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Sylvia Villeneuve
@sylv_villeneuve
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Associate Professor Department of Psychiatry, McGill University Neuroimaging, MRI, PET, Alzheimer's disease
Joined April 2018
Our new lab paper suggests that almost all (between 75-90%) cognitively intact people with abnormal plasma p-tau217 values subsequently developed MCI when followed for <10 years after their blood test. (14% in A-T-) I have mixed feeling of being happy and scarred... 😳#Alzheimer
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RT @zimmerneurolab: 🚨 New Study just out in @LancetGH 🧠 @lucasudaros, @vbwyll, @crisaguzzoli & colleagues used a machine learning model to…
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RT @sducharme66: The Center for Precision Psychiatry - Québec is releasing a first batch of open access data on its transdiagnostic SPARK c…
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RT @DBartres_Faz: 👋New in @NatMentHealth Psychological profiles related to cognition and brain changes. Distinct pathways for dementia risk…
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RT @OttoyJulie: 🧠 Our lab’s latest deep learning-based tool ‘segcsvd’ to automatically segment white matter hyperintensities #WMH, now in H…
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RT @AgustinMIbanez: Risk factors for brain health in young adults remain underexplored. In @LancetLongevity, we show how addressing lifesty…
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RT @fislarissa: Are you interested in distinguishing region-specific longitudinal changes in resting-state functional connectivity related…
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RT @sylvain_baillet: "Associations between neuromelanin depletion and cortical rhythmic activity in Parkinson’s disease" Just out in @Brai…
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RT @GaelVaroquaux: Software engineer: don't force complexity, in particular upon users. it's not that I don't understand the power of the…
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RT @mnrajah: The BHAMM Study has launched in Toronto! Please signup to participate & help fill our knowledge gap on #womensbrainhealth & #m…
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RT @UCSFmac: "Neuroimaging and Neuropathological Investigations of Alzheimer's Disease Clinical and Biological Heterogeneity" by Renaud La…
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RT @NicholasAshton: 📢 Publication alert 👉🩸 Thrilled to share our latest findings from the #DROPAD project on using capillary finger #blood…
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RT @GaelVaroquaux: 👩🎓👨🎓 Internship offers (1st step to PhD program) in my group: Topics: ◼ Health AI & causality…
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RT @SilverSanteEU: 🚨 New study from the @SilverSanteEU researchers – @MarchantLabUCL Studying 134 older adults, Lau et al. found that ru…
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RT @harald_hampel: My colleagues and I have published an article in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association wher…
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RT @susan_landau: This is a product of 20yrs of harmonization and data sharing in the ADNI PET Core
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RT @segal_eran: Our new @NatureAging paper: We built 14 "biological clocks" representing the biological age and rate of aging of 14 major b…
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I couldn't agree more with you @SuzanneESchind1 , thank you for this post.
Having started my career in basic neuroscience research, I have always understood Alzheimer disease to mean the pathophysiology associated with amyloid plaques and tau tangles. As a clinician, I appreciate that the relationship between Alzheimer disease and cognitive impairment is complex. 1. Clinically diagnosing the cause of cognitive impairment is different than diagnosing that the patient has Alzheimer disease (pathology). Many of my patients with cognitive impairment have multiple diagnoses (e.g., sleep apnea, medication-related cognitive dysfunction, depression, previous cerebral infarction), and sometimes have Alzheimer disease (based on biomarker testing). I do what I can to mitigate the effects of all of these conditions, and when Alzheimer disease is present I do not assume that it is the sole or even the primary cause of cognitive impairment. This is true across multiple potential etiologies: for example, I may diagnose someone with cerebrovascular disease and a prior infarct based on MRI findings, but determine that this condition is asymptomatic and not contributing to their cognitive impairment. 2. Given the simplicity of some biomarker tests and the difficulty of clinical assessment, there is a risk that clinicians may diagnose the etiology of cognitive impairment as Alzheimer disease without doing a full work-up. This is why appropriate use recommendations for biomarkers always mandate that biomarker results must be integrated with a clinical evaluation and not used as a “stand-alone.” 3. Alzheimer disease pathology accumulates silently for ~10-20 years before the onset of cognitive impairment. However, during this pre-clinical phase the accumulation of amyloid pathology is associated with many other biomarker changes that appear pathological (e.g., abnormal CSF synaptic biomarkers, brain atrophy, brain hypometabolism). While the brain is remarkably resilient to damage and individuals may or may not develop symptoms, the brain is sick and the pre-clinical phase is a disease state. 4. Suggesting that a disease only exists when organs are severely damaged and failing (dementia) seems counter to what we have learned in other areas of medicine. For example, patients diagnosed with hypertension or asymptomatic coronary artery disease may change their diet and medications to avoid a heart attack. Individuals with asymptomatic chronic kidney disease may or may not go on to require dialysis, but they can be monitored and sometimes treated. 5. There are valid concerns about the stigma and risks of asymptomatic individuals being labeled as having Alzheimer disease given that they may or may not develop cognitive impairment. The solution is simple—we don’t perform biomarker testing in asymptomatic individuals outside of research studies or clinical trials. Again, this has been mandated by appropriate use recommendations for biomarkers. We can help patients by promoting accurate understanding and appropriate use of biomarkers. #EndAlz
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