by Researchers from Boston University Chobanian & Avedisian School of Medicine have made significant progress in identifying a gene that may contribute to the degeneration of neurons most susceptible to Alzheimer’s disease (AD). The study, which involved collaboration with computational genomic experts from Rice University and Karolinska Institute, sheds light on the mechanisms underlying the selective vulnerability of certain brain cells during the early stages of neurodegenerative disorders.
Alzheimer’s disease is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain, leading to the degeneration of neurons. While the exact reasons behind the selective vulnerability of specific cell populations remain unclear, understanding this phenomenon could offer valuable insights into the pathological mechanisms of the disease.
The researchers focused on the entorhinal cortex, a region of the brain where neurofibrillary tangles typically first appear in AD. By employing cutting-edge analysis tools and machine learning techniques, they pinpointed the DEK gene as a potential key player in the vulnerability of entorhinal cortex neurons. Experimental models and lab-grown neurons were used to manipulate DEK gene levels, revealing that reduced DEK expression caused vulnerable neurons to accumulate tau and undergo degeneration.
The study findings suggest that targeting DEK or its associated proteins could prevent neuron degeneration and potentially halt the progression of Alzheimer’s disease before it spreads to other brain regions. Since entorhinal cortex neurons are crucial for memory formation and are particularly susceptible to damage, preserving their function could help prevent memory loss, a common early symptom of AD.
Corresponding author Jean-Pierre Roussarie emphasized the importance of further research to uncover additional genes involved in the degeneration of critical memory-forming neurons. While this study represents a significant advancement in understanding the mechanisms of neuronal vulnerability in Alzheimer’s disease, there is still much to learn in order to fully grasp the complexities of the disease progression.
The identification of the DEK gene as a potential target for therapeutic interventions opens up new possibilities for developing treatments that specifically address the underlying causes of neuronal degeneration in Alzheimer’s disease. By focusing on protecting vulnerable neurons in the entorhinal cortex, researchers hope to offer new avenues for combating the devastating effects of AD on memory and cognitive function.
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1. Source: Coherent Market Insights, Public sources, Desk research
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