Neural Vulnerabilities and Resilience in Alzheimer’s Explored
Summary: Researchers uncover how specific brain cells and circuits become vulnerable in Alzheimer’s disease and identify factors that may promote resilience to cognitive decline.
Analyzing gene expression in over 1.3 million cells across multiple brain regions, the study highlights the role of Reelin in neuron protection and choline metabolism in astrocytes for cognitive resilience. These findings pave the way for potential therapeutic targets to sustain cognition and memory amid Alzheimer’s pathology.
Key Facts:
Reelin-producing neurons are linked to cognitive resilience in Alzheimer’s patients.
Choline metabolism in astrocytes is associated with sustained cognition despite pathology.
Gene expression analysis in 1.3 million cells revealed significant insights into Alzheimer’s.
Source: Picower Institute at MIT
An MIT study published today in Nature provides new evidence for how specific cells and circuits become vulnerable in Alzheimer’s disease, and hones in on other factors that may help some people show resilience to cognitive decline, even amid clear signs of disease pathology.
To highlight potential targets for interventions to sustain cognition and memory, the authors engaged in a novel comparison of gene expression across multiple brain regions in people with or without Alzheimer’s disease, and conducted lab experiments to test and validate their major findings.
Brain cells all have the same DNA but what makes them differ, both in their identity and their activity, are their patterns of how they express those genes. The new analysis measured gene expression differences in more than 1.3 million cells of more than 70 cell types in six brain regions from 48 tissue donors, 26 of whom died with an Alzheimer’s diagnosis and 22 of whom without.
This shows neurons.
Some of the earliest signs of amyloid pathology and neuron loss in Alzheimer’s occurs in memory-focused regions called the hippocampus and the entorhinal cortex. Credit: Neuroscience News
As such, the study provides a uniquely large, far-ranging and yet detailed accounting of how brain cell activity differs amid Alzheimer’s disease by cell type, by brain region, by disease pathology, and by each person’s cognitive assessment while still alive.
“Specific brain regions are vulnerable in Alzheimer’s and there is an important need to understand how these regions or particular cell types are vulnerable,” said co-senior author Li-Huei Tsai, Picower Professor of Neuroscience and director of The Picower Institute for Learning and Memory and the Aging Brain Initiative at MIT.
“And the brain is not just neurons. It’s many other cell types. How these cell types may respond differently, depending on where they are, is something fascinating we are only at the beginning of looking at.”
Co-senior author Manolis Kellis, professor of computer science and head of MIT’s Computational Biology Group, likened the technique used to measure gene expression comparisons, single cell RNA profiling,
Analyzing gene expression in over 1.3 million cells across multiple brain regions, the study highlights the role of Reelin in neuron protection and choline metabolism in astrocytes for cognitive resilience. These findings pave the way for potential therapeutic targets to sustain cognition and memory amid Alzheimer’s pathology.
Key Facts:
Reelin-producing neurons are linked to cognitive resilience in Alzheimer’s patients.
Choline metabolism in astrocytes is associated with sustained cognition despite pathology.
Gene expression analysis in 1.3 million cells revealed significant insights into Alzheimer’s.
Source: Picower Institute at MIT
An MIT study published today in Nature provides new evidence for how specific cells and circuits become vulnerable in Alzheimer’s disease, and hones in on other factors that may help some people show resilience to cognitive decline, even amid clear signs of disease pathology.
To highlight potential targets for interventions to sustain cognition and memory, the authors engaged in a novel comparison of gene expression across multiple brain regions in people with or without Alzheimer’s disease, and conducted lab experiments to test and validate their major findings.
Brain cells all have the same DNA but what makes them differ, both in their identity and their activity, are their patterns of how they express those genes. The new analysis measured gene expression differences in more than 1.3 million cells of more than 70 cell types in six brain regions from 48 tissue donors, 26 of whom died with an Alzheimer’s diagnosis and 22 of whom without.
This shows neurons.
Some of the earliest signs of amyloid pathology and neuron loss in Alzheimer’s occurs in memory-focused regions called the hippocampus and the entorhinal cortex. Credit: Neuroscience News
As such, the study provides a uniquely large, far-ranging and yet detailed accounting of how brain cell activity differs amid Alzheimer’s disease by cell type, by brain region, by disease pathology, and by each person’s cognitive assessment while still alive.
“Specific brain regions are vulnerable in Alzheimer’s and there is an important need to understand how these regions or particular cell types are vulnerable,” said co-senior author Li-Huei Tsai, Picower Professor of Neuroscience and director of The Picower Institute for Learning and Memory and the Aging Brain Initiative at MIT.
“And the brain is not just neurons. It’s many other cell types. How these cell types may respond differently, depending on where they are, is something fascinating we are only at the beginning of looking at.”
Co-senior author Manolis Kellis, professor of computer science and head of MIT’s Computational Biology Group, likened the technique used to measure gene expression comparisons, single cell RNA profiling,
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