6 Likes

This is an interesting story, showing just how much we may be able to influence the course of Alzheimers…

Preventive neurologist Dr Richard Isaacson stared at the numbers on the fax in astonishment. Blood biomarkers of telltale signs of early Alzheimer’s disease in the brain of his patient, 55-year-old entrepreneur Simon Nicholls, had all but disappeared in a mere 14 months.

“I had to catch my breath. It was a complete shock: The blood tests on his brain had normalized,” said Isaacson, director of research at the Institute for Neurodegenerative Diseases in Boca Raton, Florida.

3 Likes

Yeah, truly is - this case and others are discussed here and in the following posts

Did anyone end up seeing the documentary that they did?

1 Like

I did not - but here is more info on it:

Its available on Amazon / Peacock to stream:
https://www.amazon.com/Dr-Sanjay-Gupta-Reports-Alzheimers/dp/B0CVDP5MS5

More details:

2 Likes

A landmark new statement released by the American Heart Association warns that three common cardiovascular diseases – heart failure, atrial fibrillation and coronary heart disease – raise the risk of developing dementia, an umbrella term describing a set of symptoms including difficulties with memory, thinking, problem-solving, judgement or language.

Research has shown that 14 to 81 per cent of patients with heart failure experience some degree of cognitive impairment. People with atrial fibrillation have a 39 per cent increased risk of memory or thinking problems, while those with heart disease have a 27 per cent higher risk of developing dementia. Following a heart attack, up to 50 per cent of patients experience cognitive decline.

https://www.telegraph.co.uk/health-fitness/conditions/heart-health/heart-conditions-dementia/

3 Likes

Dr Michael Roizen, chief wellness Officer of Cleveland Clinic on what to do to prevent brain dysfunction.

“Supplements can give you 4 more years of longevity. Stress management can give you 30 years.” -Dr. Roizen

相关:

1 Like

@RapAdmin Do you know if those talks will be online?

No, they won’t be. The above image is from the Longevity Clinics Roundtable at the Buck Institute - and they don’t seem to be recording the talks during the presentations, and don’t have any history of putting anything regarding them online. This is a very focused conference targeted at doctors doing longevity medicine and starting longevity clinics. Its production is a collaboration by the Buck Institute and the Longevity Center EU, and seems designed to accelerate and improve the quality, of longevity clinics globally.

I attended yesterday and did record some of the presentations on my phone, and took photos of the presentations - and will do a write up on what I learned (lots) and put some of the information up here when I have a chance. I was busy today, and didn’t see as much value in today’s agenda, so did not attend.

Earlier last week (Tuesday/Wednesday) were the Longevity Summit conference days, and those were video recorded and will be made available online (mostly, I think). I’m also working on a writeup of that conference.

6 Likes

Thanks a lot @RapAdmin

1 Like

Evidence Mounts for Potential of GLP-1s in Alzheimer’s Disease 2024

While preclinical studies have shown benefits of GLP-1 receptor agonists in targeting the core pathology of Alzheimer’s disease, data from clinical studies are limited, according to an article recently published in the Journal of Alzheimer’s Disease Reports. That’s set to change next year, however, when Novo is expecting readouts from two large Phase III trials, EVOKE and EVOKE Plus, testing semaglutide in patients with Alzheimer’s. Both trials are expected to be completed in September 2025.
“I’m confident that we will see some effects in the Novo Nordisk trials . . . because everything we’ve seen so far supports this concept,” Hölscher told BioSpace. “We know this is a worthwhile target and it definitely should be pursued.”
Meanwhile, Kariya is developing KP405, a first-in-class, dual GLP-1/GIP receptor agonist, initially for Parkinson’s disease with plans for a study in Alzheimer’s. Hölscher previously told BioSpace that drugs like liraglutide and semaglutide have limitations when it comes to treating diseases of the brain. “They’re actually designed to stay in the blood, which is good for diabetes but bad for Alzheimer’s because a drug that stays in the blood doesn’t get into the brain.” The key, therefore, to applying GLP-1s to dementia is getting the drug where it’s needed.
Kariya has removed “add-ons” such as fatty acids that keep GLP-1s in the blood, allowing its drugs to enter the brain at a higher rate, Hölscher explained. The addition of a TAT sequence that is recognized by cell membrane receptors further enable the drug to reach the brain faster, according to Kariya.
Hölscher credited these modifications for helping KP405 to avoid certain side effects linked to GLP-1s in the Phase I Parkinson’s study. “The GLP-1s, the ones designed to treat diabetes, they can cause nausea and stomach upset and all kinds of side effects,” he said. Because KP405 doesn’t stay in the bloodstream, “the peripheral effects are very little.”
As for Novo’s top GLP-1 competitor Eli Lilly, while there are no studies of tirzepatide in Alzheimer’s listed on the ClinicalTrials.gov database, Suvannevejh said it would be a natural fit for a company “whose entire existence is focused on neurology and neuroscience and Alzheimer’s disease.” Lilly’s monoclonal antibody Kisunla was approved in July, becoming the third disease-modifying treatment for the condition and the second actively on the market.
Eli Lilly did not respond to BioSpace‘s request for comment.
Despite the positive signs in certain studies, experts agree that GLP-1s still have a ways to go to prove their worth in Alzheimer’s.
He made a bold prediction regarding Novo’s EVOKE and EVOKE Plus studies: “If those trials show even a small effect, the amyloid strategy will be dead in the water.”

3 Likes
3 Likes

A new take on Alzheimer’s… more might be better?

A recent study published in [Brain]

(https://academic.oup.com/brain/article/147/10/3513/7754406) challenges long-held assumptions about Alzheimer’s disease treatment.

Researchers at the University of Cincinnati found that new monoclonal antibody drugs may slow cognitive decline by increasing levels of a critical brain protein called amyloid-beta 42 (Aβ42), rather than simply reducing amyloid plaques in the brain. This discovery shifts the focus from plaque buildup to the potential role of Aβ42 in maintaining brain health.

Hmmmmm…

@cl-user or other members here… does anyone have access to these Nature articles, and if you do please post the text (or screen captures of the articles):

How fast is your brain ageing? Proteins in blood offer clues

Biomarkers could monitor ageing in the brain, revealing ways to treat dementia and other age-related brain disorders.
https://www.nature.com/articles/d41586-024-04055-0

Plasma proteomics identify biomarkers and undulating changes of brain aging

Proteomics enables the characterization of brain aging biomarkers and discernment of changes during brain aging. We leveraged multimodal brain imaging data from 10,949 healthy adults to estimate brain age gap (BAG), an indicator of brain aging. Proteome-wide association analysis across 4,696 participants of 2,922 proteins identified 13 significantly associated with BAG, implicating stress, regeneration and inflammation. Brevican (BCAN) (β = −0.838, P = 2.63 × 10−10) and growth differentiation factor 15 (β = 0.825, P = 3.48 × 10−11) showed the most significant, and multiple, associations with dementia, stroke and movement functions. Dysregulation of BCAN affected multiple cortical and subcortical structures. Mendelian randomization supported the causal association between BCAN and BAG. We revealed undulating changes in the plasma proteome across brain aging, and profiled brain age-related change peaks at 57, 70 and 78 years, implicating distinct biological pathways during brain aging. Our findings revealed the plasma proteomic landscape of brain aging and pinpointed biomarkers for brain disorders.

https://www.nature.com/articles/s43587-024-00753-6

1 Like

One story on the above research:

1 Like

I wish I had access to those but unfortunately it’s not the case.
What I do to get access to the figures is an image search in google with the paper title and generally google has indexed the images so here they are:






5 Likes

Journal Source:

Debora Melo van Lent et al, Association between dietary inflammatory index score and incident dementia, Alzheimer’s & Dementia (2024). DOI: 10.1002/alz.14390

Journal information: Alzheimer’s & Dementia

4 Likes
7 Likes

DII scores were calculated for 36 dietary components, which were categorized as either anti-inflammatory (e.g., fiber, vitamins A, C, D, E, omega-3 fats) or pro-inflammatory (e.g., saturated fats, total energy intake, and carbohydrates). Higher positive scores indicated more pro-inflammatory diets.

4 Likes

Researchers used AI to analyze brain images from 70-year-olds, estimating their biological brain age and uncovering connections to lifestyle and health factors. Diabetes, inflammation, and high glucose levels were linked to older-looking brains, while regular exercise and healthy habits were associated with younger-looking brains.

The study highlights the importance of maintaining vascular health to protect cognitive resilience against aging. The researchers aim to refine the AI tool for clinical use and will explore sex differences and social health influences on brain resilience in future studies.

5 Likes

Herewith the full text: Plasma proteomics identify biomarkers and undulating changes of brain aging.pdf (8.8 MB)

4 Likes