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▎WuXi AppTec Content Team Editor Alzheimer's disease is the most common neurodegenerative disease, and tens of millions of people around the world are plagued
by symptoms such as cognitive impairment, memory imbalance and behavioral abnormalities.
For these patients, memory loss is often the earliest symptom, followed by a decline
in thinking and thinking ability.
These symptoms reflect typical features
of worsening brain tissue damage.
Toxic protein clusters first gather in the temporal lobe region of the brain, which is responsible for memory, and then spread to key brain regions
responsible for thinking and decision-making.
Now, a study led by Professor Brian Gordon of Washington University in St.
Louis has revealed why specific brain regions are particularly vulnerable
when faced with the ravages of Alzheimer's disease.
The study found that the brain region, the primary genetic risk factor for Alzheimer's disease, where the APOE gene is most active, suffered the most damage
.
The study, published in Science Translational Medicine, also explains why the symptoms of Alzheimer's disease vary from individual to individual, and that unknown biological mechanisms may play an important role
in the disease.
"Some Alzheimer's patients have atypical symptoms where they first develop language or vision impairment rather than memory problems," Professor Gordon said.
Patients with these atypical Alzheimer's diseases are often overlooked by studies because it is much
easier to study those with the same symptoms.
But this heterogeneity tells us that we still don't know much about how Alzheimer's disease progresses, how it progresses
, how it works.
Every mystery we unravel brings us one step
closer to solving these problems.
"
Alzheimer's disease begins with β-amyloid
in the brain.
More than 20 years before neurological symptoms appeared, the protein began to accumulate and form plaques
.
Years later, tangles of another disease-causing protein, tau, began to form
.
Soon after, neurons in the affected brain regions begin to weaken, die, and cognitive decline
begins.
In the study, the
authors performed brain imaging analysis on 350 volunteers to detect the content and location of their amyloid plaques and tau tangles, as well as the volume of
different brain regions.
The researchers compared the volunteers' protein clusters, brain tissue damage patterns, and expression patterns
with the APOE gene and other Alzheimer's disease-related genes.
The genetic data came from the Allen Institute for Brain Science to map gene expression in the human brain
.
"We noticed that brain regions with high expression of the APOE gene are closely related to areas where tau protein is tangled and tissue damaged," Professor Gordon said, "Not only the APOE gene, but the 20 genes most closely associated with Alzheimer's disease are expressed
in a similar pattern in the temporal lobe.
" These areas have some fundamental features that make them particularly vulnerable
to Alzheimer's disease.
This trait is likely to be present at birth and is influenced
by individual genetic factors.
"
The red and orange regions indicate: brain regions where the APOE gene is active (above); Brain regions with a concentration of tau protein tangles (below) (Credit: Diana Hobbs/Washington University) Each person carries a different version of the APOE gene, but the group carrying the APOE4 variant may have a 12-fold higher risk of Alzheimer's disease than the rest of the population and have a lower
age.
Scientists already know that the APOE4 gene promotes the accumulation
of β-amyloid in the brain.
Another study found that APOE4 exacerbated the damage
caused by tau protein even in the absence of amyloid plaques.
To assess the effects of high-risk APOE variants on tau-related damage, the research team divided volunteers into two groups based on whether they contained high-risk mutations, analyzing protein clusters and brain atrophy
.
"Carriers of the APOE4 gene are more likely to accumulate β-amyloid, which puts them at higher risk of Alzheimer's disease," Professor Gordon said, "In addition, with the same amyloid content, their tau protein tangles more, which leads to more severe brain atrophy
.
" In this way, the brain received a double whammy
.
The
research team said that next they will further explore the relationship
between gene expression patterns and tau protein damage in patients with atypical Alzheimer's disease.
These breakthroughs will provide new clues
to understand the mechanism of Alzheimer's disease and find treatment options.
References:[1] Study yields clues to why Alzheimer's disease damages certain parts of the brain.
Retrieved November 16th, 2022 from style="outline: 0px;max-width: 100%;font-size: 10px;color: rgb(178, 178, 178);box-sizing: border-box !important;overflow-wrap: break-word !important;" _mstmutation="1" _istranslated="1"> [2] Aylin Dincer et al, APOE ε4 genotype, amyloid-β, and sex interact to predict tau in regions of high APOE mRNA expression, Science Translational Medicine (2022).
DOI: 10.
1126/scitranslmed.
abl7646
by symptoms such as cognitive impairment, memory imbalance and behavioral abnormalities.
For these patients, memory loss is often the earliest symptom, followed by a decline
in thinking and thinking ability.
These symptoms reflect typical features
of worsening brain tissue damage.
Toxic protein clusters first gather in the temporal lobe region of the brain, which is responsible for memory, and then spread to key brain regions
responsible for thinking and decision-making.
Now, a study led by Professor Brian Gordon of Washington University in St.
Louis has revealed why specific brain regions are particularly vulnerable
when faced with the ravages of Alzheimer's disease.
The study found that the brain region, the primary genetic risk factor for Alzheimer's disease, where the APOE gene is most active, suffered the most damage
.
The study, published in Science Translational Medicine, also explains why the symptoms of Alzheimer's disease vary from individual to individual, and that unknown biological mechanisms may play an important role
in the disease.
"Some Alzheimer's patients have atypical symptoms where they first develop language or vision impairment rather than memory problems," Professor Gordon said.
Patients with these atypical Alzheimer's diseases are often overlooked by studies because it is much
easier to study those with the same symptoms.
But this heterogeneity tells us that we still don't know much about how Alzheimer's disease progresses, how it progresses
, how it works.
Every mystery we unravel brings us one step
closer to solving these problems.
"
Alzheimer's disease begins with β-amyloid
in the brain.
More than 20 years before neurological symptoms appeared, the protein began to accumulate and form plaques
.
Years later, tangles of another disease-causing protein, tau, began to form
.
Soon after, neurons in the affected brain regions begin to weaken, die, and cognitive decline
begins.
In the study, the
authors performed brain imaging analysis on 350 volunteers to detect the content and location of their amyloid plaques and tau tangles, as well as the volume of
different brain regions.
The researchers compared the volunteers' protein clusters, brain tissue damage patterns, and expression patterns
with the APOE gene and other Alzheimer's disease-related genes.
The genetic data came from the Allen Institute for Brain Science to map gene expression in the human brain
.
"We noticed that brain regions with high expression of the APOE gene are closely related to areas where tau protein is tangled and tissue damaged," Professor Gordon said, "Not only the APOE gene, but the 20 genes most closely associated with Alzheimer's disease are expressed
in a similar pattern in the temporal lobe.
" These areas have some fundamental features that make them particularly vulnerable
to Alzheimer's disease.
This trait is likely to be present at birth and is influenced
by individual genetic factors.
"
The red and orange regions indicate: brain regions where the APOE gene is active (above); Brain regions with a concentration of tau protein tangles (below) (Credit: Diana Hobbs/Washington University) Each person carries a different version of the APOE gene, but the group carrying the APOE4 variant may have a 12-fold higher risk of Alzheimer's disease than the rest of the population and have a lower
age.
Scientists already know that the APOE4 gene promotes the accumulation
of β-amyloid in the brain.
Another study found that APOE4 exacerbated the damage
caused by tau protein even in the absence of amyloid plaques.
To assess the effects of high-risk APOE variants on tau-related damage, the research team divided volunteers into two groups based on whether they contained high-risk mutations, analyzing protein clusters and brain atrophy
.
"Carriers of the APOE4 gene are more likely to accumulate β-amyloid, which puts them at higher risk of Alzheimer's disease," Professor Gordon said, "In addition, with the same amyloid content, their tau protein tangles more, which leads to more severe brain atrophy
.
" In this way, the brain received a double whammy
.
The
research team said that next they will further explore the relationship
between gene expression patterns and tau protein damage in patients with atypical Alzheimer's disease.
These breakthroughs will provide new clues
to understand the mechanism of Alzheimer's disease and find treatment options.
References:[1] Study yields clues to why Alzheimer's disease damages certain parts of the brain.
Retrieved November 16th, 2022 from style="outline: 0px;max-width: 100%;font-size: 10px;color: rgb(178, 178, 178);box-sizing: border-box !important;overflow-wrap: break-word !important;" _mstmutation="1" _istranslated="1"> [2] Aylin Dincer et al, APOE ε4 genotype, amyloid-β, and sex interact to predict tau in regions of high APOE mRNA expression, Science Translational Medicine (2022).
DOI: 10.
1126/scitranslmed.
abl7646
