin and zona occludens-1), and short-chain fatty acids (SCFAs) were analyzed using immunohistochemistry, alcian-blue PAS staining, and ¹H-NMR methods. Mice exposed to CD + rmTBI (CDR) displayed robust neurological dysfunctions in rotarod, anxiety- and depressive-like behavior in EZM and FST, and cognition deficits in Y-maze and NORT. Administration of CL (1 and 3 mg/kg) mitigated the above neurobehavioral abnormalities. CL treatment also normalized the levels of inflammatory markers (NF-κB, IL-6, IL-18, and TNF-α), brain-derived neurotrophic factor, and neuronal/synaptic proteins (doublecortin, synaptophysin, and postsynaptic density protein-95). Increased goblet cells and tight junction proteins in the colon and SCFAs in the cecal samples indicated improved gut integrity following CL treatment. The results indicate that CL mitigated CDR-inflicted neurological abnormalities in mice by modulating neuroinflammation and gut-brain interactions.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"81"},"PeriodicalIF":3.2,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral oxygen saturation in cirrhotic patients with gastro-intestinal bleeding, a near infrared spectroscopy study.","authors":"Maxime Mallet, Simona Tripon, Marika Rudler, Julien Mayaux, Dominique Thabut, Nicolas Weiss","doi":"10.1007/s11011-024-01466-w","DOIUrl":"10.1007/s11011-024-01466-w","url":null,"abstract":"<p><p>Near Infrared Spectroscopy (NIRS) is a non-invasive optical technique allowing a continuous measurement of brain's hemoglobin (Hb) saturation in oxygen (rSO2). It is a marker of cerebral insult and rSO2 < 50% is associated with increased neurological impairment. Cirrhotic patients with gastrointestinal bleeding (GIB) often develop hepatic encephalopathy (HE). The aims of this study were: (1) to assess brain oxygenation using NIRS in cirrhotic patients with GIB, (2) to determine if brain oxygenation was correlated to Hb level, blood pressure and liver function (3) if brain oxygenation was influencing the occurrence of HE and survival. Cirrhotic patients admitted to ICU for GIB were prospectively included and compared to non-cirrhotic patients. Bilateral recording of rSO2 was started upon admission using an INVOS 5100c Cerebral Oxymeter (Covidien). Initial, minimal, average rSO2 and AUC of rSO2 < 50% (AUC50% rSO2) were extracted. Sixty-one cirrhotic and 14 non-cirrhotic patients were included. Child-Pugh score was at 9.5 ± 0.3 and MELD score was 17.8 ± 0.9. None of the NIRS parameters differed between cirrhotic and non-cirrhotic patients. Thirty-nine patients (64%) among the 61 cirrhotic and 10 (71%) among the 14 non-cirrhotic patients displayed an initial rSO2 below the 50% threshold at least on one side. NIRS parameters correlated mainly with Hb level and MELD but not with MAP or PaO2. There was no significant correlation between NIRS parameters and survival or HE upon admission, within 5 days and after discharge. Patients with GIB frequently present rSO2 below the threshold of 50%. The significance of this finding is uncertain since it does not seem clearly correlated to a poor outcome in ICU or in the follow-up.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"80"},"PeriodicalIF":3.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective diagnostics of Amyotrophic Lateral Sclerosis, Alzheimer's and Parkinson's Diseases with machine learning and miRNA.","authors":"Juhyeok Lee, Valentina L Kouznetsova, Santosh Kesari, Igor Tsigelny","doi":"10.1007/s11011-024-01490-w","DOIUrl":"10.1007/s11011-024-01490-w","url":null,"abstract":"<p><p>The diagnosis of neurological diseases can be expensive, invasive, and inaccurate, as it is often difficult to distinguish between different types of diseases with similar motor symptoms. However, the dysregulation of miRNAs can be used to create a robust machine-learning model for a reliable diagnosis of neurological diseases. We used miRNA sequence descriptors and gene target data to create machine-learning models that can be used as diagnostic tools. The top-performing machine-learning models, trained on filtered miRNA datasets for Amyotrophic Lateral Sclerosis, Alzheimer's and Parkinson's Diseases of this research yielded 94, 97, and 96, percent accuracies, respectively. Analysis of dysregulated miRNA in neurological diseases elucidated novel biomarkers that could be used to diagnose and distinguish between the diseases. Machine-learning models developed using sequence and gene target descriptors of miRNA biomarkers can achieve favorable accuracies for disease classification and attain a robust discerning capability of neurological diseases.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"79"},"PeriodicalIF":3.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship between dyslipidemia and diabetic neuropathy: a mendelian randomization study.","authors":"Cong Li, Yu Feng, Lina Feng, Mingquan Li","doi":"10.1007/s11011-024-01448-y","DOIUrl":"10.1007/s11011-024-01448-y","url":null,"abstract":"<p><p>Some studies have shown an association between dyslipidemia and diabetic neuropathy (DN), but the genetic association has not been clarified. Therefore, the present study aimed to investigate the genetic causal association between dyslipidemia and DN through a Mendelian randomization (MR) approach. Genetic causal associations between total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL), and high-density lipoprotein cholesterol (HDL) and DN were investigated by MR to provide a basis for the prevention and treatment of DN. Significant and independent single-nucleotide polymorphisms (SNPs) identified in genome-wide association studies were selected as instrumental variables (IVs) for MR analysis. Inverse variance weighted (IVW), MR‒Egger regression, weighted median (WME), simple mode (SM), and weighted mode (WM) methods were used to analyze causal associations. Heterogeneity and multiplicity tests were also performed and analyzed using the leave-one-out method to assess the stability of the results. Genetically predicted TC and DN (OR = 0.793, 95% CI = 0.655⁓0.961, P = 0.019) and LDL and DN (OR = 0.842, 95% CI = 0.711⁓0.998, P = 0.049) may be causally associated, but no causal associations were found between TG and DN (OR = 0.837, 95% CI = 0.631⁓1.111, P = 0.221) or between HDL and DN (OR = 1.192, 95% CI = 0.940⁓1.510, P = 0.149). TC and LDL may have genetic causal associations with DN, though no genetic causal associations were found for TG or HDL with DN. However, this study may have several limitations, and further clinical studies are needed to expand the sample size for future validation.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"78"},"PeriodicalIF":3.2,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142895807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular intersections of traumatic brain injury and Alzheimer's disease: the role of ADMSC-derived exosomes and hub genes in microglial polarization.","authors":"Pengtao Li, Liguo Ye, Sishuai Sun, Yue Wang, Yihao Chen, Jianbo Chang, Rui Yin, Xiaoyu Liu, Wei Zuo, Houshi Xu, Xiao Zhang, Robert Chunhua Zhao, Qin Han, Junji Wei","doi":"10.1007/s11011-024-01503-8","DOIUrl":"10.1007/s11011-024-01503-8","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is a significant contributor to global mortality and morbidity, with emerging evidence indicating a heightened risk of developing Alzheimer's disease (AD) following TBI. This study aimed to explore the molecular intersections between TBI and AD, focusing on the role of adipose mesenchymal stem cell (ADMSC)-derived exosomes and hub genes involved in microglial polarization. Transcriptome profiles from TBI (GSE58485) and AD (GSE74614) datasets were analyzed to identify differentially expressed genes (DEGs). The hub genes were validated in independent datasets (GSE180811 for TBI and GSE135999 for AD) and localized to specific cell types using single-cell RNA (scRNA) sequencing data (GSE160763 for TBI and GSE224398 for AD). Experimental validation was conducted to investigate the role of these genes in microglial polarization using cell culture and ADMSC-derived exosomes interventions. Our results identified three hub genes-Bst2, B2m, and Lgals3bp-that were upregulated in both TBI and AD, with strong associations to inflammation, neuronal apoptosis, and tissue repair processes. scRNA sequencing revealed that these genes are predominantly expressed in microglia, with increased expression during M1 polarization. Knockdown of these genes reduced M1 polarization and promoted M2 phenotype in microglia. Additionally, ADMSC-derived exosomes attenuated M1 polarization and downregulated the expression of hub genes. This study provides novel insights into the shared molecular pathways between TBI and AD, highlighting potential therapeutic targets for mitigating neuroinflammation and promoting recovery in both conditions.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"77"},"PeriodicalIF":3.2,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parkia biglobosa Jacq. (Locust Bean) leaves and seeds extracts attenuates diabetic-linked cognitive dysfunction in streptozotocin-induced male wistar rats.","authors":"Oluwapelumi M Ajiboye, Kayode O Ogunwenmo, Aderiike G Adewumi, Clinton C Mohanye","doi":"10.1007/s11011-024-01514-5","DOIUrl":"10.1007/s11011-024-01514-5","url":null,"abstract":"<p><p>Diabetes Mellitus is a metabolic disorder characterized by high blood glucose levels, causing significant morbidity and mortality rates. This study investigated the antidiabetic, neuroprotective, and antioxidant effects of ethanol extracts of Parkia biglobosa (PB) leaves and seeds in streptozotocin (STZ)-induced diabetic rats. The administration of STZ significantly elevated fasting blood glucose levels (FBGL) to 355-400 mg/mL compared to 111 mg/mL in normal controls, indicating hyperglycemia. Treatment with PB extracts at 100 mg/kg and 200 mg/kg significantly (p < 0.05) reduced FBGL in a dose-dependent manner. No significant difference was observed between the effects of metformin and PB extracts at 200 mg/kg. Cognitive dysfunction, assessed using the Y-maze test, was significantly improved in groups treated with PB extracts (p < 0.05), particularly at 200 mg/kg, through inhibition of cholinesterase activity and protection against oxidative damage. Both PB extracts also demonstrated significant inhibition (p < 0.05) of α-amylase and α-glucosidase activity, reducing postprandial hyperglycemia, with a stronger inhibition at 200 mg/kg. Additionally, PB extracts significantly increased catalase (CAT) and superoxide dismutase (SOD) activities, reversing the diabetes-induced decline in antioxidant enzyme levels. Monoamine oxidase (MAO) activity, elevated in diabetic conditions, was significantly downregulated by PB treatment, further contributing to neuroprotection. The neuroprotective effects may be attributed to the inhibition of cholinesterase and MAO, which help maintain neurotransmitter levels, alongside the antioxidant properties that mitigate oxidative stress in the brain. These findings suggest that PB extracts could serve as a natural therapeutic agent for diabetes management, with its effects comparable to metformin at higher doses.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"76"},"PeriodicalIF":3.2,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMG-CoA reductase inhibitor simvastatin ameliorates trimethyltin neurotoxicity and cognitive impairment through reversal of Alzheimer's-associated markers.","authors":"Adel Salari, Mehrdad Roghani, Mohsen Khalili","doi":"10.1007/s11011-024-01515-4","DOIUrl":"10.1007/s11011-024-01515-4","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a prevalent neurodegenerative disorder in elderly. The neurotoxicant trimethyltin (TMT) induces neurodegenerative changes, as observed in AD. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin (SV) has shown protective and promising therapeutic effects in neurological disorders such as AD and Parkinson's disease. The present study aimed to assess neuroprotective effect of simvastatin (SV) against trimethyltin (TMT) memory decline and hippocampal neurodegeneration. For inducing AD-like phenotype, rats were i.p. injected with TMT at 8 mg/kg and were treated with simvastatin daily for 3 weeks at 10 or 30 mg/kg. Our analysis of data indicated that simvastatin-treated TMT group has lower learning and memory deficits in behavioral tasks comprising Barnes maze, Y maze, and novel object discrimination (NOD). In addition, hippocampal inflammatory, oxidative, and apoptotic factors were attenuated besides reduction of acetylcholinesterase (AChE) activity and Alzheimer's pathology factors including presenilin-1 and hyperphorphorylated Tau (p-Tau) upon simvastatin. Moreover, simvastatin treatment of TMT group inverted hippocampal changes of Wnt, β-catenin, ERK, and Akt, ameliorated astrocytic and microglial reactivity, and also prevented injury of CA1 neurons. This study unraveled that simvastatin is capable to prevent TMT-induced Alzheimer's-like phenotype in association with Wnt/β-catenin/ERK/Akt as well as restraining hippocampal neurodegeneration.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"74"},"PeriodicalIF":3.2,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactobacillus fermentum MCC2760 attenuates neurobehavioral alterations induced by oxidized oils in rats.","authors":"Vyshali Keremane, Hamsavi Kamala, Prakash Halami, Ramaprasad Talahalli","doi":"10.1007/s11011-024-01509-2","DOIUrl":"10.1007/s11011-024-01509-2","url":null,"abstract":"<p><p>The common practice of reusing deep-fried oil may derange the ability of the brain to counter free radicals and inflammatory responses and can adversely alter neurobehavioral changes. In this study, we elucidated the modulatory potentials of Lactobacillus fermentum MCC2760 (LF) on neurobehavioral changes induced by dietary intake of oxidized oils. Female Wistar rats were fed with AIN-76 diets containing native sunflower oil (N-SFO), native canola oil (N-CNO), heated sunflower oil (H-SFO), heated canola oil (H-CNO), heated sunflower oil with probiotic (H-SFO + LF) or heated canola oil with probiotic (H-CNO + LF} for 60 days. After 60 days of feeding, they were mated with adult male rats. Upon mating confirmation, pregnant dams were continued on their respective diets until delivery. After delivery and post-lactation, F2 generation males (n = 6) were continued on a diet similar to their mothers for 60 days. Memory parameters [Morris water maze, Y-maze (spontaneous alteration), and novel object recognition test], locomotor skills and endurance (open field test and rotarod test), and anxiety test (elevated plus maze) were assessed in F2 generation males weighing 270 ± 10 g. Compared to their respective controls, heated oil-fed rats showed a significant (p < 0.05) decrease in memory and motor coordination skills, whereas a significant (p < 0.05) increase in anxiety-like behavior. However, administration of LF (10⁹ CFU/day/rat) ameliorated the heated oil-induced neurobehavioral changes. Hence, the present study establishes that long-term consumption of thermally oxidized oil is detrimental to critical brain functions, including cognitive attributes. Dietary supplementation of probiotics may effectively counter the oxidized oil-induced cognitive loss.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"75"},"PeriodicalIF":3.2,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}