Comments
adnbenji t1_j3fwu33 wrote
What's the summary of this for a dumb person like me? While trying to disprove the idea that cumul of Amyloid Beta is linked to Alzheimer's, they found it could in fact be right?
ThatAndresV t1_j3g6nxv wrote
I asked OpenAI to summarise as if I was a grade 6 student and it told me:
A new study challenges existing ideas about the relationship between amyloid beta protein build-up in the brain and Alzheimer's. The study found that older, cognitively healthy brains had similar levels of one type of amyloid protein as brains of Alzheimer’s patients, although the Alzheimer's brains had higher levels of another type of amyloid protein that can form plaques linked to the disease.
ThatAndresV t1_j3g6t0y wrote
And then I asked… Human: what are the implications for other studies? AI: The findings from this study suggest that further research is needed to fully understand how amyloid beta proteins are linked to normal brain aging as well as how they may cause Alzheimer's disease. Additionally, this research may help inform the development of new treatments for Alzheimer's that are specifically designed to target amyloid beta build-up.
BafangFan t1_j3g5mdf wrote
We spend so much time and money barking up the wrong tree.
Alzheimer's is called by some researchers as Type 3 Diabetes. That indicates there is a glucose metabolism impairment in the system.
Even back in 2019 they found that scanning the brain for glucose metabolism was more accurate at predicting Alzheimer's than scanning for amyloid plaques.
https://www.beingpatient.com/alzheimers-pet-scans/
The brain can run on glucose, but it can also run on fat and ketones. And both fat and ketones can ameliorate the issue of glucose metabolism impairment.
There is a growing body of anecdotal data to show improvement in Alzheimer's and dementia symptoms in people who follow a carnivore or ketogenic diet. A clinical ketogenic diet is also a standard of care in drug resistant epilepsy in children - so it's already a medically approved technique for brain impairment issues.
calumin t1_j3hrjep wrote
Given that the data is anecdotal, you might be barking up the wrong tree. Still, it’s worth spending some time and money investigating it.
BafangFan t1_j3i4zu0 wrote
Yeah, I/we could be wrong.
But the risks of diet change are very low. Maybe so diarrhea and cravings in the early stages of transition. Maybe some boredom of a limited diet.
But the rewards can be significant. People have gone from living in Groundhogs Day to being able to remember the past few months.
calumin t1_j3i6qjq wrote
Ok but this post about the science related to something completely different.
BafangFan t1_j3ie4jf wrote
I thought it was about the science of how to detect the degree of Alzheimer's in a person ?
I'm arguing that glucose metabolism is a more insightful indicator of Alzheimer's progression than any plaques/proteins.
And I'm arguing that if glucose metabolism is functioning poorly, the brain can alternatively use more fat/ketones; and with a non-impaired fuel source metabolism, the brain can restore some of its previous function.
calumin t1_j3imrll wrote
That’s not what the scientific article is about.
BafangFan t1_j3j4jkx wrote
>Rather than Alzheimer’s simply involving increased production of Aβ protein, the more important issue may be a reduced ability to effectively clear the protein and stave off the creation of plaque-contributing fibrillary amyloid, Thorwald said.
>“These findings further support the use of aggregated, or fibrillary, amyloid as a biomarker for Alzheimer’s treatments,” Thorwald said. “The site in which amyloid processing occurs has less precursor and enzyme available for processing, which may suggest the removal of amyloid as a key issue during Alzheimer’s.”
The focus is still on amyloid plaques, is it not?
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SonUnforseenByFrodo t1_j3h8bea wrote
OK do they even know if this is produced by our body due to genetics or is it produced due to external factors?
Wagamaga OP t1_j3d7zij wrote
A new USC Leonard Davis School of Gerontology study challenges existing ideas of how buildup of a protein called amyloid beta (Aβ) in the brain is related to Alzheimer’s disease.
While buildup of amyloid protein has been associated with Alzheimer’s-related neurodegeneration, little is known about how the protein relates to normal brain aging, said University Professor Caleb Finch, the study’s senior author and holder of the ARCO/William F. Kieschnick Chair in the Neurobiology of Aging at the USC Leonard Davis School.
To explore the levels of Aβ in human brains, the researchers analyzed tissue samples from both healthy brains and brains of patients with dementia. More severe Alzheimer’s cases were indicated by higher Braak staging scores, a measurement of how widely signs of Alzheimer’s pathology are found within the brain.
The analysis revealed that older, cognitively healthy brains showed similar amounts of dissolvable, non-fibrillar amyloid protein as brains of Alzheimer’s patients. But, as the researchers expected, the brains of Alzheimer’s patients had higher amounts of insoluble Aβ fibrils, the form of amyloid protein that aggregates to form the telltale “plaques” seen in the disease, said Max Thorwald, the study’s first author and a postdoctoral researcher at the USC Leonard Davis School.
https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12896