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Image source: Shutterstock
Since 1906, researchers have known that amyloid plaques are one of the causes of Alzheimer's disease.
These plaques are stubborn sticky deposits that accumulate in our brains and contain a protein called beta amyloid.
This protein has been the focus of many studies, and we have learned a lot about its role and how it causes nerve cell death.
These plaques are stubborn sticky deposits that accumulate in our brains and contain a protein called beta amyloid.
This protein has been the focus of many studies, and we have learned a lot about its role and how it causes nerve cell death.
Beta amyloid first attacks the communication network between our nerve cells (called synapses), and then suffocates the nerve cells.
Nerve cell damage caused by amyloid is one of the causes of Alzheimer's disease symptoms.
Currently, there are no drugs that can change the amount of amyloid plaques that accumulate in the brain or prevent this accumulation from occurring.
Nerve cell damage caused by amyloid is one of the causes of Alzheimer's disease symptoms.
Currently, there are no drugs that can change the amount of amyloid plaques that accumulate in the brain or prevent this accumulation from occurring.
Amyloid comes from a protein called amyloid precursor protein (APP), which is found throughout our body, not just our brains.
The APP protein family is involved in many biological functions, including the production of other proteins and the control of communication between nerve cells.
The APP protein family is involved in many biological functions, including the production of other proteins and the control of communication between nerve cells.
However, when larger APP molecules are divided into smaller pieces by the human body, they can take two paths.
One of the pathways has nothing to do with the disease, and the other pathway has been shown to increase beta amyloid levels.
If we study the pathways that cause Alzheimer's disease, scientists have discovered that an enzyme called gamma secretase plays a key role in the process of converting APP into beta amyloid.
One of the pathways has nothing to do with the disease, and the other pathway has been shown to increase beta amyloid levels.
If we study the pathways that cause Alzheimer's disease, scientists have discovered that an enzyme called gamma secretase plays a key role in the process of converting APP into beta amyloid.
Scientists have spent a long time trying to target the secretase to prevent the sticky accumulation of beta amyloid that produces plaque.
However, the work done by researchers to inhibit the action of γ-secretase has largely failed.
Some experiments have shown that its inhibition increases the rate of brain function decline.
However, the work done by researchers to inhibit the action of γ-secretase has largely failed.
Some experiments have shown that its inhibition increases the rate of brain function decline.
Experimental molecule
However, a recent study took a different approach from the past.
Their goal is not to turn off gamma secretase, but to try to reduce its activity.
In order to do this, researchers need to generate new molecules to alter the activity of gamma secretase and provide protection from the accumulation of beta amyloid in the brain.
Their goal is not to turn off gamma secretase, but to try to reduce its activity.
In order to do this, researchers need to generate new molecules to alter the activity of gamma secretase and provide protection from the accumulation of beta amyloid in the brain.
jpg" target="_blank">
Image source: Shutterstock
The research team generated three interesting compounds that work at very low concentrations-which is essential for making new drugs.
The researchers then brought one of these compounds into an animal model of Alzheimer's disease for testing.
The researchers then brought one of these compounds into an animal model of Alzheimer's disease for testing.
To do this, they used mice that were engineered to produce more beta amyloid, which showed some signs of Alzheimer's disease.
The mice took the compound daily for three months.
The result is that the beta amyloid in the brain is reduced by half.
Although other studies have yielded similar results in animal models, the results of this study are significant because this compound can be used not only to treat dementia, but also to prevent it.
The mice took the compound daily for three months.
The result is that the beta amyloid in the brain is reduced by half.
Although other studies have yielded similar results in animal models, the results of this study are significant because this compound can be used not only to treat dementia, but also to prevent it.
They also noticed other changes in the brains of mice treated with this molecule.
This molecule suppresses the response of the brain's immune cells-microglia.
Although these cells are important for brain health, they can also be harmful when they are overactive-this is the case with Alzheimer's.
This suggests that the benefits of the drug may be twofold.
This molecule suppresses the response of the brain's immune cells-microglia.
Although these cells are important for brain health, they can also be harmful when they are overactive-this is the case with Alzheimer's.
This suggests that the benefits of the drug may be twofold.
What's the next step?
In order to apply this compound to patients with dementia, the next step is to conduct clinical trials to verify laboratory findings.
This step is often where the conclusions of laboratory work cannot be effective.
This step is often where the conclusions of laboratory work cannot be effective.
Although researchers have done a lot of research to give this compound a chance of success, the success rate of drugs targeting our brains is only about 6%.
The previous modulators of gamma secretase did not progress to become drugs due to adverse reactions reported by participants.
The previous modulators of gamma secretase did not progress to become drugs due to adverse reactions reported by participants.
But the molecules tested in this study have a stronger potency advantage, which ultimately leads to fewer molecules needed to have an impact on the user.
If it enters a clinical trial, researchers will look for various evidence to prove a positive result, such as whether it improves a person's memory test performance.
The test may also involve brain scans to monitor changes in brain structure and track beta amyloid deposits in the brain.
If it enters a clinical trial, researchers will look for various evidence to prove a positive result, such as whether it improves a person's memory test performance.
The test may also involve brain scans to monitor changes in brain structure and track beta amyloid deposits in the brain.
Although many molecules did not meet expectations during the transition from the laboratory to the clinic, the signs of the future development of this molecule are positive.
It does add a new option for experimental molecules.
This is what researchers continue to provide for Alzheimer's patients.
And those who are waiting for a diagnosis to seek treatment and preventive measures.
()
It does add a new option for experimental molecules.
This is what researchers continue to provide for Alzheimer's patients.
And those who are waiting for a diagnosis to seek treatment and preventive measures.
()
references:
Kevin D.
Rynearson, Moorthi Ponnusamy, Olga Prikhodko.
et al.
Preclinical validation of a potent γ-secretase modulator for Alzheimer's disease prevention.
J Exp Med 5 April 2021; 218 (4): e20202560.
doi: https://doi.
org/10.
1084/jem.
20202560
Rynearson, Moorthi Ponnusamy, Olga Prikhodko.
et al.
Preclinical validation of a potent γ-secretase modulator for Alzheimer's disease prevention.
J Exp Med 5 April 2021; 218 (4): e20202560.
doi: https://doi.
org/10.
1084/jem.
20202560
Müller, U.
, Deller, T.
& Korte, M.
Not just amyloid: physiological functions of the amyloid precursor protein family.
Nat Rev Neurosci 18, 281–298 (2017).
https://doi.
org/10.
1038/nrn .
2017.
29
, Deller, T.
& Korte, M.
Not just amyloid: physiological functions of the amyloid precursor protein family.
Nat Rev Neurosci 18, 281–298 (2017).
https://doi.
org/10.
1038/nrn .
2017.
29
Karran E, Mercken M, De Strooper B.
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.
Nat Rev Drug Discov.
2011;10(9):698-712.
Published 2011 Aug 19.
doi:10.
1038 /nrd3505
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.
Nat Rev Drug Discov.
2011;10(9):698-712.
Published 2011 Aug 19.
doi:10.
1038 /nrd3505
Zhang YW, Thompson R, Zhang H, Xu H.
APP processing in Alzheimer's disease.
Mol Brain.
2011;4:3.
Published 2011 Jan 7.
doi:10.
1186/1756-6606-4-3
APP processing in Alzheimer's disease.
Mol Brain.
2011;4:3.
Published 2011 Jan 7.
doi:10.
1186/1756-6606-4-3
Doody RS, Raman R, Farlow M, et al.
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
N Engl J Med.
2013;369(4):341-350.
doi:10.
1056/NEJMoa1210951
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
N Engl J Med.
2013;369(4):341-350.
doi:10.
1056/NEJMoa1210951
Panza F, Frisardi V, Imbimbo BP, et al.
REVIEW: γ-Secretase inhibitors for the treatment of Alzheimer's disease: The current state.
CNS Neurosci Ther.
2010;16(5):272-284.
doi:10.
1111/j.
1755-5949.
2010.
00164.
x
REVIEW: γ-Secretase inhibitors for the treatment of Alzheimer's disease: The current state.
CNS Neurosci Ther.
2010;16(5):272-284.
doi:10.
1111/j.
1755-5949.
2010.
00164.
x
Study: CNS drugs have lower regulatory success rate, take longer to develop style="text-align: justify;">
Tartaglia MC, Rosen HJ, Miller BL.
Neuroimaging in dementia.
Neurotherapeutics.
2011;8(1):82-92.
doi:10.
1007/s13311-010-0012-2
Neuroimaging in dementia.
Neurotherapeutics.
2011;8(1):82-92.
doi:10.
1007/s13311-010-0012-2
Kolanko MA, Win Z, Loreto F, et al.
Amyloid PET imaging in clinical practice.
Practical Neurology 2020;20:451-462.
Amyloid PET imaging in clinical practice.
Practical Neurology 2020;20:451-462.
jpg" target="_blank">
jpg" target="_blank"> Image source: Shutterstock
Since 1906, researchers have known that amyloid plaques are one of the causes of Alzheimer's disease.
These plaques are stubborn sticky deposits that accumulate in our brains and contain a protein called beta amyloid.
This protein has been the focus of many studies, and we have learned a lot about its role and how it causes nerve cell death.
These plaques are stubborn sticky deposits that accumulate in our brains and contain a protein called beta amyloid.
This protein has been the focus of many studies, and we have learned a lot about its role and how it causes nerve cell death.
Beta amyloid first attacks the communication network between our nerve cells (called synapses), and then suffocates the nerve cells.
Nerve cell damage caused by amyloid is one of the causes of Alzheimer's disease symptoms.
Currently, there are no drugs that can change the amount of amyloid plaques that accumulate in the brain or prevent this accumulation from occurring.
Nerve cell damage caused by amyloid is one of the causes of Alzheimer's disease symptoms.
Currently, there are no drugs that can change the amount of amyloid plaques that accumulate in the brain or prevent this accumulation from occurring.
Amyloid comes from a protein called amyloid precursor protein (APP), which is found throughout our body, not just our brains.
The APP protein family is involved in many biological functions, including the production of other proteins and the control of communication between nerve cells.
The APP protein family is involved in many biological functions, including the production of other proteins and the control of communication between nerve cells.
However, when larger APP molecules are divided into smaller pieces by the human body, they can take two paths.
One of the pathways has nothing to do with the disease, and the other pathway has been shown to increase beta amyloid levels.
If we study the pathways that cause Alzheimer's disease, scientists have discovered that an enzyme called gamma secretase plays a key role in the process of converting APP into beta amyloid.
One of the pathways has nothing to do with the disease, and the other pathway has been shown to increase beta amyloid levels.
If we study the pathways that cause Alzheimer's disease, scientists have discovered that an enzyme called gamma secretase plays a key role in the process of converting APP into beta amyloid.
Scientists have spent a long time trying to target the secretase to prevent the sticky accumulation of beta amyloid that produces plaque.
However, the work done by researchers to inhibit the action of γ-secretase has largely failed.
Some experiments have shown that its inhibition increases the rate of brain function decline.
However, the work done by researchers to inhibit the action of γ-secretase has largely failed.
Some experiments have shown that its inhibition increases the rate of brain function decline.
Experimental molecule
Experimental moleculeHowever, a recent study took a different approach from the past.
Their goal is not to turn off gamma secretase, but to try to reduce its activity.
In order to do this, researchers need to generate new molecules to alter the activity of gamma secretase and provide protection from the accumulation of beta amyloid in the brain.
Their goal is not to turn off gamma secretase, but to try to reduce its activity.
In order to do this, researchers need to generate new molecules to alter the activity of gamma secretase and provide protection from the accumulation of beta amyloid in the brain.
jpg" target="_blank">
jpg" target="_blank"> Image source: Shutterstock
The research team generated three interesting compounds that work at very low concentrations-which is essential for making new drugs.
The researchers then brought one of these compounds into an animal model of Alzheimer's disease for testing.
The researchers then brought one of these compounds into an animal model of Alzheimer's disease for testing.
To do this, they used mice that were engineered to produce more beta amyloid, which showed some signs of Alzheimer's disease.
The mice took the compound daily for three months.
The result is that the beta amyloid in the brain is reduced by half.
Although other studies have yielded similar results in animal models, the results of this study are significant because this compound can be used not only to treat dementia, but also to prevent it.
The mice took the compound daily for three months.
The result is that the beta amyloid in the brain is reduced by half.
Although other studies have yielded similar results in animal models, the results of this study are significant because this compound can be used not only to treat dementia, but also to prevent it.
They also noticed other changes in the brains of mice treated with this molecule.
This molecule suppresses the response of the brain's immune cells-microglia.
Although these cells are important for brain health, they can also be harmful when they are overactive-this is the case with Alzheimer's.
This suggests that the benefits of the drug may be twofold.
This molecule suppresses the response of the brain's immune cells-microglia.
Although these cells are important for brain health, they can also be harmful when they are overactive-this is the case with Alzheimer's.
This suggests that the benefits of the drug may be twofold.
What's the next step?
What's the next step?In order to apply this compound to patients with dementia, the next step is to conduct clinical trials to verify laboratory findings.
This step is often where the conclusions of laboratory work cannot be effective.
This step is often where the conclusions of laboratory work cannot be effective.
Although researchers have done a lot of research to give this compound a chance of success, the success rate of drugs targeting our brains is only about 6%.
The previous modulators of gamma secretase did not progress to become drugs due to adverse reactions reported by participants.
The previous modulators of gamma secretase did not progress to become drugs due to adverse reactions reported by participants.
But the molecules tested in this study have a stronger potency advantage, which ultimately leads to fewer molecules needed to have an impact on the user.
If it enters a clinical trial, researchers will look for various evidence to prove a positive result, such as whether it improves a person's memory test performance.
The test may also involve brain scans to monitor changes in brain structure and track beta amyloid deposits in the brain.
If it enters a clinical trial, researchers will look for various evidence to prove a positive result, such as whether it improves a person's memory test performance.
The test may also involve brain scans to monitor changes in brain structure and track beta amyloid deposits in the brain.
，，，。（）
：
Kevin D.
Rynearson, Moorthi Ponnusamy, Olga Prikhodko.
et al.
Preclinical validation of a potent γ-secretase modulator for Alzheimer’s disease prevention.
J Exp Med 5 April 2021; 218 (4): e20202560.
doi: https://doi.
org/10.
1084/jem.
20202560
Rynearson, Moorthi Ponnusamy, Olga Prikhodko.
et al.
Preclinical validation of a potent γ-secretase modulator for Alzheimer’s disease prevention.
J Exp Med 5 April 2021; 218 (4): e20202560.
doi: https://doi.
org/10.
1084/jem.
20202560
Müller, U.
, Deller, T.
& Korte, M.
Not just amyloid: physiological functions of the amyloid precursor protein family.
Nat Rev Neurosci 18, 281–298 (2017).
https://doi.
org/10.
1038/nrn.
2017.
29
, Deller, T.
& Korte, M.
Not just amyloid: physiological functions of the amyloid precursor protein family.
Nat Rev Neurosci 18, 281–298 (2017).
https://doi.
org/10.
1038/nrn.
2017.
29
Karran E, Mercken M, De Strooper B.
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.
Nat Rev Drug Discov.
2011;10(9):698-712.
Published 2011 Aug 19.
doi:10.
1038/nrd3505
The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics.
Nat Rev Drug Discov.
2011;10(9):698-712.
Published 2011 Aug 19.
doi:10.
1038/nrd3505
Zhang YW, Thompson R, Zhang H, Xu H.
APP processing in Alzheimer's disease.
Mol Brain.
2011;4:3.
Published 2011 Jan 7.
doi:10.
1186/1756-6606-4-3
APP processing in Alzheimer's disease.
Mol Brain.
2011;4:3.
Published 2011 Jan 7.
doi:10.
1186/1756-6606-4-3
Doody RS, Raman R, Farlow M, et al.
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
N Engl J Med.
2013;369(4):341-350.
doi:10.
1056/NEJMoa1210951
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
N Engl J Med.
2013;369(4):341-350.
doi:10.
1056/NEJMoa1210951
Panza F, Frisardi V, Imbimbo BP, et al.
REVIEW: γ-Secretase inhibitors for the treatment of Alzheimer's disease: The current state.
CNS Neurosci Ther.
2010;16(5):272-284.
doi:10.
1111/j.
1755-5949.
2010.
00164.
x
REVIEW: γ-Secretase inhibitors for the treatment of Alzheimer's disease: The current state.
CNS Neurosci Ther.
2010;16(5):272-284.
doi:10.
1111/j.
1755-5949.
2010.
00164.
x
Study: CNS drugs have lower regulatory success rate, take longer to develop style="text-align: justify;">
Tartaglia MC, Rosen HJ, Miller BL.
Neuroimaging in dementia.
Neurotherapeutics.
2011;8(1):82-92.
doi:10.
1007/s13311-010-0012-2
Neuroimaging in dementia.
Neurotherapeutics.
2011;8(1):82-92.
doi:10.
1007/s13311-010-0012-2
Kolanko MA, Win Z, Loreto F, et al.
Amyloid PET imaging in clinical practice.
Practical Neurology 2020;20:451-462.
Amyloid PET imaging in clinical practice.
Practical Neurology 2020;20:451-462.
