A case for chondroitinase?

 

Given that the condition is defined by the loss of specific types of neurons in the brain, any future therapy for Parkinson’s should include some form of restorative treatment. Much of the current clinical research exploring restoration in Parkinson’s is focused on cell transplantation – replacing the cells that have been lost in the brain.

But the adult brain is very different to the developing brain. While youngsters have lots of nurturing and supportive protein floating around – encouraging plasticity and survival – once we reach adulthood, our brains appear to be full of inhibitory molecules that reduce rejuvenation in the case of injury.

What if we could re-introduce some of those supportive factors and remove the inhibitory proteins? Could this help with restorative therapies for Parkinson’s?

In today’s post, we will look at new research exploring how we may be able to reduce some of those inhibitory factors and provide a more supportive environment for restorative therapy in Parkinson’s.

 


Source: restorativejustice

As we regularly state here on the SoPD, any ‘curative therapy’ for Parkinson’s is going to require three core components:

  1. A disease halting mechanism
  2. A neuroprotective agent
  3. Some form of restorative therapy

Now, the bad news is (as far as I am aware) there is no single treatment currently available (or being tested) that can do all three of these things. By this I mean that there is no disease halting mechanism therapy that can also replace lost brain cells. Nor is there a restorative therapy that stop the progression of the condition.

That statement can obviously be read as bad news, but it shouldn’t.

Let me explain:

A curative therapy for Parkinson’s is going to need to be personalised to each individual, with varying levels of each of the three component listed above. It will be a multi-modal approach designed for each individual’s needs.

Making things personal. Source: Flickr

By this I mean, there is a great deal of heterogeneity (or variability) between individuals with regards to their symptoms and the amount of time that they have had the condition. Some folks are more tremor dominant, while others do not experience tremor at all. Likewise, some individuals have only just been diagnosed, while others have lived with the condition for many years.

The treatment needs of each individual will be different, and thus what we will require is different amounts of the disease halting mechanism component, the neuroprotection component, and the restorative therapy components for each affected person.

In today’s post we are going to explore some alternative approaches being tested for restorative therapy.

What do you mean ‘alternative’?

Continue reading “A case for chondroitinase?”

The road ahead: 2020

Here at the SoPD, we are primarily interested in disease modification for Parkinson’s. While there is a great deal of interesting research exploring the causes of the condition, novel symptomatic therapies, and other aspects of Parkinson’s, my focus is generally on the science seeking to slow, stop or reverse the condition.

At the start of each year, it is a useful practise to layout what is planned and what we will be looking for over the next 12 months. Obviously, where 2020 will actually end is unpredictable, but an outline of what is scheduled over the next year will hopefully provide us with a useful resource for better managing expectations.

In this post, I will try to lay out some of what 2020 holds for us with regards to clinical research focused on disease modification for Parkinson’s.


BP

Lord Robert Baden-Powell. Source: Utahscouts

My old scout master once looked around our horse shoe, making eye contact with each of us, before asking the question:

“When did Noah build the ark?”

My fellow scouts and I looked at each other – confused. Did he want an exact date?!?

The scout master waited a moment for one of us to offer up some idiotic attempt at an answer – thankfully no one did – before he solemnly said:

“Before the rain”

It was one of those childhood moments that made little sense at the time, but comes back to haunt you as an adult when you are looking at what the future may hold and trying to plan for it.

# # # # # # # # # # #

Today’s post is our annual horizon scanning effort, where we lay out what is on the cards for the next 12 months with regards to clinical research focused on disease modification in Parkinson’s.

Source: Rand

We will also briefly mention other bits and pieces of preclinical work that we are keeping an eye on for any news of development.

To be clear, this post is NOT intended to be an exercise in the reading of tea leaves – no predictions will be made here. Nor is this a definitive or exhaustive guide of what the next year holds for disease modification research (if you see anything important that I have missed – please contact me). And it should certainly not be assumed that any of the treatments mentioned below are going to be silver bullets or magical elixirs that are going to “cure” the condition.

In the introduction to last year’s outlook, I wrote of the dangers of having expectations (Click here to read that post). I am not going to repeat that intro here, but that the same message applies as we look ahead to what 2020 holds.

Source: Unitystone

In fact, it probably applies even more for 2020, than it did for 2019.

2020 is going to be a busy year for Parkinson’s research, and I am genuinely concerned that posts like this are only going to raise expectations. My hope is that a better understanding of where things currently are and what is scheduled for the next 12 months will help in better managing those expectations. Please understand that there is still a long way to go for all of these experimental therapies.

All of that said, let’s begin:

Continue reading “The road ahead: 2020”