Roughly 5.3 million Americans are suffering from Alzheimer’s disease, and every 67 seconds someone in the US develops the disease, according to the Alzheimer’s Association. It is among the 10 leading causes of death but at this time, the medical community has found no way to prevent, cure, or even slow it.
That’s why some scientists say it might be time to look at Alzheimer’s differently. Deciphering the mechanism that underlies the development of Alzheimer’s disease in certain families but not in others, researchers at the Hebrew University have proposed that the malady is actually a collection of several diseases that should be classified and treated separately – with a variety of different approaches.
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Neurodegenerative diseases such as Alzheimer’s and Parkinson’s are debilitating conditions that result in degeneration or death of cells in the nervous system. Cases are typically diagnosed during the patient’s fifth through seventh decade of life. The late onset of the disease raises the following question: Why do individuals who carry disease-linked mutations show no clinical signs until they reach their fifties or sixties? One possible explanation is that as people age, the efficiency of the mechanisms that protect younger people from the toxic aggregation of proteins declines, thus exposing them to the disease. Indeed, previous studies clearly indicate that the aging process and this aggregation of proteins plays a key role in enabling neurodegenerative disorders to onset late in life.
The secret protein that’s responsible for the manifestation of Alzheimer’s
Since neurodegenerative disorders stem from abnormal protein folding (the process by which a protein assumes its functional shape), the researchers believe that an aging-associated decline in the activity of proteins that assist other proteins to fold properly may be one mechanism that exposes the elderly to neurodegeneration. Such abnormality can also occur due to an infectious misfolded protein or a genetic mutation. The study suggests that Alzheimer’s symptoms should be distinguished according to these underlying mechanisms, hence should be regarded as different diseases.
The international research team, led by Prof. Ehud Cohen and Dr. Tziona Ben-Gedalya of the Hebrew University, also discovered that the malfunction of a protein called “cyclophilin B,” which helps nascent proteins to attain their proper structures, can also be responsible for the manifestation of Alzheimer’s.
According to Cohen, “this study indicates that Alzheimer’s disease can emanate from more than one mechanism, suggesting that it is actually a collection of diseases that should be classified.”
The new insights derived from his study may reinforce the efforts to develop novel therapies to the different subtypes of Alzheimer’s disease, providing new hope for those who suffer from this incurable disorder.
Cohen stresses that “it is essential to carefully characterize and classify the mechanisms that underlie Alzheimer’s disease, in order to allow for the development of novel therapies that can be prescribed to the individual patient according to their relevant disease subtype.”