Who is more prone to Alzheimer’s? Scientists might have found a clue

 

With your risk of dementia post stroke, what will your competent? doctor do with this to prevent those problems? 

Parkinson’s Disease May Have Link to Stroke March 2017 

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

Oh, sorry; NOTHING AT ALL! In my opinion your doctor is completely incompetent in not using research to get you recovered!

Who is more prone to Alzheimer’s? Scientists might have found a clue

A slight difference in DNA could shape some peoples’ susceptibility to developing Alzheimer’s disease, researchers have found.

Experts based at various institutions in Hong Kong found that Chinese participants with longer repeats of a specific gene sequence in their DNA were more likely to have the disease. The association was also noted among European participants, although it was much weaker.

The study was published in the journal Nature Neuroscience on October 12.

Researchers have previously identified several genetic variants that are believed to be associated with Alzheimer’s risk, and it is understood that those who have a parent or sibling diagnosed with the disease are more likely to develop it than people without those links—although this doesn’t mean that person will develop Alzheimer’s, it only increases the odds.

That said, Alzheimer’s does not have a single genetic cause, and is believed instead to be influenced by a combination of genetic, lifestyle and environmental factors.

What the experts set out to understand in this study was whether repeats of certain genetic sequences—rather than specific genetic variants—could influence risk.

Rudolph Tanzi, a professor of neurology at Harvard University, told Newsweek that the “potentially important” study “goes beyond the normal single-base genome variants that are tested in the many genome-wide association studies of Alzheimer’s disease.”

 Related video: New study identifies possible early sign of dementia (Welltica+)

“We know that the common DNA variants that show association with Alzheimer’s in genome-wide association studies account for less than 50 percent of the heritability of Alzheimer’s disease. So finding these types of DNA repeat variants in the genome is very important,” he said.

Dr. Michael Guo, an assistant professor of neurology and genetics, and a clinician in the University of Pennsylvania Memory Center, told Newsweek: “This is an exciting study that highlights the importance of studying diverse populations and expanding our analyses to include broader sets of spelling errors in our DNA.”

“Their work may help improve our ability to predict Alzheimer’s disease risk,” he added. “Ultimately, by identifying a new gene linked to Alzheimer’s disease, this could spur further work into how FAM193B causes disease and whether it may serve as a drug target.”

A Chinese cohort of over 3,000 people were included in the study—around half of whom had Alzheimer’s disease—as well as genetic data and records obtained from UK Biobank (around 2,600 with Alzheimer’s and almost 23,000 controls) to see whether the findings were the same among different ancestries.

From 11 of the Chinese participants, the researchers built a more detailed reference of different structural DNA sets and then analyzed the collections of the other DNA readings.

They noticed that the CCG DNA string could have repeats from between four to 30 among the participants, and found that those with at least 18 repeats had twice the odds of having Alzheimer’s disease than those with no more than 11 repeats. This indicates that repeated strands of the sequence could increase likelihood of having the disease, not a person’s lifetime risk of developing the disease.

The finding was also weaker—though still identified—among the European participants’ records from UK Biobank, meaning that the estimate among the Chinese cohort cannot be translated directly across different ancestral groups.

“This isn’t unexpected, many genetic variants including APOE have different effect sizes in populations of different ancestries,” Michael Lutz, a professor of neurology and pathology at Duke University, told Newsweek. APOE is the gene that has been associated with Alzheimer’s, and its variant APOE4 is the strongest known genetic risk factor for the disease.

What’s Behind The Association?

Reasons for this association could be down to FAM193B expression. The experts found that more repeats of the CCG sequence resulted in higher FAM193B expression, and that increased activity was separately found to result in nerve cell DNA damage and cellular harm.

The researchers also noted that FAM193B protein “directly interacts” with the enzymes GSK3alpha and GSK3beta, which is notable as they said when these enzymes dysregulate it can result in increased beta-amyloid and tau—the two proteins associated with Alzheimer’s disease.

“Analyses of postmortem human brains and cultured neuronal cells showed that elevated neuronal FAM193B expression is associated with DNA damage and cell death-related pathways which are key pathways involved in Alzheimer’s disease pathophysiology,” Lutz said.

“These findings establish the common FAM193B-CCG repeat as an Alzheimer’s disease risk genetic factor and highlight the contribution of common structural variants to Alzheimer’s disease heritability,” he added.

The experts emphasized that this does not mean that longer repeats of CCG damage neurons for certain or explain the association entirely.

What This Means For Alzheimer’s

Lutz said that it is “early to consider the impact of the findings on Alzheimer’s disease prevention and treatment,” but that the “most immediate application of the finding would be for Alzheimer’s disease risk prediction.” This is because the paper provides “support that including the structural variant, with the caveat of ancestral-specific risk, will improve lifetime disease risk prediction in clinical settings.”

He added that “as is pointed out in the paper, the biological function of the FAM193B gene is unclear, so further research would be needed to understand the biochemical and physiological impact of the repeat.”

Tanzi also said that the CCG variant association was found in a “relatively small Chinese population and will need to be replicated in larger populations.”

He added that the gene implicated here is “very interesting as one can imagine how it might affect tau tangle pathology downstream of amyloid deposition (by affecting the enzyme GSK3beta).”

“Functional studies along these lines are now warranted as well as replication of the genetic association with Alzheimer’s disease in larger populations,” he said.

Reference

Cao, H., Fu, Y., Zhou, X. et al. (2026) Genome-wide analysis of common structural variants in Alzheimer’s disease identifies a risk-associated regulatory CCG repeat in FAM193B. Nature Neuroscience. https://doi.org/10.1038/s41593-026-02481-z

Contact Newsweek editors on this story: Kara Dolman and Tony Phillips.

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