TTUHSC Researcher to Uncover Mechanisms Regulating Gene Expression in Alzheimer’s Disease
Unlocking Alzheimer’s Secrets: New Research Focuses on Gene Expression Regulation
Texas Tech University Health Sciences Center (TTUHSC) researchers are delving into the complex world of gene expression to better understand Alzheimer’s disease, a devastating neurodegenerative disorder affecting over six million Americans.
alzheimer’s disease is characterized by the buildup of amyloid-β plaques and hyperphosphorylated tau (pTau) tangles in the brain, leading to brain damage and cognitive decline. While previous studies have identified changes in RNA accumulation associated with Alzheimer’s, the full picture of gene expression regulation in this disease remains unclear.
A New Approach: Option Polyadenylation
Dr. Petar Grozdanov, an assistant professor in the TTUHSC Department of Cell Biology and Biochemistry, has received a two-year, $310,000 grant from the National Institutes of Health-National Institute on Aging to investigate a specific mechanism called alternative polyadenylation.
“There are several ways to regulate gene expression,” explains Dr. Grozdanov. “The most recognized way is by changing the amount of messenger RNA (mRNA) produced. But alternative polyadenylation provides a fine-tuning of protein production, which is often overlooked.”
Alternative polyadenylation is a process that determines how an mRNA molecule ends, influencing its stability, translation, and localization within the neuron.
The Neuron’s Long Journey: Why Alternative Polyadenylation Matters
Neurons are incredibly long cells, stretching for feet in some animals. This poses a challenge for protein production, as proteins need to be delivered to specific locations within the neuron, such as synapses, crucial for learning and memory.
“Alternative polyadenylation allows mRNAs to be directed to the correct sites in neurons,” says Dr. Grozdanov. “When this process is disrupted,the balance between different mRNA transcripts is altered,perhaps interfering with protein production at specific neuronal locations.”
Hope for the future: Targeting Alternative Polyadenylation for Treatment
Dr. Grozdanov’s research aims to characterize the changes in alternative polyadenylation in Alzheimer’s patients. If triumphant,the next step will be to identify the proteins and molecules responsible for thes changes,potentially leading to new therapeutic targets.
“Can we modify this pathway or reverse its influence on the disease progression?” asks Dr. Grozdanov.”Maybe we can develop a mechanism or drug that adjusts the length of mRNA transcripts and restores more normal cognition in patients.”
While reversing brain damage in late-stage Alzheimer’s may be challenging, dr. grozdanov believes that understanding and targeting alternative polyadenylation could offer a promising avenue for slowing down the progression of this devastating disease.
Texas Tech Researchers Explore Gene Regulation as Key to Unlocking Alzheimer’s Secrets
Lubbock, TX – In a quest to unravel the complexities of alzheimer’s disease, researchers at Texas Tech University Health Sciences Center (TTUHSC) are focusing on the intricate dance of gene expression.
Alzheimer’s disease, affecting over six million Americans, is characterized by the buildup of amyloid plaques and tau tangles in the brain, leading to devastating cognitive decline. While previous studies have linked changes in RNA accumulation to Alzheimer’s, the full picture of how genes are regulated in this disease remains blurry.
Now, Dr. Petar Grozdanov, an assistant professor in TTUHSC’s Department of Cell Biology and Biochemistry, is taking a novel approach. Thanks to a two-year, $310,000 grant from the National Institutes of Health-National Institute on Aging, Dr. Grozdanov will investigate a process called alternative polyadenylation.
“Think of it like fine-tuning the volume knob on a stereo,” explains Dr. Grozdanov.”While changing the amount of messenger RNA (mRNA) produced is like adjusting the overall volume, alternative polyadenylation allows for subtle adjustments in protein production.”
This process determines how an mRNA molecule ends, influencing its stability, translation, and even where it travels within a neuron. This is particularly vital for neurons, which can stretch for remarkable distances.
“Neurons are like intricate highways within the brain,” says Dr. Grozdanov. “Alternative polyadenylation ensures that proteins are delivered to the right locations,such as synapses,which are crucial for learning and memory.”
Dr. Grozdanov believes disruption of this process might contribute to the development of Alzheimer’s disease by altering the balance of mRNA transcripts and affecting protein production at specific neuronal sites.
Dr. Grozdanov’s research aims to map these changes in Alzheimer’s patients.If successful, the next step would be to identify the proteins and molecules responsible for these shifts, potentially leading to new therapeutic targets.
“Could we develop a drug to adjust the length of mRNA transcripts and restore more normal cognition in patients?” asks Dr. Grozdanov. “
While reversing existing brain damage in late-stage Alzheimer’s might be a tall order, Dr. Grozdanov believes understanding and targeting alternative polyadenylation could offer a promising avenue for slowing down the progression of this devastating disease.
