Researchers have found that a protein may help reverse the effects of damaging plaques in the brain associated with Alzheimer’s disease.
The findings may offer clues leading to successful treatment of the disease.
The accumulation in the brain of plaques formed from deposits of a critical protein, known as amyloid beta, is a hallmark of Alzheimer’s disease, the most common form of dementia.
This study demonstrated that a multipurpose protein, known as p62, regulates the degradation or turnover of amyloid beta in living systems, which may help reverse the effects of damaging plaques in the brain.
“These exciting finding suggest that compounds aimed at increasing p62 may have beneficial effects for Alzheimer’s disease,” said one of the researchers Salvatore Oddo from Arizona State University in the US.
Currently, there is no effective therapy for Alzheimer’s that 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.
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 recognized as hallmarks of Alzheimer’s disease – tau and amyloid beta.
The authors 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, published in the journal Molecular Psychiatry, further showed that the improvement is associated with reduced levels of amyloid beta and associated plaques in the brain.
The new research also described the mechanism by which p62 activity improves Alzheimer’s disease symptoms in mice– by a process known as autophagy.
The term refers to the degradation or disassembly of unnecessary or dysfunctional components of cells – a form of biological recycling essential for cellular health.