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 - unverified

14 citing their own research

0:00:17unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Capillaries represent approximately 90 percent of the brain's vasculature.

"and remember the capillaries, it represents 90 percent of your brain vasculature, all these tiny blood vessels." (said at 0:00:17)

No published record matching the specific claim that capillaries represent approximately 90 percent of the brain's vasculature was located; this does not prove the claim false.

0:14:50unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Approximately one-fourth of the world's population carries the APOE4 genotype.

"But again, we are talking about one-fourth of the population of the world having the APOE4 genotype, so one-fourth, there's heterozygous and homozygous people." (said at 0:14:50)

No published record matching the claim that approximately one-fourth (25%) of the world's population carries an APOE4 genotype was located among the retrieved sources; this does not prove the claim false.

0:24:05unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Vascular inflammation causes brain pericytes to shorten their cellular processes, thereby reducing cerebral blood flow.

"And these processes will shorten because of the inflammation, and of course if the pericytes are shortening their processes, the flow will reduce." (said at 0:24:05)

No published record matching the claim that vascular inflammation causes brain pericytes to shorten their cellular processes and thereby reduce cerebral blood flow was located; this does not prove the claim false. While brain pericytes participate in neurovascular regulation, capillary constriction, and inflammatory signaling, a specific mechanism where inflammation-induced shortening or retraction of pericyte processes directly mediates reduced cerebral blood flow has not been demonstrated in the published literature.

0:25:26unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

The omega-3 transporter MFSD2A is specifically localized to the smallest blood vessels (capillaries) in the brain.

"and you mentioned MFSD2A, which is one of the markers we are studying carefully because it's specific to the smallest blood vessels in the brain, so the capillaries, and that's where most of the pericytes are." (said at 0:25:26)

No published record matching the claim that the omega-3 transporter MFSD2A is specifically localized to the smallest blood vessels (capillaries) in the brain was located; this does not prove the claim false.

1:19:04unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

More than one third of patients in cerebral small vessel disease cohorts do not have hypertension.

"because to give you an example here, maybe a third, even more, of the cohort of these patients that we follow, they don't have any hypertension, first of all. So it tells you that there's a big chunk of people that can move to small vessel disease" (said at 1:19:04)

No published record matching the specific proportion of patients without hypertension in the cited cerebral small vessel disease cohort was located; this does not prove the claim false. While hypertension is established as a major risk factor for cerebral small vessel disease (CSVD) and white matter hyperintensities, the exact proportion of normotensive individuals across specific longitudinal clinical cohorts varies across study cohorts and definitions.

1:20:08unverifiedvery lowAxel Montagne, PhD, on Solving Alzheimer’s and Dementia with

Hypertension in early adulthood (30s and 40s) increases the likelihood of rapid cognitive decline compared to normotensive peers, whereas hypertension onset in the 70s does not increase dementia risk.

"if you have early, like 30s, 40s—30s, 40s, if early hypertension, you will have a likelihood and more chance to develop cognitive decline quickly as compared to a normotensive person of the same age. And interestingly, they were showing also in the paper that if it's during your 70s, if I remember correctly, it doesn't impact your likelihood to develop dementia." (said at 1:20:08)

No published record matching the claim that hypertension onset specifically in the 30s and 40s leads to rapid cognitive decline while onset in the 70s has no impact on dementia risk was located; this does not prove the claim false.

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