Differential impact of eicosapentaenoic acid and docosahexaenoic acid in an animal model of Alzheimer's disease.

Dietary supplementation with n-3 polyunsaturated fatty acids improves cognitive performance in several animal models of Alzheimer's disease (AD), an effect often associated with reduced amyloid-beta and/or tau pathologies. However, it remains unclear to what extent eicosapentaenoic (EPA) provides additional benefits compared to docosahexaenoic acid (DHA). Here, male and female 3xTg-AD mice were fed for 3 months (13-16 months of age) the following diets: (1) control (no DHA/EPA), (2) DHA (1.

Impact of processing steps (filtration, creaming and pasteurization) on the botanical classification of honey using LC-QTOF-MS.

The present study investigated the impact of filtration, creaming and pasteurization on the authentication of the botanical origin of honey using the dilute-and-shoot method in liquid chromatography coupled to mass spectrometry (LC-MS). The analytical method performances were satisfactory (analyte recoveries ranging from 95 % to 103 % and inter-day precision below 12 %). Three types of raw honeys including blueberry, canola and clover were processed under controlled conditions.

Effects of summer treatments against Varroa destructor on viral load and colony performance of Apis mellifera colonies in Eastern Canada.

Despite the use of various integrated pest management strategies to control the honey bee mite, Varroa destructor, varroosis remains the most important threat to honey bee colony health in many countries. In Canada, ineffective varroa control is linked to high winter colony losses and new treatment options, such as a summer treatment, are greatly needed. In this study, a total of 135 colonies located in 6 apiaries were submitted to one of these 3 varroa treatment strategies: (i) an Apivar® fall treatment followed by an oxalic acid (OA) treatment by dripping method; (ii) same as in (i) with a summer treatment consisting of formic acid (Formic Pro™); and (iii) same as in (i) with a summer treatment consisting of slow-release OA/glycerin pads (total of 27 g of OA/colony).

Age-dependent impact of streptozotocin on metabolic endpoints and Alzheimer's disease pathologies in 3xTg-AD mice.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disease with a complex origin, thought to involve a combination of genetic, biological and environmental factors. Insulin dysfunction has emerged as a potential factor contributing to AD pathogenesis, particularly in individuals with diabetes, and among those with insulin deficiency or undergoing insulin therapy. The intraperitoneal administration of streptozotocin (STZ) is widely used in rodent models to explore the impact of insulin deficiency on AD pathology, although prior research predominantly focused on young animals, with no comparative analysis across different age groups.

Methods for Biochemical Isolation of Insoluble Tau in Rodent Models of Tauopathies.

The intracellular accumulation of microtubule-associated protein tau is a characteristic feature of tauopathies, a group of neurodegenerative diseases including Alzheimer's disease. Formation of insoluble tau aggregates is initiated by the abnormal hyperphosphorylation and oligomerization of tau. Over the past decades, multiple transgenic rodent models mimicking tauopathies have been develop, showcasing this neuropathological hallmark.

Honeybees as a biomonitoring species to assess environmental airborne pollution in different socioeconomic city districts.

Honeybees have been used in Europe as environmental bioindicators for heavy metals and polycyclic aromatic hydrocarbons (PAHs). However, their potential has been little explored in North America, especially between environments which have similar pollution levels. Many urban residents and stakeholders are concerned with air quality, mainly in regard to gradients of exposure to industrial pollution between deprived and privileged subpopulation.

In vivo induction of membrane damage by β-amyloid peptide oligomers.

Exposure to the β-amyloid peptide (Aβ) is toxic to neurons and other cell types, but the mechanism(s) involved are still unresolved. Synthetic Aβ oligomers can induce ion-permeable pores in synthetic membranes, but whether this ability to damage membranes plays a role in the ability of Aβ oligomers to induce tau hyperphosphorylation, or other disease-relevant pathological changes, is unclear. To examine the cellular responses to Aβ exposure independent of possible receptor interactions, we have developed an in vivo C.

Tau hyperphosphorylation in the brain of ob/ob mice is due to hypothermia: Importance of thermoregulation in linking diabetes and Alzheimer's disease.

Over the last few decades, there has been a significant increase in epidemiological studies suggesting that type 2 diabetes (T2DM) is linked to a higher risk of Alzheimer's disease (AD). However, how T2DM affects AD pathology, such as tau hyperphosphorylation, is not well understood. In this study, we investigated the impact of T2DM on tau phosphorylation in ob/ob mice, a spontaneous genetic model of T2DM.

Hypothermia mediates age-dependent increase of tau phosphorylation in db/db mice.

Accumulating evidence from epidemiological studies suggest that type 2 diabetes is linked to an increased risk of Alzheimer's disease (AD). However, the consequences of type 2 diabetes on AD pathologies, such as tau hyperphosphorylation, are not well understood. Here, we evaluated the impact of type 2 diabetes on tau phosphorylation in db/db diabetic mice aged 4 and 26weeks.

Conserved pharmacological rescue of hereditary spastic paraplegia-related phenotypes across model organisms.

Hereditary spastic paraplegias (HSPs) are a group of neurodegenerative diseases causing progressive gait dysfunction. Over 50 genes have now been associated with HSP. Despite the recent explosion in genetic knowledge, HSP remains without pharmacological treatment.

Tau hyperphosphorylation and deregulation of calcineurin in mouse models of Huntington's disease.

Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by polyglutamine expansions in the amino-terminal region of the huntingtin (Htt) protein. At the cellular level, neuronal death is accompanied by the proteolytic cleavage, misfolding and aggregation of huntingtin. Abnormal hyperphosphorylation of tau protein is a characteristic feature of a class of neurodegenerative diseases called tauopathies.

Anesthesia-induced hypothermia mediates decreased ARC gene and protein expression through ERK/MAPK inactivation.

Several anesthetics have been reported to suppress the transcription of a number of genes, including Arc, also known as Arg3.1, an immediate early gene that plays a significant role in memory consolidation. The purpose of this study was to explore the mechanism of anesthesia-mediated depression in Arc gene and protein expression.

Evaluation of longevity enhancing compounds against transactive response DNA-binding protein-43 neuronal toxicity.

In simple systems, lifespan can be extended by various methods including dietary restriction, mutations in the insulin/insulin-like growth factor (IGF) pathway or mitochondria among other processes. It is widely held that the mechanisms that extend lifespan may be adapted for diminishing age-associated pathologies. We tested whether a number of compounds reported to extend lifespan in C.

Pharmacological reduction of ER stress protects against TDP-43 neuronal toxicity in vivo.

C. elegans and D. rerio expressing mutant TAR DNA Binding Protein 43 (TDP-43) are powerful in vivo animal models for the genetics and pharmacology of amyotrophic lateral sclerosis (ALS).

Sex-dependent alterations in social behaviour and cortical synaptic activity coincide at different ages in a model of Alzheimer's disease.

Besides memory deficits, Alzheimer's disease (AD) patients suffer from neuropsychiatric symptoms, including alterations in social interactions, which are subject of a growing number of investigations in transgenic models of AD. Yet the biological mechanisms underlying these behavioural alterations are poorly understood. Here, a social interaction paradigm was used to assess social dysfunction in the triple-transgenic mouse model of AD (3xTg-AD).

Deregulation of protein phosphatase 2A and hyperphosphorylation of τ protein following onset of diabetes in NOD mice.

The histopathological hallmarks of Alzheimer disease (AD) include intraneuronal neurofibrillary tangles composed of abnormally hyperphosphorylated τ protein. Insulin dysfunction might influence AD pathology, as population-based and cohort studies have detected higher AD incidence rates in diabetic patients. But how diabetes affects τ pathology is not fully understood.

Cognitive and non-cognitive behaviors in the triple transgenic mouse model of Alzheimer's disease expressing mutated APP, PS1, and Mapt (3xTg-AD).

3xTg-AD mutant mice are characterized by parenchymal Aβ plaques and neurofibrillary tangles resembling those found in patients with Alzheimer's disease. The mutants were compared with non-transgenic controls in sensorimotor and learning tests. 3xTg-AD mutants were deficient in T-maze reversal, object recognition, and passive avoidance learning.

Dimethyl sulfoxide induces both direct and indirect tau hyperphosphorylation.

Dimethyl sulfoxide (DMSO) is widely used as a solvent or vehicle for biological studies, and for treatment of specific disorders, including traumatic brain injury and several forms of amyloidosis. As Alzheimer's disease (AD) brains are characterized by deposits of β-amyloid peptides, it has been suggested that DMSO could be used as a treatment for this devastating disease. AD brains are also characterized by aggregates of hyperphosphorylated tau protein, but the effect of DMSO on tau phosphorylation is unknown.

Hypothermia-induced hyperphosphorylation: a new model to study tau kinase inhibitors.

Tau hyperphosphorylation is one hallmark of Alzheimer's disease (AD) pathology. Pharmaceutical companies have thus developed kinase inhibitors aiming to reduce tau hyperphosphorylation. One obstacle in screening for tau kinase inhibitors is the low phosphorylation levels of AD-related phospho-epitopes in normal adult mice and cultured cells.

Dietary intake of unsaturated fatty acids modulates physiological properties of entorhinal cortex neurons in mice.

Dietary lipids modify brain fatty acid profile, but evidence of their direct effect on neuronal function is sparse. The enthorinal cortex (EC) neurons connecting to the hippocampus play a critical role in learning and memory. Here, we have exposed mice to diets based on canola:soybean oils (40 : 10, g/kg) or safflower : corn oils (25 : 25, g/kg) to investigate the relationship between the lipid profile of brain fatty acids and the intrinsic properties of EC neurons.

Biochemical isolation of insoluble tau in transgenic mouse models of tauopathies.

Tau is a highly soluble microtubule-associated protein (MAP) that is abundant in the central nervous system and expressed mainly in neuronal axons. Intracellular aggregates of insoluble tau protein are present in a group of neurodegenerative diseases called tauopathies, which include Alzheimer's disease. Numerous transgenic mouse models of tauopathies have been produced in the last decade, and analysis of insoluble tau in these animals has provided a powerful tool to understand the development of tau pathology.