In this interview, Claudia Gonzalez, Assistant Professor of Psychology at Thompson Rivers University, shares how her research uses neuroimaging to study neurocognitive aging. #fNIRS plays a central role in this work. Using the Brite, her lab investigates brain–behavior relationships across diverse populations, while also integrating other techniques such as eye tracking, #fMRI, and neurostimulation.

🔗 Read the full interview here https://zurl.co/Xtmon

This article examines how genetic risk for anhedonia is linked to distinct patterns of brain activity during reward processing, using polygenic risk scores and fMRI during a monetary incentive delay task. Findings suggest lower activation in reward-related regions during anticipation and feedback phases in those with higher genetic risk.

This piece is of interest to psychology readers because it connects genetic factors with neural mechanisms of motivation and pleasure, illustrating how biology can shape cognitive and affective processes involved in reward.

Article Title: Genetic risk for anhedonia linked to altered brain activity during reward processing

Link to PsyPost Article: ift dot tt/THsvVta

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#genetics #anhedonia #rewardprocessing #fMRI #psychobiology

@elduvelle_neuro

To me, fMRI is the equivalent of measuring economic activity across the world by looking at GDP amounts and growth, and trade balances across countries, regions, or continents. Nobody can claim this or that person or city was specifically responsible for the changes, and that's part of what's built into these coarse yet presumably useful economic indicators: the particulars don't matter. (To the point that many measures are averaged that shouldn't be, hiding massive inequalities in opportunity, outcomes, family budgets, education, and more.)

When an fMRI paper claims to look at neural activity patterns, benevolently I presume the authors are speaking at the analogue level of precision of GDP, economic growth, and trade balances. Perhaps here it is useful to distinguish between "neural" and "neuronal".

Any conclusions on mechanisms responsible for the observed activity patterns must be ignored for there isn't any basis whatsoever on the data. Thankfully these are written in the discussion section of the papers: the opinions of the authors about their own results. Since only the methods and results can be read from these papers, often there isn't much or anything to learn from them: all the claims are in the form of (over)interpretations listed in the discussion section.

#neuroscience #fMRI

I know I keep asking this but how can #Neuroscientists say that #fMRI lets you look at "neural activity patterns"?

The same BOLD signal, in a specific voxel, could be generated from an infinite combination of excitatory and inhibitory neurons being more or less active (and that's not even talking about glial cells). How could similar BOLD signals mean that the underlying neural activity patterns were similar?

I must be missing something, please explain 🙏

#Neuroscience

(2018) Where are the #fMRI correlates of #phosphene perception? www.frontiersin.org/journals/neu... "Threshold phosphenes are weak percepts, and their detection subjective and difficult."

Frontiers | Where Are the fMRI...
Frontiers | Where Are the fMRI Correlates of Phosphene Perception?

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Frontiers
(2018) Where are the #fMRI correlates of #phosphene perception? https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2018.00883/full "Threshold phosphenes are weak percepts, and their detection subjective and difficult."
Frontiers | Where Are the fMRI Correlates of Phosphene Perception?

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Frontiers
AI method sharply improves noise removal in brain imaging

Obtaining clearer functional MRI data about the brain and its disorders is possible using artificial intelligence, according to Boston College researchers who reported recently in Nature Methods that they developed an AI-assisted method to remove "noise", or image distortions, caused by movement, heartbeat, and other factors.

News-Medical

I've now finished Chapter 2 of "ADHD 2.0" (#Hallowell and #Ratey 2021). I've had some hard things to say about this book so far: its #extranormativity, its tone of pontificating certainty, its overconfident reliance on dubious #fMRI findings, the appalling glimpse of support for #ABA in a skimmed later chapter. But in the second half of Chapter 2, I've found something really interesting and potentially helpful, something that rings true from my experience, quite apart from any #fMRI findings.

The authors point out a way that #anxiety and #depression can arise purely from the #attentional-focus problems definitive of #ADHD, and NOT from the cognitive errors to which #CBT attributes such problems. The idea is that the obsessiveness of #ADHD, when focused on anything negative, creates a self-sustaining, self-amplifying vortex of negativity. Their description makes it sound almost like a bad trip on #psychedelics. The solution is NOT to try to debunk the negative thoughts that make up the vortex, #CBT-style; indeed, that approach might make things worse by reinforcing the focus on the negative thoughts. Instead, try to refocus on — indeed, obsess about! — something positive instead.

Indeed, #anxiety and (especially) #depression were my own psychiatric diagnoses (not counting bipolar disorder, which later psychiatrists rejected decisively as a misdiagnosis). #CBT was worse than useless. Instead, I got help from antidepressant drugs — and I don't think it was an accident that the best one for me turned out to be Wellbutrin (bupropion), which doubles as a third-line #ADHD drug. And the subjective experience of depression, and of recovery from it, matched Hallowell and Ratey's attentional account, rather than the error-correcting story #CBT tells. I suspect that if there were such a thing as "attentional psychotherapy", I might have benefited from getting that instead of #CBT.

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@autistics