A5020591693- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Inflammation biomarkers and pathways
- Tryptophan and brain disorders
- Parkinson's Disease Mechanisms and Treatments
- Mitochondrial Function and Pathology
- Cholinesterase and Neurodegenerative Diseases
- Neurological Disorders and Treatments
- Genetic Neurodegenerative Diseases
- Natural Antidiabetic Agents Studies
- Intensive Care Unit Cognitive Disorders
- Receptor Mechanisms and Signaling
- Intracerebral and Subarachnoid Hemorrhage Research
- Photochromic and Fluorescence Chemistry
- Traumatic Brain Injury and Neurovascular Disturbances
- Cardiovascular Health and Disease Prevention
- Cerebrovascular and genetic disorders
- Sleep and Wakefulness Research
- Barrier Structure and Function Studies
- Anesthesia and Neurotoxicity Research
- Peroxisome Proliferator-Activated Receptors
- Adenosine and Purinergic Signaling
- Immune cells in cancer
Université Laval
2013-2024
Institut de Neurophysiopathologie
2023-2024
Centre National de la Recherche Scientifique
2017-2024
Hope Center for Neurological Disorders
2018-2023
Aix-Marseille Université
2023
University of Missouri–St. Louis
2023
Washington University in St. Louis
2019-2021
Centre hospitalier de l'Université Laval
2014-2019
Saint Louis University
2018
Centre hospitalier universitaire de Québec
2014-2017
Alzheimer's disease (AD) is characterized by plaques containing amyloid-β (Aβ) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau. Beyond tau Aβ, evidence suggests that microglia play an important role in AD pathogenesis. Rare variants the microglia-expressed triggering receptor expressed on myeloid cells 2 (TREM2) gene increase risk 2- to 4-fold. It likely these TREM2 decreasing response Aβ its local toxicity. However, neocortical pathology occurs many years before...
In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well seeding spreading of tau aggregates. Whether this Aβ-enhanced seeding/spreading is due to loss microglial function or a toxic gain TREM2-deficient microglia unclear. Depletion mice with established brain amyloid has no effect on but results less spine neuronal loss. Microglial repopulation aged improved cognitive...
The ε4 allele of the apolipoprotein E (APOE) gene is strongest genetic risk factor for late-onset Alzheimer's disease (AD) and greatly influences development amyloid-β (Aβ) pathology. Our current study investigated potential therapeutic effects anti-human APOE antibody HAE-4, which selectively recognizes human that co-deposited with Aβ in cerebral amyloid angiopathy (CAA) parenchymal In addition, we tested whether HAE-4 provoked brain hemorrhages, a component amyloid-related imaging...
Sleep loss is associated with cognitive decline in the aging population and a risk factor for Alzheimer’s disease (AD). Considering crucial role of immunomodulating genes such as that encoding triggering receptor expressed on myeloid cells type 2 (TREM2) removing pathogenic amyloid-β (Aβ) plaques regulating neurodegeneration brain, our aim was to investigate whether how sleep influences microglial function mice. We chronically sleep-deprived wild-type mice 5xFAD mouse model cerebral...
Background Arterial stiffness is associated with cognitive decline and dementia; however, the precise mechanisms by which it affects brain remain unclear. Methods Results Using a mouse model based on carotid calcification this study characterized that could contribute to degeneration due arterial stiffness. At 2 weeks postcalcification, attenuated resting cerebral blood flow in several regions including perirhinal/entorhinal cortex, hippocampus, thalamus, determined autoradiography ( P...
Abstract Background Alzheimer Disease (AD) and cerebral amyloid angiopathy (CAA) are both characterized by amyloid-β (Aβ) accumulation in the brain, although Aβ deposits mostly brain parenchyma AD cerebrovasculature CAA. The presence of CAA can exacerbate clinical outcomes patients promoting spontaneous intracerebral hemorrhage ischemia leading to CAA-associated cognitive decline. Genetically, share ε4 allele apolipoprotein E ( APOE ) gene as strongest genetic risk factor. Although...
Huntington's disease (HD) is an autosomal-dominant neurodegenerative disorder caused by polyglutamine expansions in the amino-terminal region of huntingtin (Htt) protein. At cellular level, neuronal death accompanied proteolytic cleavage, misfolding and aggregation huntingtin. Abnormal hyperphosphorylation tau protein a characteristic feature class diseases called tauopathies. As number studies have reported pathology HD patients, we investigated whether may promote if so tackle some its...
Abstract Abnormally hyperphosphorylated tau aggregated as intraneuronal neurofibrillary tangles is one of the two neuropathological hallmarks Alzheimer’s disease (AD). The majority AD cases are sporadic with numerous environmental, biological and genetic risks factors. Interestingly, insulin dysfunction hyperglycaemia both risk factors for AD. However, how affect pathology, not well understood. In this study, we examined effects deficiency on pathology in transgenic hTau mice by injecting...
The brain's complex microconnectivity underlies its computational abilities and vulnerability to injury disease. It has been challenging illuminate the features of this synaptic network due small size dense packing elements. Here, we describe a rapid, accessible super-resolution imaging analysis workflow-SEQUIN-that quantifies central synapses in human tissue animal models, characterizes their nanostructural molecular features, enables volumetric mesoscale networks without production large...
APOE is the strongest genetic factor for late-onset Alzheimer's disease (AD). A specific conformation of ApoE protein present in amyloid-β (Aβ) containing plaques. Immunotherapy targeting plaques reduces brain Aβ deposits mice. Here, we evaluated effects anti-human antibody HAE-4 on amyloid plaques, Aβ-mediated tau seeding and spreading, neuritic dystrophy 5XFAD mice expressing human ApoE4. reduced as well Aβ-driven seeding/spreading dystrophy. These results demonstrate that may provide...
Abstract Study Objectives Aggregates of hyperphosphorylated tau protein are a hallmark Alzheimer’s disease (AD) and other tauopathies. Sleep disturbances common in AD patients, insufficient sleep may be risk factor for AD. Recent evidence suggests that phosphorylation is dysregulated by mice. However, the physiological regulation during sleep–wake cycle currently unknown. We thus aimed to determine whether regulated circadian rhythms, inherently linked cycle. Methods To answer these...
Parenchymal border macrophages (PBMs) reside close to the central nervous system parenchyma and regulate CSF flow dynamics. We recently demonstrated that PBMs provide a clearance pathway for amyloid-β peptide, which accumulates in brain Alzheimer’s disease (AD). Given emerging role AD, we explored how tau pathology affects PBM populations PS19 mouse model of pathology. reduction flow, an increase MHCII + subpopulation mice compared with WT littermates. Consequently, asked whether dysfunction...