Should the Source of Alzheimer's Disease Dictate Treatment?

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the Neurology Advisor take:

Alzheimer’s disease may actually be a group of conditions that should each be treated differently, according to new research.

Since neurodegenerative disorders result from an abnormal folding of protein, researchers at the Hebrew University Faculty of Medicine thought that the decline in the activity of proteins that assist other proteins to fold properly as a result of aging may be one mechanism that exposes seniors to neurodegeneration.

With this in mind, the researchers looked for similar mutational patterns in different proteins that are linked to the development of neurodegenerative disorders. They found that the development of Alzheimer’s disease in certain families, and of a familial prion disorder in other families, originate from very similar mutational patterns.

They then discovered that the malfunction of the protein cyclophilin B, which helps new proteins attain their proper structures, is responsible for the formation of Alzheimer’s and other prion disorders.

“This study provides important new insights: first, it shows that the development of distinct neurodegenerative disorders stems from a similar mechanism,” Ehud Cohen, PhD, of Hebrew University, said in a statement. “More importantly, it 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.”

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Should the Source of Alzheimer's Disease Dictate Treatment?

Deciphering the mechanism that underlies the development of Alzheimer's disease in certain families but not in others, researchers at the Hebrew University of Jerusalem's Faculty of Medicine have proposed that the malady is actually a collection of diseases that probably should be treated with a variety of different approaches.

The late disease onset typical to distinct neurodegenerative diseases, and the common temporal emergence patterns of these maladies, raise key questions: first, why do individuals who carry disease-linked mutation show no clinical signs until their fifth or sixth decade of life? In addition, why do apparently distinct disorders share a common temporal emergence pattern?

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 disease. Indeed, previous studies clearly indicate that the aging process plays key roles in enabling neurodegenerative disorders to onset late in life.

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