December 19, 2025
Timothy Birdnow
You know I thought this was going to be about climate and the alleged 98% "concesus" which is itself a kind of climatological Alzheimers...
The 98% Mystery: Scientists Just Cracked the Code on "Junk DNA” Linked to Alzheimer’s
Turns out all the "junk DNA" is actually busily controlling the machinery that causes or prevents Alzheimers.
From the article:
This stands to reason; there is no such thing as junk in the human genome because any such thing would long ago have been deleted as irrelevant, just as we have deleted genes for beaks or gills (or, more accurately, have suppressed them epigenetically). It seems entirely likely "junk DNA" has an important role to play but we just haven't understood it until now.
I would also point out that memory MUST be edited or the brain would quickly become saturated. So there are editing mechanisms in place and they no doubt tie in with our DNA. Alzheimers appears to be a systemic failure of such as, well:
So basically if the enhancers are switched off memory starts to degrade.
So does cognitive ability and thus my reference to climate change alarmism.
This is a most welcome development; if we come to understand which genes influence the enhancers, and can work up ways to switch them off, we could reverse or at least help prevent memory loss in Alzheimers patients.
I watched my grandmother lose her memory (and mind) from this disease; it's a terrible thing.
At any rate the more we learn the more we realize we don't know.
You know I thought this was going to be about climate and the alleged 98% "concesus" which is itself a kind of climatological Alzheimers...
The 98% Mystery: Scientists Just Cracked the Code on "Junk DNA” Linked to Alzheimer’s
Turns out all the "junk DNA" is actually busily controlling the machinery that causes or prevents Alzheimers.
From the article:
December 19, 2025
Source:
University of New South Wales
Summary:
Researchers have revealed that so-called "junk DNA” contains powerful switches that help control brain cells linked to Alzheimer’s disease. By experimentally testing nearly 1,000 DNA switches in human astrocytes, scientists identified around 150 that truly influence gene activity—many tied to known Alzheimer’s risk genes. The findings help explain why many disease-linked genetic changes sit outside genes themselves. The resulting dataset is now being used to train AI systems to predict gene control more accurately.
Source:
University of New South Wales
Summary:
Researchers have revealed that so-called "junk DNA” contains powerful switches that help control brain cells linked to Alzheimer’s disease. By experimentally testing nearly 1,000 DNA switches in human astrocytes, scientists identified around 150 that truly influence gene activity—many tied to known Alzheimer’s risk genes. The findings help explain why many disease-linked genetic changes sit outside genes themselves. The resulting dataset is now being used to train AI systems to predict gene control more accurately.
This stands to reason; there is no such thing as junk in the human genome because any such thing would long ago have been deleted as irrelevant, just as we have deleted genes for beaks or gills (or, more accurately, have suppressed them epigenetically). It seems entirely likely "junk DNA" has an important role to play but we just haven't understood it until now.
I would also point out that memory MUST be edited or the brain would quickly become saturated. So there are editing mechanisms in place and they no doubt tie in with our DNA. Alzheimers appears to be a systemic failure of such as, well:
Researchers from UNSW Sydney have now pinpointed DNA switches that help regulate astrocytes. Astrocytes are brain cells that support neurons, and they are known to be involved in Alzheimer's disease.
In research published on December 18 in Nature Neuroscience, a team from UNSW's School of Biotechnology & Biomolecular Sciences reported that they tested nearly 1000 possible switches in lab-grown human astrocytes. These switches are strings of DNA called enhancers. Enhancers can sit far from the genes they influence, sometimes separated by hundreds of thousands of DNA letters, which makes them difficult to investigate.
To tackle that problem, the researchers combined CRISPRi with single-cell RNA sequencing. CRISPRi is a method that can switch off small stretches of DNA without cutting it. Single-cell RNA sequencing measures gene activity in individual cells. Together, the tools let the team examine the effects of nearly 1000 enhancers in a single large-scale test.
"We used CRISPRi to turn off potential enhancers in the astrocytes to see whether it changed gene expression," says lead author Dr. Nicole Green.
"And if it did, then we knew we'd found a functional enhancer and could then figure out which gene -- or genes -- it controls. That's what happened for about 150 of the potential enhancers we tested. And strikingly, a large fraction of these functional enhancers controlled genes implicated in Alzheimer's disease."
Cutting the list from 1000 candidates to about 150 confirmed switches greatly reduces the search area in the non-coding genome for genetic clues linked to Alzheimer's disease.
In research published on December 18 in Nature Neuroscience, a team from UNSW's School of Biotechnology & Biomolecular Sciences reported that they tested nearly 1000 possible switches in lab-grown human astrocytes. These switches are strings of DNA called enhancers. Enhancers can sit far from the genes they influence, sometimes separated by hundreds of thousands of DNA letters, which makes them difficult to investigate.
To tackle that problem, the researchers combined CRISPRi with single-cell RNA sequencing. CRISPRi is a method that can switch off small stretches of DNA without cutting it. Single-cell RNA sequencing measures gene activity in individual cells. Together, the tools let the team examine the effects of nearly 1000 enhancers in a single large-scale test.
"We used CRISPRi to turn off potential enhancers in the astrocytes to see whether it changed gene expression," says lead author Dr. Nicole Green.
"And if it did, then we knew we'd found a functional enhancer and could then figure out which gene -- or genes -- it controls. That's what happened for about 150 of the potential enhancers we tested. And strikingly, a large fraction of these functional enhancers controlled genes implicated in Alzheimer's disease."
Cutting the list from 1000 candidates to about 150 confirmed switches greatly reduces the search area in the non-coding genome for genetic clues linked to Alzheimer's disease.
So basically if the enhancers are switched off memory starts to degrade.
So does cognitive ability and thus my reference to climate change alarmism.
This is a most welcome development; if we come to understand which genes influence the enhancers, and can work up ways to switch them off, we could reverse or at least help prevent memory loss in Alzheimers patients.
I watched my grandmother lose her memory (and mind) from this disease; it's a terrible thing.
At any rate the more we learn the more we realize we don't know.
Posted by: Timothy Birdnow at
02:24 PM
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