Parkinson’s-related protein can spread from the nose to the brain

The takeaway

Abnormal alpha-synuclein proteins, which are associated with the spread of Parkinson’s, travel from the part of the brain responsible for sense of smell to other areas of the brain. Many people experience problems with their sense of smell years before they experience issues with movement; these findings present a clearer picture of what happens early on in this process.

Why is it important?

This is an important development for two reasons:

  1. The study confirms that alpha-synuclein moves between part of the brain that controls sense of smell to other regions of the brain.
  2. It outlines a new model for the disease, which will help scientists better study the earliest stages of Parkinson’s.

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IMPACT

  • Novelty 100%
  • Proximity 60%
  • Deliverability 60%

Impact

“The study provides fascinating evidence that a protein associated with Parkinson’s disease can spread pathology throughout the brain following injection into the olfactory bulb (i.e., the nose). It might mean that inhaled toxins or infections that affect the nose may trigger the disease process.” Dr. Patrik Brundin

Background

Much like sticky grains of rice, abnormal alpha-synuclein proteins clumps together, forming the Lewy bodies found in the brains and nervous systems of people with Parkinson’s. It is thought that cells’ inability to clean out these proteins causes inflammation and, ultimately, damage or death to the cell. When enough of the dopamine-producing cells in the brain are damaged or killed, Parkinson’s hallmark movement problems begin. Understanding how alpha-synuclein moves from cell to cell could provide insight into ways to slow or stop this process, ultimately interfering with the disease’s progression.

Related work

As many people with Parkinson’s experience a reduced sense of smell early on, a recent review article has evaluated much of the clinical, pathological and neuroimaging evidence for the involvement of the olfactory system in the underlying mechanisms of prodromal Parkinson’s (the period between the appearance of initial symptoms and full development of Parkinson’s) and how this might differ in people who do not experience loss of sense of smell.

Original article: Rey NL, Steiner JA, Maroof N, Luk KC, Madaj Z, Trojanowski JQ, Lee VMY, Brundin P. Aug 8, 2016. Widespread transneuronal propagation of a-synucleinopathy triggered in olfactory bulb mimics prodromal Parkinson’s disease. J Exp Med.

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