Washington | Scientists have identified a protein that may help reverse the effects of damaging plaques in the brain associated with Alzheimer’s disease.
The findings offer new insights that may help unravel the mysteries of one of the most intractable and shattering human illnesses, researchers said.
The multi-purpose protein p62 has already been associated with one of the two classic neurological symptoms of Alzheimer’s disease.
Known as neurofibrillary tangles, these twisted strands of tau protein form inside dying cells, destroying vital pathways for nutrients.
Researchers from Biodesign Neurodegenerative Disease Research Centre (NDRC) in the US have shown that p62 is associated with the other hallmark of Alzheimer’s disease, the accumulation in the brain of plaques formed from deposits of another critical protein, known as amyloid beta (AB).
The study demonstrates for the first time that p62 regulates the degradation or turnover of AB in living systems, which may help reverse the effects of damaging plaques in the brain.
The association of p62 with both plaques and tangles points to a central role in the onset and trajectory of Alzheimer’s disease and may offer clues leading to successful treatment of the disease, researchers said.
Currently, there is no effective therapy for Alzheimer’s.
“These exciting finding suggest that compounds aimed at increasing p62 may have beneficial effects for Alzheimer’s disease,” said Salvatore Oddo from NDRC.
Alzheimer’s disease causes nerve cell death and tissue loss throughout the brain. During the course of the disease, the brain shrinks dramatically, affecting nearly all its functions.
Shrinkage of the brain is acute in the cortex, damaging areas critical for thinking, planning and remembering.
Atrophy is particularly severe in the hippocampus, an area of the cortex that plays a crucial role in formation of new memories. By contrast, the fluid-filled spaces in the brain known as ventricles grow larger.
The protein p62 is known to perform an array of vital functions in cells. Of particular interest is p62′s role in the aggregation and degradation of a pair of proteins long recognised as hallmarks of Alzheimer’s disease – tau and AB, researchers said.
They demonstrated, for the first time, that a modified strain of mice generated to display human-like symptoms of Alzheimer’s show significant cognitive improvements, including a reversal of spatial memory deficit, when the brain’s expression of p62 is restored.
The study further shows that the improvement is associated with reduced levels of AB and associated plaques in the brain.
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