HoldsUp

Axel Montagne

UK Dementia Research Institute at the University of Edinburgh Centre for Clinical Brain Sciences

Axel Montagne, PhD, is a Chancellor's Fellow and group leader at the UK Dementia Research Institute at the University of Edinburgh Centre for Clinical Brain Sciences. His research focuses on the role of brain vasculature and blood-brain barrier dysfunction in the early stages of dementia and age-related cognitive decline. His published studies cover topics including glial-vascular interactions, pericytes, transcriptomics of brain vascular cells, cerebral small vessel disease, and neurodegenerative mechanisms in Alzheimer's disease.

62 claims checked on air: 5 context 5 contradicted 3 overstated 43 supported 6 unverified

What they said on air - overstated

14 citing their own research

0:00:56overstatedlowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Lack of exercise accelerates age-related vision loss.

"It's true for the eyes, obviously, or if you don't exercise you're gonna tend to lose eye vision quicker than the normal person as you age" (said at 0:00:56)

Observational cohort studies show that higher physical activity is associated with a modest reduction in the risk of certain age-related eye conditions, primarily cataract (relative risk ~0.90) and diabetic retinopathy, but evidence for age-related macular degeneration is weak and statistically inconsistent (relative risk ~0.92, 95% CI: 0.84–1.01), and studies find no clear association with glaucoma. Furthermore, these epidemiological associations do not demonstrate that physical inactivity directly accelerates the rate of normal age-related visual decline (such as presbyopia) or vision loss in general.

0:45:55overstatedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Administering omega-3 fatty acids to aged mice reduces brain endothelial VCAM-1 levels.

"A couple of studies have given some omega-3 to the mice, and I remember seeing the reduction of one particular protein that I really like to study and we are currently studying is VCAM-1, vascular cell adhesion molecule 1. And omega-3 was able to reduce these levels" (said at 0:45:55)

While omega-3 fatty acids have been shown to attenuate vascular cell adhesion molecule 1 (VCAM-1) expression under neuroinflammatory conditions, this reduction was demonstrated in an in vitro human microfluidic blood-brain barrier model stimulated with interleukin-1β rather than directly measured in the brain endothelium of aged mice in vivo. In mice subjected to orthopedic surgical trauma, intravenous omega-3 fatty acid administration inhibited surgery-induced blood-brain barrier impairment and microglial activation, but the claim overstates the evidence by extrapolating the specific endothelial VCAM-1 attenuation from the cell model to in vivo mouse studies.

1:24:42overstatedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Chronic alcohol consumption leads to blood-brain barrier leakage in males, whereas age-matched female chronic drinkers show relatively preserved vascular function.

"there is a gender effect, a sex effect. So the males tend to have—if you're a chronic drinker of alcohol, you will have some vascular issues. It has been linked, so if you chronically drink alcohol, you have a leakier blood-brain barrier, it has been shown. But if a woman drank the same, as age-matched and everything, they will have almost preserved vascular functions." (said at 1:24:42)

The speaker extrapolates findings from preclinical rodent experiments directly to human men and women. In animal models of chronic and intermittent ethanol exposure, male rats demonstrate increased blood-brain barrier (BBB) permeability and vascular dysfunction across several brain regions, whereas age-matched female rats show resistance to ethanol-induced BBB hyperpermeability. However, direct evidence establishing that human females are protected from alcohol-induced neurovascular or BBB disruption compared to males is lacking, and broader human epidemiological literature indicates that women often experience equal or heightened susceptibility to alcohol-related systemic and organ toxicity at equivalent exposure levels.

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