A New Way to Evaluate Parkinson’s Disease: Brain First and Body First

According to a recent article in Parkinson’s News Today, Dr. Per Borghammer, Research Professor at Denmark’s Aarhus University, proposed a new model that has the potential to identify early Parkinson’s symptoms. The new model addresses the symptoms as they appear and monitors their progression through the nervous system.

Dr. Borghammer’s model called the alpha-synuclein Origin and Connectome (SOC), has been designed using imaging and clinical studies of patients living with Parkinson’s as well as evidence from postmortem brain tissues. Parkinson’s animal models were also used in the study.

Dr. Borghammer points out that the SOC model shows that the alpha-synuclein disease is symmetrical and widespread throughout the body. It identifies the involvement of specific brainstem neurons associated with dementia and cognitive decline.

About Body First

In the SOC model, during the development of Parkinson’s, when the original site is located in the gut’s peripheral nervous system, the name of the sub-type is ‘Body-First’.

There are two main parts to the nervous system. The peripheral nervous system made up of nerves that branch off from the spinal cord and lead to all parts of the body, and the central nervous system composed of the spinal cord and brain.

In body-first, the disease spreads slowly because neurons separate the gut’s peripheral nervous system from the central nervous system. In addition, connections in the peripheral nervous system overlap so that the disease spreads evenly (symmetrically) from the gut to the brain. However, body-first patients characteristically have a heavier burden of alpha-synuclein disease causing a faster progression accompanied by cognitive decline.

Alpha-synuclein is a protein that is usually found in the body and brain. However, in Parkinson’s disease, it tends to cluster into abnormal deposits that are called Lewy bodies. These deposits affect chemicals in the brain that disrupt thinking, movement, behavior, and mood. The SOC model is applicable to any disease associated with Lewy bodies.

About Brain First

The ‘brain-first’ subtype is almost the complete opposite of body first. In the brain-first, protein clumping begins in the brain and the pre-diagnostic phase is shorter. All other symptoms such as motor, non-motor progression, and cognitive decline progress at a slower pace. There are usually fewer sleep problems than with body-first subtypes.

The other dissimilar factor is that Parkinson’s is often asymmetric in patients classified as brain-first. In this scenario, the alpha-synuclein disorder begins in the brain’s right or left hemisphere and spreads within that same hemisphere, creating motor symptoms that are one-sided.

When Brain-First Meets Body-First

However, when Parkinson’s progresses and alpha-synuclein moves into the other hemisphere of the brain and then throughout the body, body-first and brain-first subtypes will have similar non-motor and motor symptoms.

And Then There is the Connectome

The Connectome is defined as the physical wiring of an organism’s nervous system. It is known as neuronal connectivity and it allows for toxic protein spread.

Looking Forward

Dr. Borghammer summarized the study by saying that he believes Parkinson’s motor asymmetry should be viewed in terms of brain-first vs. body-first in order to produce a better understanding of the disease.

Dr. Borghammer acknowledges that the SOC model must now be studied further to find out if it is an improvement on previous models with respect to Parkinson’s development.

He also acknowledges that SOC does not completely describe the deficits in Parkinson’s disease and should be refined further.

Rose Duesterwald

Rose Duesterwald

Rose became acquainted with Patient Worthy after her husband was diagnosed with Acute Myeloid Leukemia (AML) six years ago. During this period of partial remission, Rose researched investigational drugs to be prepared in the event of a relapse. Her husband died February 12, 2021 with a rare and unexplained occurrence of liver cancer possibly unrelated to AML.

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