Out today in @NatureComms our 🐁+👨work where we show that in #Autism
➡️(mTOR-related) excess of synapses causes aberrant fronto-striatal activity
➡️ this signature can be decoded in human fMRI scans, defining an identifiable autism subtype
@IITalk
1/4
tinyurl.com/265xy8ha
An important implication of our work is that it unifies two major pathological domains that in #Autism had long been regarded as distinct i.e. synaptic pathology & macroscale dysconnectivity

An expanded account of our results was reported here
➡️

2/4
All our previous results hold. We have now just added further evidence that Tsc2 mice lack major white matter/myelin alterations, further implicating synaptic pathology as cause for our findings, and documented that human findings are robust to multiple denoising strategies

3/4
Very grateful to @SFARIorg for funding this back in 2016 (we are slow, I know..) and to @mvlombardo @LabPasqualetti @alibert_ @RaffaellaTonini indomitable @MarcoPagani1985 my entire lab @lauraUlysse and all twitterless folks including 🌟🌟#Gustavo_Deco and #Vinod_Menon

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More from @Gozzi_Ale

16 Oct 20
Can we ‘see’ #autism in the brain? And is there a specific brain signature for the condition?

This is what we found by comparing brain connectivity maps across 16 mouse autism models
➡️tinyurl.com/yxfu2gzn

➡️Majestically led 👏👏👏by @Valerio_Zerbi @NCMLabETH

Thread 1/n
Autism is diagnosed based on behavior - but is this condition associated with a specific brain signature of circuit dysfunction?
Despite decades of work, brain imaging has failed to identify such signature as we have evidence of under-connectivity... tinyurl.com/y5uxoe3s

2/n
.....over-connectivity....
linkinghub.elsevier.com/retrieve/pii/S…

3/n
Read 14 tweets
9 Oct 20
#Autism is often associated with an excess of synapses:
but how does this trait affect large-scale circuit function?

Here's what we found by modelling autism-related pruning deficits across-species🧠🐭
➡️tinyurl.com/y2yfj74o

By @MarcoPagani1985 @mvlombardo & al.

Thread 1/n
Postmortem investigations in idiopathic #Autism have consistently revealed an excess of excitatory synapses
tinyurl.com/y57cc4r5
tinyurl.com/y59mdffp
tinyurl.com/y3t64yfe

2/n
Seminal work form the #Sulzer_Lab @Columbia has shown that postmortem synaptic surplus in #Autism is associated with hyperactive mTOR signalling
➡️this is a molecular pathway often dysregulated in autism and a key point of convergence of many autism-risk genes

3/n
Read 19 tweets
7 Aug 20
Wondering whether axonal input *drives* fMRI-based functional connectivity? Us too!

Here is what we found using #chemogenetic deconstruction of rsfMRI in the mouse🐁🐭

➡️Cortical silencing results in paradoxical fMRI overconnectivity tinyurl.com/yy269j92

Thread below 1/n
Computational and empirical evidence suggest that structural and functional connectivity are robustly related

➡️ this recent review from @richardfbetzel @misicbata summarizes it all tinyurl.com/yyy5u3zm

2/n
⚠️A key prediction of structurally based models of fMRI coupling is that *inactivation* of a brain node would result in reduced rsfMRI connectivity with its targets⚠️

But is that really the case?

3/n
Read 19 tweets
15 May 20
**New preprint from the lab**

Regional, layer and cell-class specific connectivity of the mouse default mode network tinyurl.com/yddanw5w

Conceived & majestically led by @DrJigsaww @harrisjuliea @AllenInstitute

Thread covering DMN basics + implications of findings
1/n 👇
What is the Default Mode Network (DMN)?

👉Network identified in human PET/fMRI studies
👉Active and strongly synchronized during rest
👉Desynchronized by goal-oriented tasks
👉Encompasses associative cortices - Prefrontal, Cingulate, Retrosplenial, Parietal, Temporal

2/n
Why study the DMN?

👉Most prominent large-scale network of human brain
👉Pivotal substrate for higher-order cognitive and social functions
👉Key point of vulnerability for autism, schizophrenia, Alzhemier's and other brain disorders (seminal feature review below)

3/n
Read 13 tweets

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