Increased cerebrospinal fluid and plasma apoE glycosylation is associated with reduced levels of Alzheimer's disease biomarkers.

The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). ApoE is glycosylated with an O-linked Core-1 sialylated glycan at several sites; however, the impact and function of this glycosylation on AD biomarkers remain unclear. We examined apoE glycosylation (total and secondary) in a cohort of cerebrospinal fluid (CSF, n = 181) and plasma (n = 178) samples from the Alzheimer's Disease Neuroimaging Initiative (ADNI) stratified into 4 groups: cognitively normal (CN), Mild Cognitive Impairment (MCI), progressors, and non-progressors based on delayed word recall performance over 4 years.

Utility of plasma GFAP as a secondary endpoint for clinical trials in Alzheimer's disease.

Background: Clinical trials have recently incorporated plasma glial fibrillary acidic protein (GFAP) as an exploratory endpoint. To include plasma GFAP as a secondary endpoint, it is essential to characterize its longitudinal progression in target populations.

Objective: To evaluate the potential use of plasma GFAP changes as a secondary endpoint in Alzheimer's disease trials.

Deregulation of Neuroinflammatory and Neurotrophic Factors as Biological Events Triggered by D-Galactose Chronic Administration in Wistar Rats.

The chronic administration of D-galactose (D-gal) is widely used to model brain senescence in rodents. However, the effects of prolonged oral exposure of D-gal on the neuroinflammatory cytokines in rats remain poorly characterized. Therefore, we administered D-gal (100 mg/kg) in male Wistar rats aged 3-4 months, via oral gavage once a day for 1, 2, 4, 6, or 8 weeks.

Increased cerebrospinal fluid and plasma apoE glycosylation is associated with reduced levels of Alzheimer's disease biomarkers.

The apolipoprotein E ( ) ε4 allele is the strongest genetic risk factor for Alzheimer's disease (AD). ApoE is glycosylated with an O-linked Core-1 sialylated glycan at several sites, yet the impact and function of this glycosylation on AD biomarkers remains unclear. We examined apoE glycosylation in a cohort of cerebrospinal fluid (CSF, n=181) and plasma (n= 178) samples from the Alzheimer's Disease Neuroimaging Initiative (ADNI) stratified into 4 groups: cognitively normal (CN), Mild Cognitive Impairment (MCI), progressors and non-progressors based on delayed word recall performance over 4 years.

Histone 3 Trimethylation Patterns are Associated with Resilience or Stress Susceptibility in a Rat Model of Major Depression Disorder.

Major Depressive Disorder (MDD) is a severe and multifactorial psychiatric condition. Evidence has shown that environmental factors, such as stress, significantly explain MDD pathophysiology. Studies have hypothesized that changes in histone methylation patterns are involved in impaired glutamatergic signaling.

Microglia contribute to cognitive decline in hypercholesterolemic LDLr mice.

Familial hypercholesterolemia (FH) is caused by mutations in the gene that encodes the low-density lipoprotein (LDL) receptor, which leads to an excessive increase in plasma LDL cholesterol levels. Previous studies have shown that FH is associated with gliosis, blood-brain barrier dysfunction, and memory impairment, but the mechanisms associated with these events are still not fully understood. Therefore, we aimed to investigate the role of microgliosis in the neurochemical and behavioral changes associated with FH using LDL receptor knockout (LDLr) mice.

Sodium Butyrate Protects Against Intestinal Oxidative Damage and Neuroinflammation in the Prefrontal Cortex of Ulcerative Colitis Mice Model.

Inflammatory bowel diseases (IBD) cause increased inflammatory signalling and oxidative damage. IBDs are correlated with an increased incidence of brain-related disorders suggesting that the gut-brain-axis exerts a pivotal role in IBD. Butyrate is one of the main microbial metabolites in the colon, and it can cross the blood-brain barrier, directly affecting the brain.

Role of Oxidative Stress on Insulin Resistance in Diet-Induced Obesity Mice.

Insulin resistance is the link between obesity and type 2 diabetes mellitus. The molecular mechanism by which obese individuals develop insulin resistance has not yet been fully elucidated; however, inconclusive and contradictory studies have shown that oxidative stress may be involved in the process. Thus, this study aimed to evaluate the effect of reactive species on the mechanism of insulin resistance in diet-induced obese mice.

Neuroprotective effects of combined therapy with memantine, donepezil, and vitamin D in ovariectomized female mice subjected to dementia model.

Women older than 60 have a higher risk of dementia, aging-related cognitive decline, and Alzheimer's Disease (AD) than the rest of the population. The main reason is hormonal senescence after menopause, a period characterized by a decline in estrogen levels. Since the effectiveness of drugs currently approved for the treatment of AD is limited, it is necessary to seek the development of new therapeutic strategies.

Gold nanoparticles application to the treatment of brain dysfunctions related to metabolic diseases: evidence from experimental studies.

Nanotechnology is an emerging and expanding technology worldwide. The manipulation of materials on a nanometric scale generates new products with unique properties called nanomaterials. Due to its significant expansion, nanotechnology has been applied in several fields of study, including developing materials for biomedical applications, i.

Inflammatory Cascade in Alzheimer's Disease Pathogenesis: A Review of Experimental Findings.

Alzheimer's disease (AD) is the leading cause of dementia worldwide. Most AD patients develop the disease in late life, named late onset AD (LOAD). Currently, the most recognized explanation for AD pathology is the amyloid cascade hypothesis.

Nanotechnology as a therapeutic strategy to prevent neuropsychomotor alterations associated with hypercholesterolemia.

Hypercholesterolemia has been linked to neurodegenerative disease development. Previously others and we demonstrated that high levels of plasma cholesterol-induced memory impairments and depressive-like behavior in mice. More recently, some evidence reported that a hypercholesterolemic diet led to motor alterations in rodents.

Reduction of oxidative stress improves insulin signaling in cardiac tissue of obese mice.

Objective: To evaluate the effects of oxidative stress on insulin signaling in cardiac tissue of obese mice.

Methods: Thirty Swiss mice were equally divided (n=10) into three groups: Control Group, Obese Group, and Obese Group Treated with N-acetylcysteine. After obesity and insulin resistance were established, the obese mice were treated with N-acetylcysteine at a dose of 50mg/kg daily for 15 days via oral gavage.

Fish oil reduces subclinical inflammation, insulin resistance, and atherogenic factors in overweight/obese type 2 diabetes mellitus patients: A pre-post pilot study.

Objective: Insulin resistance-associated obesity and type 2 diabetes mellitus (T2DM) are commonly accompanied with metabolic lipid abnormalities and are characterized by hypertriglyceridemia and low HDL-c levels (atherogenic index plasma, AIP). The primary molecular mechanism that is known to cause insulin resistance is chronic low-grade inflammation. Considering that omega-3 fatty acid reduces subclinical inflammation, we hypothesized that fish oil could affect insulin resistance and AIP.

Strength training and aerobic exercise alter mitochondrial parameters in brown adipose tissue and equally reduce body adiposity in aged rats.

With aging, there is a reduction in mitochondrial activity, and several changes occur in the body composition, including increased adiposity. The dysfunction of mitochondrial activity causes changes and adaptations in tissue catabolic characteristics. Among them, we can mention brown adipose tissue (BAT).