How does physics inform neurodegeneration? Supersaturation lowers the nucleation barrier for the precipitation of monomeric proteins into their pathological state. In normal aging, replacement matches loss; in accelerated aging, it does not. (1/4)
https://t.co/KFchGr1N4w
#Parkinsons with and without detectable pathological α-synuclein (αSyn-SAA) are remarkably similar. What does that mean for the idea that α-syn aggregates "biologically define" PD? My take on a new #PPMI analysis:
https://t.co/dBwWCBRSxF
𝐀𝐥𝐳𝐡𝐞𝐢𝐦𝐞𝐫'𝐬 𝐭𝐚𝐮 𝐛𝐢𝐨𝐦𝐚𝐫𝐤𝐞𝐫𝐬 𝐜𝐨𝐫𝐫𝐞𝐜𝐭𝐞𝐝. 𝐀𝐥𝐳𝐡𝐞𝐢𝐦𝐞𝐫'𝐬 𝐝𝐢𝐬𝐞𝐚𝐬𝐞 𝐮𝐧𝐜𝐡𝐚𝐧𝐠𝐞𝐝.
~10 anti-tau monoclonal antibodies tested to date in #Alzheimers. They change tau, not the disease.
https://t.co/vl1Knb4NpN
I now understand why we can look at the same data on studies of tests of pathology and come to very different conclusions. My thoughts here. https://t.co/8leTj7E92J
A faux vignette illustrates a flawed causal inference in Parkinson's research: pathology ('calcification') is mistaken for a pathogenic mechanism ('toxicity') rather than a marker of protein dyshomeostasis ('calcium metabolism'). @ajlees@movedisorder
https://t.co/Al5UW4mzNB
If Parkinson’s is “biologically defined” by a positive α-synuclein test, what do we do with the 10% who are negative? Can we distinguish between detecting pathology and defining disease?
https://t.co/kk9LGNCFQC
This treatment can kill. But counting is legally prohibited until 2036–2037.
Deaths occur with lecanemab & donanemab, but excess mortality can’t be estimated: it is proprietary data and can be withheld for a decade.
https://t.co/WLNmANS8wI
𝐘𝐨𝐮𝐫 𝐛𝐫𝐚𝐢𝐧 𝐰𝐢𝐥𝐥 𝐬𝐡𝐫𝐢𝐧𝐤 𝐛𝐮𝐭 𝐭𝐡𝐢𝐬 𝐢𝐬 “𝐩𝐬𝐞𝐮𝐝𝐨-𝐚𝐭𝐫𝐨𝐩𝐡𝐲,” 𝐭𝐫𝐮𝐬𝐭 𝐮𝐬. We need independent analysis, not trust. The dry weight of Aβ accounts for <1/1,000 of the observed volume change in #Alzheimers with treatment. https://t.co/AtIaKMpI1D
Protective or Pathogenic? Kinase activity and the neurodevelopmental origins of G2019S LRRK2-Associated Parkinson's disease
#kinase#LRRK2#G2019S#PD#Parkinson
Log in :
https://t.co/5lZlLtlaPv
In Parkinson’s, we obsess over what α-synuclein becomes when aggregated, and ignore what neurons lose when its normal form disappears. New data in α-syn KO mice: hyposmia, apoptosis, impaired autophagy. Depletion may matter more than we think. https://t.co/hwXeLZH5fQ
Tuning Forks
"If you want to find the secrets of the universe, think in terms of energy, frequency, and vibration"
Nikola Tesla (1856 –1943), Serbian-American engineer
1/
An important call to save the mouth that fed AI. "Academics’ failure to support Wikipedia while benefiting from it is not just hypocrisy, but a betrayal of our mission to create and disseminate knowledge." https://t.co/vS8k0AWcEr
We know Painful Leg and Moving Toes; now it's time to remember 'Painful Jaw and Moving Tongue' as a clue for anti-IgLON5 @AlbertoEspay#neurotwitter@MDCP_Journal
https://t.co/sjymwMyUGS
@barttels2 That we’re entering a "better" futuristic world where blood tests can label people with “Alzheimer’s” before symptoms, and justify preventive anti-pathology therapy (he says nothing about failed preclinical trials). A very Huxleyan Brave New World.
“Alzheimer’s is caused by pathology decades before symptoms.” If so, removing pathology in preclinical AD should prevent decline. It didn't—most preclinical AD trials (4/6) worsened outcomes in treated vs placebo. Pathology ≠ disease.
https://t.co/zEJqvTR13m