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Spanish researchers find possible cause of Alzheimer's
19/07/2019
NEUROSCIENTISTS have discovered a protein in the brain which could be the main cause of Alzheimer's, and which they may one day be able to inhibit in order to slow down or halt the disease.
Known as the SFRP1, the protein is found in 'abnormally-high' levels in Alzheimer's sufferers and continues to increase as the condition progresses.
Researchers a the Severo Ochoa Molecular Biology Centre – part of Spain's National Research Council (CSIC) and Madrid Autonomous University – helped by funding from the Tatiana Pérez de Guzman el Bueno Foundation decided to test the cause-and-effect relationship to see whether the increase in SFRP1 was a symptom of Alzheimer's or whether it influenced the onset and decline of the illness.
Dr Paola Bovolenta and Dr Pilar Esteve carried out tests on mice and found a positive correlation between the progresssion of the disease and increasing levels of SFRP1, and also discovered that when they inhibited the protein, rendering it inactive, the advance of the condition halted altogether.
Neutralising the functions of SFRP1, says Dr Bovolenta, could be key in stopping Alzheimer's getting worse in humans, and detecting it in the bloodstream or spinal chord fluid may be a way of diagnosing the condition before symptoms begin to manifest themselves.
Alzheimer's typically starts in early middle age, in the 60s or 70s, but can begin as late as the 90s and is one of the main forms of senile dementia in the very elderly.
But it can appear in much younger adults and its progression is often quicker, with reports of people in their late 30s or early 40s dying within three to five years of diagnosis.
Although rare, early-age Alzheimer's appears to be on the rise.
A devastating condition for close family and friends in particular, Alzheimer's does not just affect short-term memory processing, but takes its toll on cognitive functions in general – spatial ability declines, the patient is unable to judge the height and width of steps, for example; decision-making and other executive functions become depleted, meaning even the apparently easiest tasks such as what to have for dinner become difficult and distressing; susceptibility to stress heightens, meaning even the most stoic and resilient of patients can become overwhelmed; too much 'going on around them' can cause a 'meltdown', and carers often say they seem to operate using a 'parallel logic system' at odds with reality and become stubborn, intolerant and rebellious when diverted from it.
Paranoia and suspicion are frequently present, fear of change or the unknown, and inability to articulate their thoughts can lead to frustration which becomes anger, sometimes attacking those closest to them – even physically.
Most Alzheimer's patients have 'lucid' flashes in between 'Alzheimer's moments', when they are able to think clearly, recognise people whom they may have forgotten, or understand what is going on around them, but these become fewer and shorter over time.
It is now one of the main causes of elderly care needs in the western world, since physically, older people tend to be in better shape and are living longer and healthier lives.
Given its huge significance in modern society and with predictions for the first-world demographic structure in future decades pointing at between a third and a half of society being aged over 65, finding a suitable remedy or management system for Alzheimer's is becoming more and more vital in public health and welfare terms.
But there is still a 'very long way to go' before the research in Madrid can provide any practical benefit, Dr Bovolenta reveals.
“Experiments and results in mice do not always work in the same way in humans, but we have a good base,” she says.
“But the origin of Alzheimer's is based upon numerous factors, and new lines of research need to work on acting on as many of these processes as possible that are pathologically altered in human sufferers.”
The next stage would be to develop drugs that neutralise SFRP1 and continue to work to find out if other proteins present alterations in patients.
Only then can clinical trials be carried out.
Also, future research will need to look into whether high levels of SFRP1 in those who apparently do not suffer Alzheimer's are an indicator of this being in the process of developing, by monitoring these subjects to see whether the condition does in fact appear.
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NEUROSCIENTISTS have discovered a protein in the brain which could be the main cause of Alzheimer's, and which they may one day be able to inhibit in order to slow down or halt the disease.
Known as the SFRP1, the protein is found in 'abnormally-high' levels in Alzheimer's sufferers and continues to increase as the condition progresses.
Researchers a the Severo Ochoa Molecular Biology Centre – part of Spain's National Research Council (CSIC) and Madrid Autonomous University – helped by funding from the Tatiana Pérez de Guzman el Bueno Foundation decided to test the cause-and-effect relationship to see whether the increase in SFRP1 was a symptom of Alzheimer's or whether it influenced the onset and decline of the illness.
Dr Paola Bovolenta and Dr Pilar Esteve carried out tests on mice and found a positive correlation between the progresssion of the disease and increasing levels of SFRP1, and also discovered that when they inhibited the protein, rendering it inactive, the advance of the condition halted altogether.
Neutralising the functions of SFRP1, says Dr Bovolenta, could be key in stopping Alzheimer's getting worse in humans, and detecting it in the bloodstream or spinal chord fluid may be a way of diagnosing the condition before symptoms begin to manifest themselves.
Alzheimer's typically starts in early middle age, in the 60s or 70s, but can begin as late as the 90s and is one of the main forms of senile dementia in the very elderly.
But it can appear in much younger adults and its progression is often quicker, with reports of people in their late 30s or early 40s dying within three to five years of diagnosis.
Although rare, early-age Alzheimer's appears to be on the rise.
A devastating condition for close family and friends in particular, Alzheimer's does not just affect short-term memory processing, but takes its toll on cognitive functions in general – spatial ability declines, the patient is unable to judge the height and width of steps, for example; decision-making and other executive functions become depleted, meaning even the apparently easiest tasks such as what to have for dinner become difficult and distressing; susceptibility to stress heightens, meaning even the most stoic and resilient of patients can become overwhelmed; too much 'going on around them' can cause a 'meltdown', and carers often say they seem to operate using a 'parallel logic system' at odds with reality and become stubborn, intolerant and rebellious when diverted from it.
Paranoia and suspicion are frequently present, fear of change or the unknown, and inability to articulate their thoughts can lead to frustration which becomes anger, sometimes attacking those closest to them – even physically.
Most Alzheimer's patients have 'lucid' flashes in between 'Alzheimer's moments', when they are able to think clearly, recognise people whom they may have forgotten, or understand what is going on around them, but these become fewer and shorter over time.
It is now one of the main causes of elderly care needs in the western world, since physically, older people tend to be in better shape and are living longer and healthier lives.
Given its huge significance in modern society and with predictions for the first-world demographic structure in future decades pointing at between a third and a half of society being aged over 65, finding a suitable remedy or management system for Alzheimer's is becoming more and more vital in public health and welfare terms.
But there is still a 'very long way to go' before the research in Madrid can provide any practical benefit, Dr Bovolenta reveals.
“Experiments and results in mice do not always work in the same way in humans, but we have a good base,” she says.
“But the origin of Alzheimer's is based upon numerous factors, and new lines of research need to work on acting on as many of these processes as possible that are pathologically altered in human sufferers.”
The next stage would be to develop drugs that neutralise SFRP1 and continue to work to find out if other proteins present alterations in patients.
Only then can clinical trials be carried out.
Also, future research will need to look into whether high levels of SFRP1 in those who apparently do not suffer Alzheimer's are an indicator of this being in the process of developing, by monitoring these subjects to see whether the condition does in fact appear.
Related Topics
You may also be interested in ...
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