Globally, dementia is becoming a more prevalent issue as people live longer on average. Studies indicate that around 150 million people will suffer from dementia by 2050.
Numerous symptoms, including memory loss, cognitive impairments, and personality changes, are associated with Alzheimer's disease . These symptoms are commonly attributed to an accumulation of two proteins in the brain : beta-amyloid and tau.
Most current therapies focus on symptom relief, with several more recent disease-modifying therapies like aducanumab and lecanemab showing promising results. Nevertheless, there are adverse effects associated with these monoclonal antibody treatments, which some specialists feel may exceed their therapeutic advantages.
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A new study has described a potential treatment that targets the tau protein, which accumulates into neurofibrillary tangles and slows down nerve impulse transmission across synapses, the junctions between nerve cells.
Researchers discovered that PHDP5, a synthetic peptide, restored memory and learning deficits in transgenic mice by blocking a mechanism that causes tau accumulation. Microtubules and dynamin are two materials that are essential for the transfer of nerve impulses between synapses. Together, these enable the recycling of neurotransmitter-filled vesicles, which are responsible for sending impulses from one nerve cell to another.
Tau helps to stabilize the microtubules in healthy people. Nevertheless, tau detaches from microtubules in Alzheimer's disease, eliminating dynamin from nerve cells and ultimately resulting in tangles. Due to these modifications, vesicles are unable to recycle effectively, which stops nerve impulses from traveling between nerve cells.
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Previous studies conducted in vitro by the researchers show that the synthetic peptide PHPD5 released dynamin, allowing it to be recycled into vesicles and restoring synaptic transmission.
Cognition Health's CEO and consultant neuroradiologist, Dr. Emer MacSweeney, who was not involved in the study, stated: “This research appears to be pioneering in specifically targeting the dynamin-microtubule interaction with the synthetic peptide PHDP5. While other treatments for Alzheimer’s focus on different mechanisms, such as amyloid-beta plaques and tau tangles, targeting the dynamin-microtubule pathway is relatively novel.”
“The researchers have shown in vitro and in vivo evidence of the positive effects of inhibiting this interaction, suggesting this could be the first time it has been targeted in this manner,” she added.
After demonstrating PHPD5's effectiveness in vitro, the researchers employed transgenic Tau609 mice—mice that experience tau tangles, neuronal degeneration, and memory loss—in their investigation. For four weeks, they put two milligrams of PHDP5 in saline solution into each of their nostrils once daily. Using the same procedure, control Tau609 mice were given only saline solution.
The Morris Water Maze (MWM) test was used to evaluate the mice's memory and learning three weeks into the treatment. Initially, the mice were trained for four times to locate an escape platform in one quadrant of a circular water trough with a diameter of 100 cm and a depth of 30 cm.
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