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Dementia prevention can’t rely on individual choices alone, new study finds | News at Curtin

Researchers found far less attention is paid to social and environmental influences such as education, housing, neighbourhood safety, healthcare access, clean air and social connection — despite growing evidence these factors affect people’s ability to protect their brain health.”

curtin.edu.au

Efforts to prevent dementia may be placing too much responsibility on people’s choices while overlooking the wider social and environmental conditions that ...

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Dementia prevention can’t rely on individual choices alone, new study finds | News at Curtin

Researchers mapped 61 potentially modifiable dementia risk and protective factors to assess whether prevention efforts are overlooking the broader social, environmental and policy influences that shape lifelong brain health.

curtin.edu.au

Efforts to prevent dementia may be placing too much responsibility on people’s choices while overlooking the wider social and environmental conditions that ...

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Dementia prevention can’t rely on individual choices alone, new study finds | News at Curtin

“Efforts to prevent dementia may be placing too much responsibility on people’s choices while overlooking the wider social and environmental conditions that shape brain health, according to new Curtin University research published in The Lancet Public Health.

curtin.edu.au

Efforts to prevent dementia may be placing too much responsibility on people’s choices while overlooking the wider social and environmental conditions that ...

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Josh Taylor @joshtaylor.bsky.social · 24/09/2026

NSW Health once again hiding comments that don’t fit their narrative. Having a healthy lifestyle is good for everyone, but that alone won’t prevent dementia. Outsourcing public health to individuals doesn’t work for COVID, won’t work for dementia.

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Reposted by Angry Redhead

If ultimately there's no criminal responsibility for this incident here then FOI just became a lot easier if we ask AI agents to go find those documents for us. www.theguardian.com/australia-ne...

theguardian.com

Albanese says OpenAI hacked Medicare and told Australia months later via email to generic inbox

Prime minister says he told Sam Altman he was disappointed it had taken OpenAI ‘way too long’ to disclose breach

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Reposted by Angry Redhead

Crowbar @crowbar.wtf · 24/09/2026

4 Corners do a dodgy investigation into Chinese EVs being susceptible to “hacking”, meanwhile an AI has a nosy around private data in an Australian government system. Make the world make sense.

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@szupraha @ZdravkoOnline @VZPtweetuje Hedberg at al., Cognitive fatigue is related to reduced cerebral perfusion & sustained attention in patients with post COVID-19 condition: An fMRI study. www.sciencedirect.com/science/arti... #COVIDisnotover #mask4yourlife #cleantheair

sciencedirect.com

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Every scan like this is one person routine workup would have sent home healthy.

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The objective evidence exists - & the illness is still communicated as functional, as a thing in the head. Prevention gets written off on that basis. Yet the denominator is population-scale - mild infections times reinfections times prevalence.

What's left. An objective, instrument-measurable hemodynamic deviation in people with clean routine MRI, nearly three years after a mild infection, converging with metabolic & microvascular findings from elsewhere. A group signal, not an individual diagnosis. As a population picture, it holds.

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The cohort is overwhelmingly pre Omicron - ancestral + Alpha/Delta, with only a few percent in the Omicron era.

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In long COVID we have the finding without the therapy. It is cross-sectional, no follow-up, so nothing about whether perfusion stays low or reverses. Controls couldn't be tested for prior infection - silent infections among them would shrink the difference, not inflate it.

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A viral parallel this field knows well. HIV. In HIV-Hand, cerebral hypoperfusion is documented - chronic viral involvement in the CNS, with cognition & fatigue grinding along below the clinical threshold, missed by routine imaging. Hand, we've learned to hold back with treatment.

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The authors point at microvascular & endothelial dysfunction & at a leaky BBB. Rubin 2025 found long-term increased barrier permeability even where CBF was unchanged - so these don't have to move together, & the barrier can be quietly compromised.

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It doesn't sit in isolation. Ganesh this year showed cortical hypometabolism on PET in long COVID with fatigue, also ~2 years out. Kim, Qin independently reported reduced CBF. Retinal work points at the microvasculature. Metabolism & perfusion are two windows onto the same lowered activity.

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Perfusion & performance track together. Global blood flow correlated with reaction times even after statistically adjusting for the global level - so it isn't one region driving it, but a system level sensitivity of attention networks to under perfusion.

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Sounds like a footnote, but in multiple sclerosis & mild brain injury, performance variability is a stronger predictor of fatigue than average speed. & almost nobody measures it - which is why it's novel here.

Variability. Reaction times swung more in patients in every segment of the test, in controls they didn't.

The global difference is modest - around 5% (49 vs 52 mL/100g/min). You may see 38% lower perfusion quoted somewhere. That figure comes from clusters selected precisely because they differed most. Important. The second signal may be firmer than the perfusion itself.

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The authors computed how unevenly perfusion was distributed across gray matter - proxy for how staggered the arrival is. In patients it was significantly higher (46 vs 41%). So even the it's mostly delayed, scattered inflow reading is a real finding, not a measurement artifact.

This study can't separate the two (technical). But neither reading says the vessels are fine. It moves the abnormality from the tissue to the delivery. It doesn't erase it. That delay isn't just a convenient escape hatch.

What lower perfusion actually means. Blood flow is tightly coupled to metabolism - to how hard the tissue is working. A lower value can mean two things. Either less blood reaches the tissue, or blood arrives late & unevenly - what's called arterial transit time.

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What it found instead - they were slower from the first minute, & their performance swung far more. Not running out of gas - more like running the whole task on a smaller tank at a higher cost.

Measured with ASL, a technique that magnetically tags your own blood as contrast. The study is framed around cognitive fatigue & went hunting for fatigability - the idea that performance progressively decays during a demanding task as you run out. It didn't find that.

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22 people with long COVID. Mild infection, no hospitalization, nearly three years out. Routine MRI clean - the radiologist found nothing. Their brains still perfuse measurably worse than matched controls. Not in one spot, but globally.🧵

Via Zdenek Vrozina Comments below theirs. Cognitive fatigue is related to reduced cerebral perfusion and sustained attention in patients with post COVID-19 condition: An fMRI study

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Thank you. I don’t have either, no menopause symptoms meant I didn’t go to a O&G or menopause clinic. I’ll ask my GP.

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SARS-CoV-2 triggers a wide range of dysregulation that can induce a wide range of symptoms. ACE2 dysregulation and lipid metabolism: Mechanistic interplay between COVID-19 and neurodegeneration'” #COVIDisnotover #mask4yourlife #cleantheair

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The overlapping mechanisms also involve RAS (renin-angiotensin system) imbalance, including ACE2 (primary host receptor for SARS-CoV-2) dysregulation, which has been suggested to contribute to both Long COVID and neurological diseases."

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Moreover, in both AD and PD, aberrant lipid metabolism is increasingly recognised as a key contributor to neuroinflammation, synaptic dysfunction, and neuronal death..

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This BBB impairment may allow peripheral inflammation to affect the brain, potentially accelerating the onset or progression of diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD).

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