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With fractured genomes, Alzheimer’s neurons call for help

With fractured genomes, Alzheimer’s neurons call for help

Think of your brain as a sprawling city with a bustling downtown, countless neighborhoods, and a vast and intricate system of highways and side roads. Now imagine that the city is slowly being consumed by a invasive species of plant, one that strangles the buildings and chokes off the roads.

This isn’t a metaphor for some impending environmental disaster. It’s a pretty accurate description of what happens in Alzheimer’s disease.

The plant in question is a tangle of proteins known as amyloid beta. As Alzheimer’s progresses, these proteins gradually overtake the brain, killing off neurons and disrupting essential neural functions.

But amyloid beta doesn’t act alone. In order to cause such widespread destruction, it recruits an unwitting accomplice: a protein called tau.

Tau is essential for the health of neurons. It helps stabilize the cell’s internal skeleton, which in turn supports the cell’s ability to send and receive electrical signals.

In Alzheimer’s, tau goes awry. It loses its ability to stabilizer neurons and instead starts to form clumps inside of them. These clumps, known as neurofibrillary tangles, further damage the cells and contribute to the progression of the disease.

Fractured Genomes

One of the most intriguing aspects of Alzheimer’s is its propensity for attacking specific regions of the brain. The disease usually starts in the hippocampus, a small, seahorse-shaped structure that plays a vital role in memory and learning.

From there, it typically spreads to the cortex, the outer layer of the brain that controls higher-level functions like language and decision-making.

Why does Alzheimer’s target these areas of the brain?

Scientists believe that it has to do with the structure of our genomes.

The human genome is made up of two sets of DNA, one from each parent. This means that we have two copies of each gene, one from mom and one from dad.

In most cases, both copies of a gene are identical. But in some cases, they can be slightly different, a phenomenon known as genomic variance.

Genomic variance is thought to be important for brain development. It’s been linked to increased synaptic activity, which is essential for learning and memory.

But it also seems to make the brain more vulnerable to Alzheimer’s.

Studies have found that people with Alzheimer’s are more likely to have genomic variance in the regions of the brain that are typically affected by the disease. This suggests that the disease may be able to take advantage of these small differences to cause neuronal damage.

In order to understand how genomic variance contributes to Alzheimer’s, scientists are studying a group of neurological disorders known as familial Alzheimer’s diseases (FADs).

FADs are rare forms of Alzheimer’s that are caused by mutations in genes that are involved in the production of amyloid beta and tau.

These mutations are typically passed down from one generation to the next, which makes FADs ideal for studying the role of genetics in Alzheimer’s.

Studying FADs has revealed that the mutations that cause the disease can have a wide range of effects on amyloid beta and tau. In some cases, the mutations cause amyloid beta to be produced at higher levels. In others, they cause tau to be more prone to forming clumps.

But in all cases, the mutations seem to exacerbate the damaging effects of these proteins on the brain.

FADs are rare, but they’re not the only form of Alzheimer’s that’s linked to genomic variance. Studies have also found that people with the more common, late-onset form of the disease are more likely to have genomic variance in the same regions of the brain that are typically affected by FADs.

This suggests that genomic variance may be a general risk factor for Alzheimer’s, not just for rare, inherited forms of the disease.

The Link Between Amyloid Beta and Tau

Recent studies have uncovered another important connection between amyloid beta and tau. It turns out that these two proteins may not just be coincidentally involved in the same disease. They may actually have a causal link.

The evidence for this comes from studies of mice that have been genetically engineered to produce high levels of amyloid beta.

These mice typically develop neurofibrillary tangles, even though they don’t have any of the genetic mutations that are typically associated with FADs.

This suggests that amyloid beta is enough to cause tau to start forming clumps. And once tau starts to clump, the damage to neurons is swift and severe.

This is a major breakthrough in our understanding of Alzheimer’s. It suggests that the disease may be caused by a build-up of amyloid beta, rather than by tau tangles.

It also suggests that amyloid beta may be the key to developing new treatments for the disease.

If we can find a way to stop amyloid beta from accumulating in the brain, we may be able to prevent Alzheimer’s from ever taking hold.

Alzheimer’s is a devastating disease that takes a terrible toll on patients and their families. But with each new discovery, we inch closer to a cure.

A new study has found that neurons in the brains of Alzheimer’s patients have fractured genomes.

The study, conducted by researchers at the University of British Columbia, looked at the brains of people with Alzheimer’s and found that their neurons had fragmented DNA.

The researchers believe that this fragmentation may be a key factor in the development of Alzheimer’s disease.

“Our findings suggest that the neuronal genome is under stress in Alzheimer’s disease, and that this stress may contribute to the progressive decline in brain function seen in this condition,” said study author Weihong Song.

The study is published in the journal Nature Neuroscience.

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