Health and Me

Itisha Arya

Ending Alzheimer’s Could Start With Fruit Flies, UK Scientists Suggest

alzheimers disease fruits

UK researchers say fruit flies could help unlock why devastating brain and nerve conditions such as Alzheimer’s, Parkinson’s and <span>motor neurone disease</span> develop, despite decades of medical research. Scientists have known for years that many neurodegenerative disorders are linked to genetic mutations. What has remained unclear is how those mutations actually trigger disease inside the nervous system.

According to the Mirror, new findings published in the journal Current Biology suggest a breakthrough may lie in studying fruit flies, insects whose genes behave in strikingly similar ways to those in humans.

<h2>UK Scientists Say Fruit Flies May Hold Answers to <span rel="noindex">Neurodegenerative Diseases</span></h2>

The study was led by Professor Andreas Prokop from the University of Manchester, who examined the role of so-called motor proteins using fruit flies as a model. These proteins are responsible for transporting materials inside nerve cells. Fruit flies are widely used in genetic research because experiments can be carried out quickly and at low cost while still offering insights relevant to human biology.

Professor Prokop explained that many human genes linked to neurodegenerative disease have close equivalents in fruit flies, performing nearly identical roles in nerve cells.

<h2>Axons and the Role of Motor Proteins</h2>

The research focused on axons, the long and fragile nerve fibres that act like cables, carrying messages between the brain and the rest of the body to control movement and behaviour. For axons to stay healthy, motor proteins must move essential materials along internal tracks called microtubules.

These motor proteins are vulnerable to genetic mutations, which can interfere with their function and ultimately cause axons to break down.

<h2>Why Different Mutations Cause Similar Damage</h2>

Professor Prokop said scientists have long struggled to explain why both disabling mutations, which reduce motor protein activity, and hyperactivating mutations, which keep them constantly switched on, can result in very similar forms of neurodegeneration.

To investigate this puzzle, his team studied fruit flies carrying different types of motor protein mutations.

<h2>What Happens Inside Damaged Nerve Fibres?</h2>

The researchers found that both disabling and hyperactivating mutations lead to the same physical damage inside axons. Healthy microtubules, which normally form straight bundles, begin to decay and curl into disorganised structures. Professor Prokop compared this change to the difference between dry spaghetti and overcooked spaghetti. This curling is a clear sign that axons are breaking down.

<h2>Transport, Damage and Repair Inside Axons</h2>

Axons rely on a complex internal system to survive over time. Materials must be transported from the nerve cell body to distant parts of the axon, a process carried out by motor proteins moving along microtubules.

Professor Prokop explained that if mutations prevent motor proteins from transporting cargo, axons begin to decay. Many inherited neurodegenerative diseases can be traced back to this failure. However, the study also showed that hyperactivating mutations cause a different but equally damaging problem.

<h2>Why Too Much Activity Can Be Harmful?</h2>

When motor proteins are constantly active and unable to pause, they generate excessive wear and tear along microtubules. Even under normal conditions, transport damages microtubules over time, much like traffic creates potholes on roads. This damage usually triggers repair and replacement mechanisms inside the cell.

The researchers found that when motor proteins are either overactive or when repair systems fail, the balance between damage and repair breaks down. The result is microtubule curling and axon decay.

At first glance, disabling mutations might seem less harmful because fewer motor proteins mean less internal traffic and therefore less damage. However, the researchers discovered the opposite effect.

Reduced transport means vital supplies fail to reach the axonal machinery. This shortage triggers oxidative stress, a harmful condition linked to cell damage. Oxidative stress, the team showed, disrupts microtubule maintenance and leads to the same curling seen with hyperactive motor proteins.

Based on these findings, Professor Prokop and his team proposed what they call the dependency cycle of axon homeostasis. This model suggests that axon maintenance depends on motor proteins and microtubules, but those same systems rely on ongoing transport to function properly.

If mutations interfere with this balance, either by causing oxidative stress or by upsetting the repair process, the entire cycle collapses.

Professor Prokop said parallel research from his group strongly supports this model. He added that because the genetic foundations of fruit flies and humans are surprisingly alike, it is highly likely that the same mechanisms operate in people. According to Professor Prokop, there are already strong signs that these findings apply beyond fruit flies and could reshape how scientists understand and eventually treat neurodegenerative disease.

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UK researchers say fruit flies could help unlock why devastating brain and nerve conditions such as Alzheimer’s, Parkinson’s and motor neurone disease develop, despite decades of medical research. Scientists have known for years that many neurodegenerative disorders are linked to genetic mutations. What has remained unclear is how those mutations actually trigger disease inside the nervous system.According to the Mirror, new findings published in the journal Current Biology suggest a breakthrough may lie in studying fruit flies, insects whose genes behave in strikingly similar ways to those in humans.UK Scientists Say Fruit Flies May Hold Answers to Neurodegenerative DiseasesThe study was led by Professor Andreas Prokop from the University of Manchester, who examined the role of so-called motor proteins using fruit flies as a model. These proteins are responsible for transporting materials inside nerve cells. Fruit flies are widely used in genetic research because experiments can be carried out quickly and at low cost while still offering insights relevant to human biology.Professor Prokop explained that many human genes linked to neurodegenerative disease have close equivalents in fruit flies, performing nearly identical roles in nerve cells.Axons and the Role of Motor ProteinsThe research focused on axons, the long and fragile nerve fibres that act like cables, carrying messages between the brain and the rest of the body to control movement and behaviour. For axons to stay healthy, motor proteins must move essential materials along internal tracks called microtubules.These motor proteins are vulnerable to genetic mutations, which can interfere with their function and ultimately cause axons to break down.Why Different Mutations Cause Similar DamageProfessor Prokop said scientists have long struggled to explain why both disabling mutations, which reduce motor protein activity, and hyperactivating mutations, which keep them constantly switched on, can result in very similar forms of neurodegeneration.To investigate this puzzle, his team studied fruit flies carrying different types of motor protein mutations.What Happens Inside Damaged Nerve Fibres?The researchers found that both disabling and hyperactivating mutations lead to the same physical damage inside axons. Healthy microtubules, which normally form straight bundles, begin to decay and curl into disorganised structures. Professor Prokop compared this change to the difference between dry spaghetti and overcooked spaghetti. This curling is a clear sign that axons are breaking down.Transport, Damage and Repair Inside AxonsAxons rely on a complex internal system to survive over time. Materials must be transported from the nerve cell body to distant parts of the axon, a process carried out by motor proteins moving along microtubules.Professor Prokop explained that if mutations prevent motor proteins from transporting cargo, axons begin to decay. Many inherited neurodegenerative diseases can be traced back to this failure. However, the study also showed that hyperactivating mutations cause a different but equally damaging problem.Why Too Much Activity Can Be Harmful?When motor proteins are constantly active and unable to pause, they generate excessive wear and tear along microtubules. Even under normal conditions, transport damages microtubules over time, much like traffic creates potholes on roads. This damage usually triggers repair and replacement mechanisms inside the cell.The researchers found that when motor proteins are either overactive or when repair systems fail, the balance between damage and repair breaks down. The result is microtubule curling and axon decay.The Role of Oxidative StressAt first glance, disabling mutations might seem less harmful because fewer motor proteins mean less internal traffic and therefore less damage. However, the researchers discovered the opposite effect.Reduced transport means vital supplies fail to reach the axonal machinery. This shortage triggers oxidative stress, a harmful condition linked to cell damage. Oxidative stress, the team showed, disrupts microtubule maintenance and leads to the same curling seen with hyperactive motor proteins.Based on these findings, Professor Prokop and his team proposed what they call the dependency cycle of axon homeostasis. This model suggests that axon maintenance depends on motor proteins and microtubules, but those same systems rely on ongoing transport to function properly.If mutations interfere with this balance, either by causing oxidative stress or by upsetting the repair process, the entire cycle collapses.Professor Prokop said parallel research from his group strongly supports this model. He added that because the genetic foundations of fruit flies and humans are surprisingly alike, it is highly likely that the same mechanisms operate in people. According to Professor Prokop, there are already strong signs that these findings apply beyond fruit flies and could reshape how scientists understand and eventually treat neurodegenerative disease.