Marianne Chapleau

Neuropsychologist turned Medical Science Liaison. Passionate about patient care & improving the dx and tx of neurodegenerative diseases. Views are my own.

[Marianne Chapleau @M_Chapleau]

@financedon2024 @vivekramaswami The implication that a man of color following a woman is suspicious or predatory… 🙃

[Marianne Chapleau @M_Chapleau]

@grinberg_t @UCSFmac @MayoClinic @gowoon_son @MayoPathology Congrats Lea! Enjoy the sunny Florida weather! ☀️

[Marianne Chapleau @M_Chapleau]

Big day for Life Molecular Imaging! 👏

https://t.co/DYUM1u5quI

[RikOssenkoppele @RikOssenkoppele]

🚨NEW PREPRINT: An atypical phenotype is a risk factor for higher mortality in Alzheimer’s disease

@ilse_bader shows that an atypical (non-amnestic-predominant) clinical presentation is an important risk factor for mortality beyond age, sex, education, APOEε4-carriership and disease severity.

Link @medrxivpreprint: https://t.co/emJwxQwnzL

@Colin__Groot @AlzheimerAms

[Marianne Chapleau @M_Chapleau]

Happy to share this great review on florbetaben, led by Aleksandar Jovalekic, highlighting its pivotal role in imaging Alzheimer’s pathology since its approval 10 years ago. Grateful to have collaborated on this work!

https://t.co/DTfrnM4ouu

[Anna Marseglia @anna_marseglia_]

📣 Postdoc Hiring📣

Join our project on how social health impacts cognition & resilience with a focus on women’s health

✅ Longitudinal data expertise 
✅ Passion for aging research
✅ Team-oriented mindset

📍Karolinska Institutet 🇸🇪 
💼 Apply now:
https://t.co/GKwX4dFYpo

[Nico Franzmeier @nfranzme]

Massive paper alert: We performed extensive profiling of PI-2620 for 4R tauopathies. PI-2620 tau PET signals in PSP stem from neuronal and oligodendroglial tau, not astrocytes. Signals correlate with fibrillary tau, autoradiography, and autopsy data in PSP https://t.co/zEF9fwBlsN

[JAMA Neurology @JAMANeuro]

ARIA-E in Alzheimer disease is more likely in those with APOE ε4, microhemorrhages, low CSF Aβ42, and high Fazekas scores, but it does not generally worsen long-term cognition or function. https://t.co/9ZzJu0esle

[Marianne Chapleau @M_Chapleau]

Exciting news for Alzheimer’s treatment in Europe! National decisions on access, pricing, and reimbursement are next, but this is a big step forward! 🎉

[EU Medicines Agency @EMA_News]

📢The CHMP recommends authorising a new treatment for early #AlzheimersDisease in the EU.

Leqembi is intended for treatment of mild dementia and cognitive impairment in a restricted patient population with a specific genetic make-up.

👉 https://t.co/0rUpn7K7ri

[CurePSP @CurePSP]

#CurePSP is now accepting applications for the Student Fellowship Program. This program supports students engaged in research on PSP and CBD, providing resources to drive meaningful advances in the field.

Deadline: January 31, 2025, by 5pm ET
https://t.co/3ENeOqtuod

#Research

[JAMA Neurology @JAMANeuro]

Study found frailty accelerates up to 9 years before dementia onset and is a key early marker. Frailty was linked to higher dementia risk even when measured years before dementia onset and may represent a target for prevention efforts.

https://t.co/cN6TI5jqvW

[Sara Nolin, PhD 🧠 @SaraNolin_neuro]

📢 Looking for a postdoc opportunity in neuroimaging research! 🎓 My focus: Alzheimer’s disease, cognitive aging, & functional networks. Skilled in multiple MRI modalities and neuropsych. Excited to connect with labs! #Postdoc #AlzheimersResearch #Neuroimaging

[Maria C Carrillo PhD @DrMariaALZ]

Join us at #AAICAdvancements Exploring Equity in Diagnosis, Nov. 18-19 in Chicago and online! Be a part of the conversation around addressing disparities in an era of modernizing diagnosis for Alzheimer’s and other dementias. #ExploringEquity24 https://t.co/A4mETBueE7

[Jake Vogel @_JakeVogel_]

Whelp. Maybe a good time to mention that I am about to open a new PhD position in Sweden that just happens to be exactly four years in length. Any aspiring PhD candidates in neurodegenerative imaging or multiomics who want to "take a break" from the US, please get in touch!

[Marianne Chapleau @M_Chapleau]

@elvisha9 Yep… 😞 This feels unreal.

[Marianne Chapleau @M_Chapleau]

Well said! And this framework does not diminish the importance of syndromic diagnosis or the quantification of clinical impairment.

[Suzanne E Schindler @SuzanneESchind1]

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

[Marianne Chapleau @M_Chapleau]

@MilanNigam2 Pour attirer plus de psychologues dans le public, ça prend une meilleure rémunération… Les médecins sont biens au Québec 🙂

[Marianne Chapleau @M_Chapleau]

@MilanNigam2 Quand j’ai obtenu mon diplôme en 2020, on nous obligeait, en tant que psys/neuropsys, à accepter un poste dans notre dernier milieu de stage si l’opportunité se présentait. La plupart trouvaient une excuse pour y échapper, car le salaire de base dans le public était de 66 000$.

[Marianne Chapleau @M_Chapleau]

@jme_walker 🤣

[RikOssenkoppele @RikOssenkoppele]

Lewy body pathology exacerbates brain hypo-metabolism and cognitive decline in Alzheimer’s disease

Great work led by @LECollij. Using ADNI data, she showed that the presence of LB pathology (CSF SAA) exacerbates global cognitive decline in symptomatic AD and is associated with more pronounced hypo-metabolism (FDG PET), particularly in posterior cortical regions.

Link @NatureComms (open access): https://t.co/aldXoZufLl

@biofinder_study @SEMastenbroek @NiklasMattsson4 @SebastianPalmqv @OskarHansson9