Alzheimer’s Developments

Alzheimer’s disease researchers have long believed that plaque was the culprit that causes the brain cell death that characterizes the degenerative condition. Now, new data reported in the October 29, 2014 issue of Molecular Neurodegeneration, suggests that it is actually another protein that kills brain cells, and that plaque build up is actually a by-product of the protein in question. According to researchers from Georgetown Medical Center, it is the cell death caused by a protein called tau that leads to the memory and behavioral interferences associated with Alzheimer’s.

Alzheimer’s disease is the most common type of dementia. It is associated with a disruption in the storage and retrieval of memory, and a decline in cognitive abilities. It is a degenerative condition, meaning that symptoms get worse over time. Approximately 5.2 million people currently suffer from Alzheimer’s disease in the United States, the majority of whom are over the age of 65, making it a condition associated mainly with old age. In approximately five percent of cases, however, younger people are affected, proving that the disease can affect individuals in middle age.

Age-related neurodegenerative disorders such as Alzheimer’s place a great strain on society, so preventative measures to forestall the disease are being keenly sought by the medical profession. It is estimated that $214 billion will be spent on healthcare for all forms of dementia in 2014 alone. As the population ages, the number of patients is expected to increase so that, by the year 2050, 16 million people over the age of 65 will suffer from Alzheimer’s disease.

Tangles of the tau protein and plaque consisting of amyloid-beta protein fragments are often observed in the brains of Alzheimer’s disease patients. New research has pointed to the tau protein as the element that accelerates the death of neurons, rather than the plaque that is seen alongside it. This theory provides an explanation to the anomaly seen some individuals, who have evidence of plaque build-up, but no signs of cognitive decline. These findings could lead to the establishment of new medication and treatment protocol for the disease.

Charbel E-H Moussa, study leader and department head at Georgetown University School of Medicine’s Laboratory for Dementia and Parkinsonism, says that, for almost a century, the prevailing belief was that Alzheimer’s disease was largely due to the build up of amyloid-beta plaques.Animal studies indicate that when tau protein is functioning well, less plaque is present outside brain cells.He believes that the finding that the tau protein may be responsible for the deterioration observed in Alzheimer’s patients is major step forward because it removes a longstanding distraction posed by the belief that plaque was the culprit.

Tau is a protein that provides a cell a structure in which waste products can be transported out of the body’s cells. When tau is functioning optimally, the cell has a route to eliminating toxins, an activity vital for its health. Should tau cease to function in such a manner, this important process is disrupted and the cell is unable to dispose of toxic materials, which ultimately results in the cell’s death.

Moussa explains how the cell attempts to eliminate any malfunctioning tau protein blockage it by spitting it out. As these proteins are sticky, clumps are formed which turn into plaque when they are ejected, which cling to the outside of the cell. He believes that it is the protein inside of the cell, the parts that were not removed, that ultimately causes cell death, rather than the plaque as seen outside of the cell.

To investigate this, the researchers used nilotinib, an anti-cancer medication normally given to adults suffering from leukemia. Nilotinib is believed to enter into a cell and remove toxic material, in the context of the recent investigation, it was applied as a potential disposal route for excess tau and intercellular waste.

Moussa says that nilotinib is also effective at reducing the build up of plaque outside of a cell. He has plans to begin clinical trials on dementia patients within the next month. He believes that tau build-up will be the most effective indicator of Alzheimer’s disease onset, and that screening for this will help doctors recognize the earliest signs of the disease.

The application of medications designed to interfere with the development of tau accumulation could, according to Moussa, help patients avoid dementia. According to Dr. Ronald Peterson, director of the Mayo Clinic Alzheimer’s Disease Research Center, knowing that tau is a factor in the progression of the disease will be key to the development of therapeutics to treat and prevent Alzheimer’s disease in the future.

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