Giovanna Mallucci facts for kids
Quick facts for kids
Giovanna Mallucci
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| Born | 29 June 1963 |
| Alma mater | St Hilda's College, Oxford University College London Imperial College London |
| Known for | mechanisms of neurogenerative diseases; translational neuroscience |
| Awards | Potamkin Prize (2021) |
| Scientific career | |
| Fields | Neuroscience Neurodegeneration Prion diseases |
| Institutions | University of Cambridge University of Leicester |
| Thesis | Prion protein gene knockout in the mouse using the Cre/1oxP system (2001) |
Giovanna Rachele Mallucci (born 29 June 1963) is a leading scientist who studies the brain. She is a professor at the University of Cambridge in England. She also helps lead the UK Dementia Research Institute there. Her main work is understanding and treating brain diseases where brain cells get sick and die.
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About Giovanna Mallucci
Giovanna Mallucci went to school at Haberdashers' Aske's School for Girls. She then studied medicine at St Hilda's College, Oxford and University College London. After that, she chose to focus on brain and nerve problems.
She earned her Ph.D. in 2001 from Imperial College London. Her research looked at how certain brain diseases work in mice. Since then, she has worked as both a scientist and a doctor.
In 2008, she joined the MRC Toxicology Unit. Here, she studied common ways that brain cells get sick. In 2014, she became a professor at the University of Cambridge. She also became the director of the Cambridge Centre of the UK Dementia Research Institute in 2017. She is also a doctor at Addenbrooke's Hospital, helping people with memory problems.
How Brain Cells Get Sick
Giovanna Mallucci's team studies brain diseases using mice. They look at how brain cells get damaged. They also try to find new ways to treat these problems.
Her group found that early changes in brain connections in mice with a specific brain disease could be fixed. This helped the mice think better and act normally again. It also protected their brain cells for a long time. This showed that brain cell damage can be stopped by fixing these early problems.
Her team uses different models to understand how brain cells get damaged and die. They use mice, special brain cells, and even tiny worms called C. elegans. They also study how brain cells can repair themselves.
Her lab wants to understand why brain cells get sick. They look for common problems in many brain diseases, like Alzheimer's disease. They focus on things that harm brain cells and ways to help them heal.
They found that a stress response in cells, called the unfolded protein response (UPR), plays a role in brain cell damage. They even found a medicine that could stop this process in living things. They also discovered that brain cells sometimes fail to repair themselves. This happens because another stress response, involving 'cold shock' proteins, doesn't work right. They have found ways to use this to protect brain cells. Their goal is to turn this research into new treatments for memory diseases.
Working to Cure Dementia
Professor Mallucci leads a new center at the UK Dementia Research Institute. This center is on the Cambridge Biomedical Campus. Its main job is to find new ways to find, treat, prevent, and care for people with memory problems.
This center is part of a bigger group called the UK Dementia Research Institute (UK DRI). Other centers are at Cardiff University, the University of Edinburgh, Imperial College London, and King's College London.
Professor Mallucci explained that the DRI wants to deeply understand how brain cells go wrong in memory diseases. They hope to find new treatments based on this knowledge. She said Cambridge has many experts in different fields. They work together, mixing chemistry and physics with biology. This makes Cambridge a great place for dementia research. She believes they can find important new ways to change the course of these diseases.
Her team has made a very important discovery. They found a main pathway that causes brain cells to die in mice. Now, they have found two medicines that can block this pathway. These medicines stop brain cell damage with few side effects in rodents.
One of these medicines, trazodone hydrochloride, is already used in people as an antidepressant.
Professor Mallucci said this is exciting because it speeds up finding new drugs. She added that since trazodone is already known to be safe for people, they can start a study soon. This study will check if the drug protects brain cells in people with early Alzheimer's disease or other memory problems. She thinks they could know in 2-3 years if this approach can slow down the disease. This would be a huge first step.
She also noted that trazodone has been used to help people with later stages of memory problems. So, it is safe for them. Now, they need to see if giving the drug earlier can stop or slow the disease.
Scientists know that misfolded proteins build up in the brains of people with brain diseases. This is a big problem in diseases like Alzheimer's disease, Parkinson's disease, and prion disease. Professor Mallucci's team first found that these misfolded proteins in mice caused a natural defense system to turn off. This stopped brain cells from making new, important proteins.
They found that turning protein production back on with an experimental drug stopped brain cell damage. However, that drug was harmful to other parts of the body. In a new study, they tested many different compounds. They first tested them in worms, which have a working nervous system. Then they tested them in mice.
They found two drugs that helped brain cells make proteins again. These were trazodone hydrochloride and dibenzoylmethane (DBM). Trazodone is an antidepressant. DBM is being studied as a cancer drug. Both drugs stopped signs of brain cell damage in most mice with prion disease. They also helped restore memory in mice with a type of frontotemporal dementia. In both mouse models, the drugs also reduced brain shrinkage.
Research with the MRC
A team of scientists, led by Professor Mallucci, found a major pathway that causes brain cells to die in mice. They have now found two drugs that block this pathway and prevent brain cell damage. These drugs had very few side effects in mice. One of them is already approved for use in humans. This means it can be tested in people sooner.
In many brain diseases, like Alzheimer's disease, Parkinson's disease, and prion diseases, proteins in the brain fold incorrectly. Professor Mallucci's team previously found that these misfolded proteins caused a natural defense system in brain cells to turn off. This stopped the brain cells from making new, vital proteins. They then found that turning protein production back on with an experimental drug stopped brain cell damage. But this drug was harmful to the pancreas and could not be used in people.
In their latest study, the team tested over 1000 compounds. They first tested them in worms, which are good for testing drugs for the nervous system. Then they tested them in mammal cells. This helped them find good candidate compounds. They then tested these in mouse models of prion disease and a type of dementia called frontotemporal dementia (FTD).
The researchers found two drugs that helped brain cells make proteins again. These were trazodone hydrochloride, an antidepressant, and dibenzoylmethane (DBM), an anti-cancer drug. Both drugs stopped signs of brain cell damage in most mice with prion disease. They also helped restore memory in the FTD mice. In both mouse models, the drugs also reduced brain shrinkage, which is common in brain diseases.
Giovanna Mallucci, who led the team, said that since trazodone is safe for humans, a study can now check its effects in people. This study would look at people in the early stages of Alzheimer's disease and other dementias. She hopes they will know in 2-3 years if this approach can slow down the disease. This would be a very exciting first step.
She also mentioned that trazodone has been used to treat symptoms in people with later stages of dementia. So, it is known to be safe for them. Now, they need to find out if giving the drug earlier can stop or slow the disease.
This research was supported by the Medical Research Council. Professor Mallucci also received funding from Alzheimer's Society and the Alzheimer's Drug Discovery Foundation.
Rob Buckle, from the MRC, said this study shows how new scientific discoveries can quickly lead to possible treatments. He added that the two drugs are still experimental. But they protected mice even after brain cell damage had started. He said it is very exciting to think about finding drugs that can slow or stop these diseases. Especially since these drugs have already been tested for safety in other studies.
Dr. Doug Brown, from the Alzheimer's Society, said these findings are promising. They suggest that a treatment found in mice with prion disease might also stop brain cells from dying in some forms of dementia. He noted that this research is still early. But since one drug is already used for depression, it could reach people much faster.
He explained that the drug blocks a natural defense system in cells. This system is too active in the brains of people with frontotemporal dementia, Alzheimer's disease, and Parkinson's disease. So, it could potentially work for several conditions. So far, it has only been tested in mice with frontotemporal dementia. But the Alzheimer's Society is now funding research to test it in models of Alzheimer's too.
