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Together, the two studies show that memory loss is not caused by a single molecule or pathway and that multiple molecular systems likely contribute to how the brain ages. Credit: Neuroscience News<\/p>\nSummary: Researchers have identified molecular mechanisms behind age-related memory decline \u2014 and shown they can be reversed. Two studies revealed that correcting specific molecular processes in the hippocampus and amygdala, and reactivating a silenced memory-supporting gene called IGF2, improved memory in older rats.<\/p>\n
Using CRISPR-based gene-editing tools, scientists restored proper signaling and communication between neurons linked to memory storage and recall. The findings suggest memory loss may not be an inevitable part of aging and could eventually be treated at the molecular level.<\/p>\n
Key Facts:<\/p>\n
Molecular Targets Identified: Disruptions in K63 polyubiquitination and IGF2 gene silencing drive age-related memory decline.CRISPR Success: Editing these pathways in older rats improved memory performance.Therapeutic Promise: Findings suggest future gene-based treatments could help prevent or reverse age-related memory loss.<\/p>\n
Source: Virginia Tech<\/p>\n
Memory loss may not simply be a symptom of getting older. New research from Virginia Tech shows that it\u2019s tied to specific molecular changes in the brain and that adjusting those processes can improve memory.<\/p>\n
In two complementary studies,\u00a0Timothy Jarome, associate professor in the\u00a0College of Agriculture and Life Sciences\u2019\u00a0School of Animal Sciences, and his graduate students used gene-editing tools to target those age-related changes to improve memory performance in older subjects. The work was conducted on rats, a standard model for studying how memory changes with age.<\/p>\n
Together, the two studies show that memory loss is not caused by a single molecule or pathway and that multiple molecular systems likely contribute to how the brain ages. Credit: Neuroscience News<\/p>\n
\u201cMemory loss affects more than a third of people over 70, and it\u2019s a major risk factor for Alzheimer\u2019s disease,\u201d said Jarome, who also holds an appointment in the\u00a0School of Neuroscience.<\/p>\n
\u201cThis work shows that memory decline is linked to specific molecular changes that can be targeted and studied.\u00a0If we can understand what\u2019s driving it at the molecular level, we can start to understand what goes wrong in dementia and eventually use that knowledge to guide new approaches to treatment.\u201d<\/p>\n
Targeting memory loss in two key brain regions<\/p>\n
In\u00a0the first study, published in\u00a0the journal Neuroscience\u00a0and led by Jarome and doctoral student Yeeun Bae, the team examined a process called K63 polyubiquitination. This process acts as a molecular tagging system that tells proteins inside the brain how to behave. When the system functions normally, it helps brain cells communicate and form memories.<\/p>\n
Jarome and his team found that aging disrupts K63 polyubiquitination in two distinct areas of the brain. In the\u00a0hippocampus, which helps form and retrieve memories, levels of K63 polyubiquitination\u00a0increase\u00a0with age. Using the\u00a0CRISPR-dCas13 RNA editing system\u00a0to reduce these levels, the researchers were able to improve memory in older rats.<\/p>\n
In the amygdala, which is important for emotional memory, the researchers noted that K63 polyubiquitination declines with age. By reducing it even further, they were able to boost\u00a0memory in older rats.<\/p>\n
\u201cTogether, these findings reveal the important functions of K63 polyubiquitination in the brain\u2019s aging process,\u201d\u00a0Jarome said. \u201cIn both regions, adjusting this one molecular process helped improve memory.\u201d<\/p>\n
Reactivating a gene that supports memory<\/p>\n
A second study, published in\u00a0the Brain Research Bulletin\u00a0and led by Jarome with doctoral student Shannon Kincaid, focused on IGF2, a growth-factor gene that supports memory formation. As the brain ages, IGF2 activity drops as the gene becomes chemically silenced in the hippocampus.<\/p>\n
\u201cIGF2 is one of a small number of genes in our DNA that\u2019s imprinted, which means it\u2019s expressed from only one parental copy,\u201d Jarome said. \u201cWhen that single copy starts to shut down with age, you lose its benefit.\u201d<\/p>\n
The researchers found that this silencing happens through DNA methylation, a natural process in which chemical tags accumulate on the gene and switch it off. Using a precise gene-editing tool, CRISPR-dCas9, they removed those tags and reactivated the gene. The result was better memory in older rats.<\/p>\n
\u201cWe essentially turned the gene back on,\u201d Jarome said. \u201cWhen we did that, the older animals performed much better. Middle-aged animals that didn\u2019t yet have memory problems weren\u2019t affected, which tells us timing matters. You have to intervene when things start to go wrong.\u201d<\/p>\n
Together, the two studies show that memory loss is not caused by a single molecule or pathway and that multiple molecular systems likely contribute to how the brain ages.<\/p>\n
\u201cWe tend to look at one molecule at a time, but the reality is that many things are happening at once,\u201d he said. \u201cIf we want to understand why memory declines with age or why we develop Alzheimer\u2019s disease, we have to look at the broader picture.\u201d<\/p>\n
Collaborative, graduate-led research<\/p>\n
Both studies were driven by graduate researchers in Jarome\u2019s lab and supported through collaborations with scientists at Rosalind Franklin University, Indiana University, and Penn State.\u00a0Yeeun Bae, who completed her doctoral work with Jarome in the\u00a0School of Animal Sciences, led the study on K63 polyubiquitination.\u00a0Shannon Kincaid, a doctoral student in the same program, led the study on IGF2.<\/p>\n
\u201cThese projects represent the kind of graduate-led, collaborative research that defines our work,\u201d Jarome said. \u201cOur students are deeply involved in designing experiments, analyzing data, and helping shape the scientific questions we pursue.\u201d<\/p>\n
\u201cEveryone has some memory decline as they get older,\u201d he said. \u201cBut when it becomes abnormal, the risk for Alzheimer\u2019s disease rises. What we\u2019re learning is that some of those changes happening at a molecular level can be corrected \u2014 and that gives us a path forward to potential treatments.\u201d<\/p>\n
Funding: The research was supported by the National Institutes of Health and the American Federation for Aging Research.<\/p>\n
Key Questions Answered:Q: What causes memory loss as we age?<\/p>\n
A: Researchers found that aging alters key molecular processes, including K63 polyubiquitination and silencing of the IGF2 gene, which are critical for forming and maintaining memories.<\/p>\n
Q: How did scientists improve memory in older subjects?<\/p>\n
A: By using CRISPR-based gene-editing tools to restore normal molecular signaling in the hippocampus and amygdala, they enhanced memory in older rats.<\/p>\n
Q: Could this research lead to human treatments?<\/p>\n
A: While still early, the findings suggest targeting specific molecular changes could form the basis of future gene therapies for age-related memory loss and possibly Alzheimer\u2019s disease.<\/p>\n
About this memory and gene editing research news<\/p>\n
Author: Margaret Ashburn<\/a> Original Research: Open access.
Source: Virginia Tech
<\/a>Contact: Margaret Ashburn \u2013 Virginia Tech
Image: The image is credited to Neuroscience News<\/p>\n
\u201cIncreased DNA methylation of\u00a0Igf2\u00a0in the male hippocampus regulates age-related deficits in synaptic plasticity and memory<\/a>\u201d by Timothy Jarome et al. Brain Research Bulletin<\/p>\n