Discover and read the best of Twitter Threads about #Amyloid
Most recents (22)
Everything begins with A
Aluminum -> Amyloid -> Autism & Alzheimer's
Aluminum is the main adjuvant in most childhood 💉s
Aluminum is also proven to cause amyloid or misfolded proteins in the brain.
Amyloid plaques are associate with Alzheimer's and autism. 🧵
Aluminum -> Amyloid -> Autism & Alzheimer's
Aluminum is the main adjuvant in most childhood 💉s
Aluminum is also proven to cause amyloid or misfolded proteins in the brain.
Amyloid plaques are associate with Alzheimer's and autism. 🧵
The CDC states that Aluminum is the main adjuvant, or immune system "stimulator," in many 💉 on their childhood 💉 schedule >
cdc.gov/vaccinesafety/…
cdc.gov/vaccinesafety/…
Aluminum transforms normal proteins into misfolded, messy, junk or Amyloid proteins. >
"The results demonstrated that Al(III) induced the transformation of the initial random coil structure to the β-sheet configuration in the Aβ40 peptides."
sciencedirect.com/science/articl…
"The results demonstrated that Al(III) induced the transformation of the initial random coil structure to the β-sheet configuration in the Aβ40 peptides."
sciencedirect.com/science/articl…
Teaming up again with the great @VerwerftJan to share our experience with #echoCPET in #HFpEF. This hot-of-the-press paper @ESC_Journals demonstrates myriad of opportunities for diagnosis & treatment, far beyond #SGLT2i only. Tweetorial below!
@SarahStroobant2 @HerbotsLieven
@SarahStroobant2 @HerbotsLieven
We have recently described our set-up for a dedicated #dyspnoeaclinic in detail @JACCJournals
In #HFpEF, early & correct diagnosis are important, #phenotyping is everything. There are a lot of mechanisms for dyspnoea involved
In #HFpEF, early & correct diagnosis are important, #phenotyping is everything. There are a lot of mechanisms for dyspnoea involved
Current @ESC_Journals paper goes one step further: "In patients with confirmed HFpEF or probability >90% according to well-validated HFpEF scores (both are complimentary in our view), why #echoCPET within a dedicated #dyspnoea clinic? What is the impact of findings?"
1/5 "The analysis revealed that older, #cognitively #healthy #brains showed similar amounts of #dissolvable, #non-#fibrillar #amyloid #protein as #brains of #Alzheimer’s #patients."
#aβ #Aβ #fibrils
gero.usc.edu/2023/01/05/new…
#aβ #Aβ #fibrils
gero.usc.edu/2023/01/05/new…
2/5 "But, as the researchers expected, the brains of #Alzheimer’s patients had higher amounts of #insoluble #Aβ #fibrils, the form of #amyloid #protein that aggregates to form the telltale “#plaques” seen in the #disease,..."
3/5 "... higher levels of #fibrillary #amyloid appear to be a better indicator of #poorer #brain #health."
1/5 "#SARSCoV2 #infection is associated with a #surprising number of #morbidities."
#amyloidogenesis #aβ #fibrils #COVID19 #SARSCoV2
#spike
#protein
pubs.acs.org/doi/10.1021/ja…
#amyloidogenesis #aβ #fibrils #COVID19 #SARSCoV2
#spike
#protein
pubs.acs.org/doi/10.1021/ja…
2/5 "#Uncanny #similarities with #amyloid-#disease associated #blood #coagulation and #fibrinolytic #disturbances together with #neurologic and #cardiac problems led us to investigate the #amyloidogenicity of the #SARSCoV2 #spike #protein (#S-protein)."
3/5 "#Amyloid #fibril #assays of peptide library mixtures and theoretical predictions identified seven #amyloidogenic #sequences within the S-protein."
And another from my former institution, this as a first author!
We found that higher levels of GFAP, an #astroglial marker, were related to higher glucose metabolism 🧠in early stages of #Alzheimer's, especially when GFAP was measured in blood🩸
link.springer.com/article/10.100…
We found that higher levels of GFAP, an #astroglial marker, were related to higher glucose metabolism 🧠in early stages of #Alzheimer's, especially when GFAP was measured in blood🩸
link.springer.com/article/10.100…
This suggests that a higher astrocytic reactivity in early stages of Alzheimer's, probably in response to #amyloid accumulation, is related to higher glucose consumption. This may (in part) explain why we see higher levels of glucose metabolism in these early stages.
This relationship between GFAP and glucose metabolism became negative in subjects with tau pathology (A+T+), suggesting a failure to sustain the higher energetic demands required by astrocytes. Notably, this was observed in areas of typical AD hypometabolism seen in later stages.
🚨 Our paper on p-tau231 and p-tau217 as blood 🩸biomarkers 🧪 in preclinical #Alzheimers 🧠 is now published in @NatureMedicine
nature.com/articles/s4159…
@goteborgsuni #BarcelonaBeta @fpmaragall
@hospitaldelmar @IMIM_research @KingsCollegeLon
🧵 summary
👇🏾
(1/6)
nature.com/articles/s4159…
@goteborgsuni #BarcelonaBeta @fpmaragall
@hospitaldelmar @IMIM_research @KingsCollegeLon
🧵 summary
👇🏾
(1/6)
We investigated 6 blood 🩸 biomarkers in 397 cognitively unimpaired individuals of the ALFA study at #BarcelonaBeta :
🟤 p-tau181
🟣 p-tau217
🟠 p-tau231
🟢 GFAP
🔵 NfL
🔴 Abeta42/40
and all were significantly increased in preclinical #Alzheimers
but ..
(2/6)
🟤 p-tau181
🟣 p-tau217
🟠 p-tau231
🟢 GFAP
🔵 NfL
🔴 Abeta42/40
and all were significantly increased in preclinical #Alzheimers
but ..
(2/6)
Plasma 🩸 p-tau231 🟠 and p-tau217 🟣 had:
👉🏾 the highest increase with the lowest #amyloid burden
👉🏽 the strongest association with amyloid PET
👉🏿 a significant association with longitudinal increases in amyloid PET uptake
(3/6)
👉🏾 the highest increase with the lowest #amyloid burden
👉🏽 the strongest association with amyloid PET
👉🏿 a significant association with longitudinal increases in amyloid PET uptake
(3/6)
Are #Amyloid and #Tau #PET positive cognitively unimpaired individuals destined to decline?
Find out in our new preprint: bit.ly/3yXRrOf.
See a thread👇1/11
Find out in our new preprint: bit.ly/3yXRrOf.
See a thread👇1/11
A major unanswered question in the field is whether cognitively unimpaired (CU) individuals who harbor both #Alzheimer’s disease neuropathological hallmarks (abeta #plaques and tau neurofibrillary #tangles) can preserve their #cognition over time or are destined to decline. 2/11
There is fundamental disagreement about the nomenclature. E.g. a CU individual with positive Abeta (A+) and tau (T+) biomarkers is classified as “preclinical AD” by the NIA-AA criteria, while the IWG criteria would label such an individual “at risk for progression to AD”. 3/11
While #science thought us that we can even cut and paste #genes with #CRISPR technology…even with that we only influence 3% to 5% of #chronicillness. The rest depends on #how you #live your #life!!! So how do we #SelfRegulate our #body?
There are 6 main steps to #selfregulation:
1. #Sleep
2. #Meditation & #StressManagement
3. #Movement / #Yoga / #Pranayama
4. #Emotions
5. #Nutrition / #Nourishment
6. #Biological Rhythms / #Grounding
1. #Sleep
2. #Meditation & #StressManagement
3. #Movement / #Yoga / #Pranayama
4. #Emotions
5. #Nutrition / #Nourishment
6. #Biological Rhythms / #Grounding
1. Good #sleep is more important than most think! What happens during sleep? The fluctuation of consciousness…that we call the waking state. But in many wisdom traditions of the world, the waking state is merely a lucid dream that consciousness is having…
#Hochinzidenz #Strategie in #UK führt zu massenhaft #LongCovid. 1,7% der Bevölkerung haben LC-Symptomatik >3Mo, fast #700k Menschen leiden seit über einem Jahr unter LC, ~1.000.000 Menschen sind #funktional in #Arbeitsfähigkeit #eingeschränkt.
1/x
#Niedriginzidenz #Strategie
1/x
#Niedriginzidenz #Strategie
Wer leidet am häufigsten unter #LongCovid? ☡Höchstes Risiko für #Lehrkräfte, Arbeitende im #Gesundheitswesen. Hier erschreckendes #LongCovid -Risiko. 3fach #Impfung reduziert Risiko wahrscheinlich um 50%. Da reicht #nicht aus bei hoher Exposition!
2/x
2/x
Wer ist besonders betroffen? #Alte? #Vorerkrankte? Menschen mit #schwerem #Verlauf?
Nein, nein und nochmals #Nein !
Dänische Studie zeigt klar : #96_Prozent hatten milden Verlauf ⤵⤵⤵
#LongCovid tritt bei Frauen im Alter ~30-60 bes. häufig auf.
3/x
Nein, nein und nochmals #Nein !
Dänische Studie zeigt klar : #96_Prozent hatten milden Verlauf ⤵⤵⤵
#LongCovid tritt bei Frauen im Alter ~30-60 bes. häufig auf.
3/x
Da es gerade das #Tabuthema während der #Nachdurchseuchung und #Kinderdurchseuchung ist. Einige wichtige Infos zu #LongCovid & #LongCovidKids die viele nicht wissen die in dem Thema nicht drin sind:
1.) Long Covid bedeutet #nicht dass die Covid Symptomatik nur schwer abklingt
1x
1.) Long Covid bedeutet #nicht dass die Covid Symptomatik nur schwer abklingt
1x
oder eine längere Rekonvaleszenzphase bei schweren Verlauf. #LongCovid Risiko ist vollkommen entkoppelt, von der individuellen Verlaufsschwere. Große Studie aus England zeigt dass Long Covid Betroffene zu 90% während Covid nicht ins Krankenhaus mussten,
2x
2x
Auch zwischen denen die es richtig weg gehauen hat und denen die nur wenige respiratorische Symptome für kurzen Zeitraum hatten keinen Unterschied. Risiko scheint von Verlaufsschwere fast #entkoppelt. Wenn eine Familie #Covid hatte
3x
3x
#WeekendLecture
#GeneticsAndStroke
#Genetics is involved in several #stroke related conditions, such as small vessel disease #SVD, aneurysms, dissections, cavernomas, and intracranial #hemorrhages
Check this 🧵!
Prepared by @J_Rosales_MD
Edited by @interneurona
#GeneticsAndStroke
#Genetics is involved in several #stroke related conditions, such as small vessel disease #SVD, aneurysms, dissections, cavernomas, and intracranial #hemorrhages
Check this 🧵!
Prepared by @J_Rosales_MD
Edited by @interneurona
#Weekendlecture
#Genetic & #SVD
🧬🧠
✅1,5% of cerebral #SVD are #monogenic disorders
✅AR, AD or X-linked
☝🏼Absence of family history doesn't rule out diagnosis because of
👉de novo mutation
👉reduced expression or
👉incomplete penetrance
✅ahajournals.org/doi/10.1161/ST…
#Genetic & #SVD
🧬🧠
✅1,5% of cerebral #SVD are #monogenic disorders
✅AR, AD or X-linked
☝🏼Absence of family history doesn't rule out diagnosis because of
👉de novo mutation
👉reduced expression or
👉incomplete penetrance
✅ahajournals.org/doi/10.1161/ST…
#Weekendlecture
#Genetic & #SVD
When to #suspect?🕵️♀️
✅early onset stroke without vascular RFs
✅systemic features and neuroimaging of an specific monogenic disorder
✅consanguinity
✅negative work up for other causes of SVD
👉ahajournals.org/doi/10.1161/ST…
#Genetic & #SVD
When to #suspect?🕵️♀️
✅early onset stroke without vascular RFs
✅systemic features and neuroimaging of an specific monogenic disorder
✅consanguinity
✅negative work up for other causes of SVD
👉ahajournals.org/doi/10.1161/ST…
1/🧵Wake-Up to how #SLEEP flushes waste from your brain 🧠 @JAMA_current
I may get more done when I 💤 less, but I lose the long-game! #Evolution dictated that we gain an advantage by spending 1/3rd of our lives asleep.
I’ll tell you WHY? bit.ly/3qPgzAA
#MedTwitter
I may get more done when I 💤 less, but I lose the long-game! #Evolution dictated that we gain an advantage by spending 1/3rd of our lives asleep.
I’ll tell you WHY? bit.ly/3qPgzAA
#MedTwitter
2/ Why do we sleep? Brain rest? To process bad decisions or incomplete conversations? Maybe. But the coolest reason is removal of #amyloid & #tau proteins that cause #dementia. Our #glymphatic system does this most efficiently during deep sleep.
🚨🧠📄🍾 🤪🥳 For some reason all our papers are coming our within 2 weeks!
Here’s the latest in @GreenJournal, on the relationships between 1) patterns #tau and #amyloid PET and 2) #Alzheimer’s clinical #heterogeneity and #APOE4.
n.neurology.org/content/early/…
1/n
Here’s the latest in @GreenJournal, on the relationships between 1) patterns #tau and #amyloid PET and 2) #Alzheimer’s clinical #heterogeneity and #APOE4.
n.neurology.org/content/early/…
1/n
#Alzheimer is associated with #heterogeneous clinical presentations. Patients develop symptoms at different ages (even sporadic AD can start early) and clinical syndromes vary: not everyone shows a “typical” amnestic syndrome (which is not very sensitive nor specific to AD!)
2/n
2/n
Specific non-amnestic syndromes are often associated with AD, like #PosteriorCorticalAtrophy (PCA, the visual variant of AD) or the logopenic variant of Primary Progressive Aphasia (lvPPA).
#APOE4 is associated with an earlier onset but also a more amnestic syndrome.
3/n
#APOE4 is associated with an earlier onset but also a more amnestic syndrome.
3/n
@jenbrea Hey! So I'm getting to the point where I could write a long paper about potential overlapping connections b/t #Alzheimer's and #MECFS, but I'll summarize a few top trends in this thread! First, I brainstormed often on topic with the late Rob Moir
@jenbrea 2/ Rob’s research (done w/ Rudy Tanzi + Will Eimer at Harvard) forms the core of a potential ongoing paradigm shift in Alzheimer’s - namely that #amyloid beta may be an antimicrobial peptide that forms in response to pathogens in #brain tissue: pubmed.ncbi.nlm.nih.gov/30001512/
@jenbrea 3/ To better understand that research, read this #interview I did with Rob before he passed away last year from glioblastoma. Key to ME/CFS is his work indicates that amyloid may form in response to herpesviruses like HSV1 in the Alzheimer’s brain: microbeminded.com/2017/12/18/int…
Our new paper in paper in blood 🩸 and CSF p-tau in #preclinical #Alzheimers 🧠 is out in @EmboMolMed ‼️
A great collaboration between #BarcelonaBeta @fpmaragall and @goteborgsuni
1/n
embopress.org/doi/full/10.15…
A great collaboration between #BarcelonaBeta @fpmaragall and @goteborgsuni
1/n
embopress.org/doi/full/10.15…
A collaboration between great scientists!
@TommyKakari @NicholasAshton @Marta_Mila_ @JuandoGispert @gesalbla @CarolinaMingui2 @ArenazaEider @GSBenavides and all the team of #BarcelonaBeta and the Blennow/Zetterberg lab in @goteborgsuni
A summary below
2/n
@TommyKakari @NicholasAshton @Marta_Mila_ @JuandoGispert @gesalbla @CarolinaMingui2 @ArenazaEider @GSBenavides and all the team of #BarcelonaBeta and the Blennow/Zetterberg lab in @goteborgsuni
A summary below
2/n
We investigated novel CSF and plasma p‐tau biomarkers in the preclinical stage of the Alzheimer’s continuum and compared them with the widely used CSF Mid‐p-tau181.
We hypothesized that they change when subtle changes in Aβ are detectable.
3/n
We hypothesized that they change when subtle changes in Aβ are detectable.
3/n
This is a really important preprint. @dbkell, @resiapretorius used a range of techniques to image clotting in the blood of #COVID-19 patients vs. controls...and found MAJOR differences in COVID-19 blood clotting patterns: medrxiv.org/content/10.110…
Ooof interesting! This team found Ljungan #virus (LV) antigens in autopsied #brain tissue from the hippocampus region of 18 #Alzheimer’s brains. No LV antigen was identified in any of their 11 age-matched control brains: ncbi.nlm.nih.gov/pmc/articles/P…
2/ The LV virus antibodies reacted with #neurons and #astrocytes and also showed distinct positive reaction in the #amyloid/neuritic plaques. The team thinks the findings indicate LV #virus may persist in the Alzheimer’s brain
3/ Here’s an image from one of the #Alzheimer’s brains. The red stain visualizes presence of LV viral antigen in neurons, astrocytes + #glial cells. In Panel C, an amyloid/neuritic plaque is shown staining positive in the glial compartment + in dystrophic neurites
This same pattern applies to much of the #microbiome community 👉 It’s hard to challenge the “consensus” that the human brain, CSF + womb are “sterile”...when the #NIH barely funds such topics, and novel results from privately funded studies are repeatedly blocked in peer-review
Example 👉 Robert Moir’s novel finding that #amyloid beta functions a potent antimicrobial peptide strongly suggests that communites of #pathogens persist in the #Alzheimer’s brain☝️But read how often his papers have been blocked in peer review: statnews.com/2018/10/29/alz…
Quote from the article 👉 “The first journal [Moir] submitted his results to, #Science, “looked like they would take it,”....But after what editors told him was “a consultation with our #Alzheimer’s disease experts,” it rejected the paper. So did three other journals.”
The study of persistent #infection as a driver of #Alzheimer’s disease is on 🔥👇!
From the study 👉 “Ezzat and his colleagues found that #HSV-1 is able to accelerate the transformation of soluble #amyloid proteins into thread-like structures that constitute the amyloid plaques”: reliawire.com/viral-protein-…
Here’s the full paper 👉 “Our results highlight the #viral protein corona as an acquired structural layer that is critical for viral–host interactions and illustrate a mechanistic convergence between viral and amyloid pathologies”: nature.com/articles/s4146…
Thanks to everyone who alerted me abt this study! 👉 Oral #pathogen p. gingivalis + the toxic enzymes (gingipains) it creates...were identified in the #Alzheimer’s brain☝️P. gingivitis was also found in the #spinal fluid of living people with Alzheimer’s
Cortexyme (the company doing the #Alzheimer’s trial) also developed molecules that block p. gingivalis gingipains 👉 Giving these molecules to mice reduced their #infections, halted #amyloid production + lowered brain inflammation ☝️(Very cool new #treatment possibility!)
One thing: As interesting as the findings are, I suspect p. gingivalis is just one of several #microorganisms that may “work together” to drive #Alzheimer’s pathology 👉 (In other words I still think infection in Alzheimer’s is #polymicrobial)
THIS 👉 #Mitochondria play a role in helping white blood cells target human #pathogens☝️Below, mitochondria-derived vesicles delivered #antimicrobial reactive oxygen species to control phagosome-localized S. aureus (a #bacterial infection)
So let’s add #mitochondria to the growing list of human organelles/proteins/pathways recently shown to have #antimicrobial activity 👉 Other compounds already on that list include #amyloid beta, alpha-syn, PrP, #HMOs etc☝️More context here: microbeminded.com/2018/12/30/myf…
Also #mitochondria are derived from #bacterial ancestors, and can become infected by a range of viral/bacterial #pathogens 👉 Suggests mitochondria’s antimicrobial activities may be defense mechanisms that stem from their #evolutionary history as a free-living organisms
So @Merck’s BACE-1 inhibitor Verubecestat resulted in “near-maximal reduction” of amyloid-beta in cerebrospinal fluid and “modest reduction” in brain amyloid. But it didn’t help even #Alzheimer’s disease, even "mild" Alzheimer's. A few thoughts:
1. Many companies are holding on to the hope that giving #tau- and #amyloid-busting drugs earlier, before Alzheimer's sets in, could prevent the disease. The FDA might even be open to using tau and amyloid as biomarkers to approve #Alzheimers drugs cen.acs.org/articles/96/i9…
2. But if we already know these drugs can lower amyloid-beta levels and *not* stop disease progression, is that really a good idea? I'd love to see the long term studies done, but the idea of drug approval based on biomarkers, and not cognitive markers, seems like a can of worms.
