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Columbia and MIT studies point to two possible Alzheimer’s research approaches

The New York Post reports that researchers at Columbia and MIT identified two biological findings that could guide future Alzheimer’s research. One concerns a rare FN1 mutation that appeared to keep fibronectin under control; the other links suppressed Wnt signaling with fat buildup in cells that produce myelin.

AI-assisted synthesis · Based on 3 outlets' reporting · Article text read from 1 of 3 outletsHow it's made

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3 outletsLatest reporting 3 min read
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What happened

Key facts

  • Researchers at Columbia and MIT identified two findings that could inform future Alzheimer’s therapies (per New York Post).
  • The New York Post says about one in nine people over 65 have Alzheimer’s (per New York Post).
  • Columbia researchers found that some people with APOE4 also had a mutation in the FN1 gene, which provides instructions for making fibronectin (per New York Post).
  • MIT researchers found that APOE4 was associated with suppressed Wnt signaling and fat buildup in oligodendrocytes, the cells that make myelin (per New York Post).

The brief

Researchers at Columbia and MIT identified two biological findings that could inform future Alzheimer’s research, according to the New York Post. One involves a rare mutation in the FN1 gene that appeared to keep fibronectin under control. The other links disrupted Wnt signaling to fat buildup in brain cells that produce myelin.

The findings point to possible research approaches, not established treatments. The New York Post describes APOE4 as a common gene variant used in Alzheimer’s research. It says one in four people carry the variant and that carriers face at least twice, and up to 12 times, the risk of developing Alzheimer’s. The outlet also says about one in nine people over 65 have the disease.

It notes that not every APOE4 carrier develops Alzheimer’s. Columbia researchers found that some people with APOE4 also had a mutation in FN1, which provides instructions for making fibronectin.

The outlet says this gene mutation is often seen in APOE4 carriers who develop Alzheimer’s, while the rare mutation identified by the researchers appeared to have a different effect: keeping fibronectin under control. The account does not provide further details about how the researchers studied the mutation or how it might affect disease development.

Caghan Kizil, identified by the outlet as an author of the study, said the work moves from a genetic clue toward a disease mechanism. That comment characterizes the significance of the Columbia finding; it does not establish that the mutation prevents Alzheimer’s or can be used as a treatment.

Separately, MIT researchers found that Wnt signaling was suppressed in people carrying APOE4, according to the New York Post. The outlet says this suppression led to fat accumulating inside oligodendrocytes, cells that make myelin. Myelin forms fatty protective insulation around nerve fibers, and the account says faulty oligodendrocytes produce less of it.

The New York Post identifies CHIR99021 as an experimental compound that inhibits GSK3B in connection with the MIT finding. The account does not say that the compound has been shown to prevent or treat Alzheimer’s in people. Both findings are presented as avenues for further research, rather than demonstrated ways to prevent the disease.

Why it matters

  • The New York Post says about one in nine people over 65 have Alzheimer’s, giving the disease’s reported prevalence context.
  • The outlet says one in four people carry APOE4 and that carriers face at least twice, up to 12 times, the risk of developing Alzheimer’s.
  • The findings identify distinct biological mechanisms for research: fibronectin regulation associated with an FN1 mutation, and Wnt signaling linked to fat buildup in myelin-producing oligodendrocytes.
  • CHIR99021 is identified as an experimental compound that inhibits GSK3B; the outlet does not describe it as an established treatment.

What to watch next

  • Whether further research tests the apparent effect of the rare FN1 mutation on fibronectin control.
  • Whether further research examines the relationship between suppressed Wnt signaling and fat buildup in oligodendrocytes.
  • Whether researchers study CHIR99021 further in connection with the MIT finding.
  • Whether either research avenue demonstrates a role in preventing or treating Alzheimer’s.

How it's being covered

Coverage analysisShow details
3 source articles · 3 unique outlets
Outlet political mix: Too few rated· 1 Left · 1 Right · 1 unrated
Where the outlets are based: US/Canada 67% · Unknown 33%
Outlet political mix
Too few rated
Left
Center
Right
1 outlet
0 outlets
1 outlet
The marker shows coverage balance: each unique outlet counts once. 1 unrated outlet is not included.
Geography
Where the outlets covering this story are based.
3 unique outletsDominant coverage: US/Canada
How we measure coverage

How outlets' accounts compare

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Timeline

Developments from this story's sources, dated background we compiled and fact-checked, and our earlier coverage. Each row says which.
  1. Alzheimer’s disease was first described by German psychiatrist Alois Alzheimer in 1906, after he reported changes in the brain of patient Auguste Deter.
    Background · from our historical context
  2. In 1910, psychiatrist Emil Kraepelin used the name “Alzheimer’s disease” in a textbook.
    Background · from our historical context
  3. Research subsequently established that the disease involves more than amyloid: in 1986, scientists identified the tau protein as the main component of neurofibrillary tangles, another characteristic brain change.
    Background · from our historical context
  4. In 1993, researchers identified the APOE gene variant as a major genetic risk factor for late-onset Alzheimer’s, though carrying it does not mean a person will develop the disease.
    Background · from our historical context
  5. The FDA approved lecanemab for people with early Alzheimer’s disease.
    Background · compiled and fact-checked by Updat3
  6. The FDA approved donanemab for people with early Alzheimer’s disease.
    Background · compiled and fact-checked by Updat3

How we got here

The treatment backdrop before these studies included two U.S. approvals of drugs that target amyloid, a protein that accumulates in Alzheimer’s disease: the Food and Drug Administration approved lecanemab in January 2023 and donanemab in July 2024 for people with early Alzheimer’s.

In 1993, researchers identified the APOE gene variant as a major genetic risk factor for late-onset Alzheimer’s, though carrying it does not mean a person will develop the disease. Alzheimer’s disease was first described by German psychiatrist Alois Alzheimer in 1906, after he reported changes in the brain of patient Auguste Deter.

Original sources

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