Vincent Planche
@vincentplanche.bsky.social
140 followers 120 following 19 posts
Professor of Neurology, Bordeaux University - Head of Memory Clinic, Bordeaux University Hospital
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Reposted by Vincent Planche
brain1878.bsky.social
Using brain charts that map structural changes in the brain across the human lifespan, Planche et al. estimate the neurodegenerative trajectories of the three major genetic forms of frontotemporal lobar degeneration. tinyurl.com/2s3uhdpw
vincentplanche.bsky.social
By combining brain charts for the human lifespan and 1,341 MRIs from subjects with a FTLD mutation, we described the age of onset of the first anatomical abnormalities, the duration of the presymptomatic phase, the chronological staging of atrophy progression, and the severity of regional atrophy.
vincentplanche.bsky.social
This letter, co-written with @suzanneeschindler.bsky.social , David Knopman, Giovanni Frisons, Douglas Galasko, Joshua Grill, Lon S. Schneider, Jason Karlawish and @nvillain-alz.bsky.social , is a response to the previously published Perspective Article by Paul Aisen and colleagues.
vincentplanche.bsky.social
Many thanks to Erwan Bezard, who co-lead this work, and to all the co-authors: Valentine Kulifaj, Marie-Laure Arotçarena, Qin Li, Taxiarchis Katsinelos, William A. McEwan, Maria Xilouri, and @benjamindehay.bsky.social DEHAY!
vincentplanche.bsky.social
Taken together, our findings align with the growing body of literature indicating that co-pathologies can significantly influence the severity and progression of neurodegenerative diseases.
vincentplanche.bsky.social
We found that the distant injection of LB or AD-tau induced nigral TH neuronal loss of 26.5% and 38.4%, respectively. Notably, the co-injection of these aggregates into distinct but anatomically connected regions to the mesencephalon resulted in an additive effect with 53.5% neuronal loss
vincentplanche.bsky.social
we reported for the first time the cooperation between LB and tau pathologies in this experimental context. We found that the injection of AD-tau could induce distant pSyn, whereas we did not observe the reverse phenomenon; the injection of LB did not induce distant AT8-positive tau phosphorylation
vincentplanche.bsky.social
We used in this study our innovative approach consisting of injecting patient-derived proteopathic aggregates into macaques’ brains, to address the issue of a putative contribution of tau versus α-synuclein pathologies to the survival of dopaminergic mesencephalic neurons.
Reposted by Vincent Planche
chu-bordeaux.fr
Lien vers le communiqué de presse "vers la définition d’un cadre d’utilisation des biomarqueurs sanguins
de la maladie d’Alzheimer en pratique clinique" : www.chu-bordeaux.fr/Espace-m%C3%...
www.chu-bordeaux.fr
Reposted by Vincent Planche
walaszek.medsky.social
Interpreting p-tau-17 results depends on characterizing the clinical phenotype.

Positive predictive value in those w/ subjective cognitive impairment was only 60%. It was 90% in those with MCI & a typical Alzheimer phenotype.

Important to consider before widespread use of blood-based biomarkers.
Reposted by Vincent Planche
nvillain-alz.bsky.social
Just out in JAMA Neurol blood biomarkers are powerful—but without cognitive phenotyping, we risk more noise than signal.
Plasma p-tau217 needs clinical context or we’ll end up in a false-positive factory!
Clinico-biological AD is a reality!
👉🏻 jamanetwork.com/journals/jam...

bsky.app/profile/vinc...
vincentplanche.bsky.social
The main message of this study is that neuropsychological examination remains fundamental for interpreting the results of AD plasma biomarkers (ptau217)
Reposted by Vincent Planche
vincentplanche.bsky.social
AD and PD, same battle! Biology, yes, but not in isolation from clinical practice! Happy to share David Bendetowicz paper: Biological definitions of synucleinopathies should be anchored in clinical trajectories and encompass the complex biology of the disease journals.sagepub.com/doi/10.1177/...
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Reposted by Vincent Planche
nvillain-alz.bsky.social
Should amyloid-lowering therapies be approved based on biomarker evidence alone?

With @vincentplanche.bsky.social we argue for prioritizing clinical endpoints over unvalidated surrogates like amyloid load in AD trials. Read our full critique on AlzForum: www.alzforum.org/news/researc...
Is It Time to Approve Drugs Based on Amyloid Removal? | ALZFORUM
www.alzforum.org