Home Health Alzheimer’s may be able to SPREAD to organ transplant patients, study suggests – as experts call for dementia screening for ALL donors

Alzheimer’s may be able to SPREAD to organ transplant patients, study suggests – as experts call for dementia screening for ALL donors

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Researchers in Canada found that mice who received bone marrow transplants containing stem cells with defective genes developed Alzheimer's faster than those who did not receive it.
  • Researchers from Canada suggested that Alzheimer’s could spread in mice
  • The spread was due to bone marrow transplants containing defective genes.
  • READ MORE: NIH launches urgent investigation into whether Alzheimer’s can spread

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Alzheimer’s disease could be transmitted to patients who receive transplants that contain potentially toxic genes, a study suggests.

Researchers in Canada are now calling for all donors to be tested for the disease if no cases are detected.

The new study examined mice that were transplanted with stem cells from their bone marrow from donors with familial Alzheimer’s disease.

This type is caused by a single genetic mutation passed from parent to child and affects almost 350,000 Americans and 1 percent of Alzheimer’s cases in the United Kingdom.

Researchers in Canada found that mice that received bone marrow transplants containing stem cells with defective genes developed Alzheimer's faster than those that did not receive it.

Researchers in Canada found that mice that received bone marrow transplants containing stem cells with defective genes developed Alzheimer’s faster than those that did not receive it.

Alzheimers may be able to SPREAD to organ transplant patients

Alzheimers may be able to SPREAD to organ transplant patients

A spectacular study from the United Kingdom evaluated five patients who were injected with growth hormones infected with toxic amyloid beta protein “seeds” as children. All five suffered from the same rare, early-onset form of devastating dementia. Other people who received the same treatment are now considered “at risk”

Patients with this form of Alzheimer’s carry a defective version of the amyloid precursor protein (APP) gene, which can develop into plaques and degrade the brain.

For the first time, the study appeared to show that this process begins outside the central nervous system and then travels to the brain where it causes the cognitive decline associated with Alzheimer’s disease.

The team found that the mice showed signs of cognitive decline starting at six months of age, in almost half the time as those that did not receive transplants.

The study comes amid explosive evidence from the UK suggesting that at least five people “catched” the memory-robbing disorder through a now-banned hormone treatment that was contaminated with toxic proteins from the bodies of sick people.

The authors of the new research called for blood, tissue and organ donors to be screened for Alzheimer’s disease to prevent possible spread of the disease.

But they noted that more research is needed to see if the effect is the same in humans and other species.

Dr Wilfred Jefferies, lead author of the study and an immunologist at the University of British Columbia, said: “This supports the idea that Alzheimer’s is a systemic disease in which amyloids expressed outside the brain contribute to the pathology of the brain. Central Nervous System”.

“As we continue to explore this mechanism, Alzheimer’s disease may be the tip of the iceberg and we need to have much better controls and screening of donors used in blood, organ and tissue transplants, as well as stem cell transfers. derived from humans. or blood products.’

It is unclear whether any cases of Alzheimer’s to date have been linked to organ or bone marrow donations.

The new study was published Thursday in the journal Stem cell reports.

The researchers transplanted bone marrow, a spongy substance in the center of bones, with APP-containing stem cells into two different groups of mice: those without an APP gene (APP Knockouts) and those with a normally functioning one.

They found that mice with a normally functioning APP gene developed signs of cognitive decline within nine months, and those without the gene experienced features of Alzheimer’s within just six months.

Typically, mice prone to familial Alzheimer’s begin to show symptoms around 11 to 12 months of age.

In mice, these symptoms typically include short- and long-term memory loss and lack of fear. Signs in the brain include a buildup of amyloid in the brain and leaks in the blood-brain barrier.

Dr Chaahat Singh, lead author of the study and a neuroscientist at the University of British Columbia, said: “The fact that we could see significant behavioral and cognitive impairment differences in the APP knockouts at six months was surprising but also intriguing because it only showed the appearance of the disease that was accelerating after being transferred.’

The findings suggest that the mutated APP gene in donor stem cells could cause the disease in those without the gene and that those with a normal APP gene are more susceptible to it.

The team also concluded that Alzheimer’s disease can form from amyloid proteins found outside the central nervous system.

The findings come after a UK study found evidence that at least five patients who were injected with growth hormones containing “seeds” of amyloid beta protein, taken from the bodies of dead people, “contracted” Early-onset Alzheimer’s later in life.

More than 1,800 patients who received the treatment were considered “at risk.”

An NIH panel announced in January that it would launch an “urgent” investigation into the research, since nearly 8,000 American children were injected with the therapy between the 1960s and 1980s.

CanadaAlzheimer’s disease

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