Fingolimod, a drug used in multiple sclerosis, prevents memory problems in HD mice. Would it work in patients?

By Melissa Christianson on November 24, 2015Edited by Dr Ed Wild

Thinking problems in Huntington’s disease take a huge toll from early in the disease. Now, new work suggests that a drug already approved by the FDA to treat another brain disease – multiple sclerosis – may stave off these problems in HD mice. Could these results be real, or are they too good to be true?

Although movement disturbances are the most obvious symptom of Huntington’s disease, Huntington’s also causes cognitive problems – like changes in memory, planning, decision-making, and communication – that take a huge toll on patients and their families early in the disease. Understanding why these cognitive changes arise and how we might prevent them is really important for treating Huntington’s.

In Huntington’s disease, thinking or ‘cognitive’ problems typically arise long before brain cells die. If these problems begin before brain cell death, though, what causes them?

One likely culprit is a change in how well brain cells communicate.

To understand this idea, remember that the brain is made up of a huge network of cells (called neurons) that talk to each other by passing messages back and forth. You can think of brain communication like a giant game of ‘telephone’: one neuron (brain cell) passes a message to another, which passes it to a third, and so on down the line. Because the brain has about 86 billion neurons, however, this game is huge beyond the scale of what you probably played as a kid.

Problems occur when messages in this giant game of telephone get garbled – in other words, when neurons don’t reliably hear or pass along the messages they receive.

This garbling can happen in a few different ways. First, messages can get garbled if a neuron gets sick. Just like it would be difficult for you to play telephone if you lost your voice, being sick makes it difficult for a neuron to pass messages to other neurons.

Alternatively, a neuron’s environment can influence how well it hears or passes along messages. Just like it would be harder to play telephone in a room full of screaming two-year-olds than in a quiet room, certain brain environments make it harder for neurons to communicate. For example, we know that neurons in the brain are surrounded by helper cells that have a bit of a split personality. These helper cells are normally ‘good guys’ that make communication easier; when the brain gets damaged by injury or disease, however, helper cells can become ‘bad guys’ that can interfere with brain communication.

So, to keep messages flowing through the brain’s giant game of telephone in Huntington’s disease, we may need to protect neurons, their helper cells, or both at the same time.

Wouldn’t it be nice if a drug that’s already in use, could protect both neurons and helper cells, and was already being used in humans?

One possible drug that fits the bill is fingolimod. It’s approved around the world for treating multiple sclerosis (MS). MS is a disease where excessive inflammation harms the brain.

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