Cognitive Changes in Parkinson's Disease: What You Need to Know
Learn how Parkinson's impacts cognitive function and early warning signs.
Daniel Weintraub, Anuprita R Nair, Ryan Kurth, Michael C. Brumm, Michele K. York, Roseanne Dobkin, Kenneth Marek, Caroline Tanner, Tanya Simuni, Andrew Siderowf, Douglas Galasko, Lana M. Chahine, Christopher Coffey, Kalpana Merchant, Kathleen L. Poston, Tatiana Foroud, Brit Mollenhauer, Ethan G. Brown, Karl Kieburtz, Mark Frasier, Todd Sherer, Sohini Chowdhury, Roy N. Alcalay, Aleksandar Videnovic
― 7 min read
Table of Contents
- Early Signs of Cognitive Changes
- What is Neuronal Alpha-Synuclein Disease?
- The Importance of Cognitive Assessment
- Enrollment in Studies
- How the Stages Work
- Cognitive Scores Among Groups
- The Impact of iRBD
- Dopaminergic Dysfunction and Cognition
- Why Does This Matter?
- Strengths and Limitations of Research
- Conclusion
- Original Source
- Reference Links
Parkinson’s disease (PD) is not just about shaking hands and shuffling feet. It can also mess with your mind. Many people with Parkinson’s experience cognitive issues over time, with studies showing that up to 80% of patients could develop dementia later on. Even those who are newly diagnosed or in the early stages often face mild cognitive impairment. These cognitive changes can show up earlier than people expect, sometimes even before the classic motor symptoms emerge.
Early Signs of Cognitive Changes
Before we get to the nitty-gritty of cognitive decline in Parkinson’s, let’s talk about some early warning signs. Two key prodromal symptoms linked to Parkinson's are hyposmia (fancy talk for a reduced sense of smell) and isolated REM sleep behavior disorder (iRBD), where folks act out their dreams. Studies indicate that people with these conditions might already be experiencing subtle changes in their thinking skills.
In fact, researchers found both global and specific cognitive deficits in individuals who had both hyposmia and iRBD. That’s like your brain giving you a wink before the real problems start.
What is Neuronal Alpha-Synuclein Disease?
Let’s get a bit technical here, but don’t worry—I’ll keep it simple. Researchers have proposed a way to classify Parkinson’s and related issues based on a biological marker known as neuronal α-synuclein. Think of this marker as a flag that raises when something isn’t quite right in the brain. The presence of pathological α-synuclein signals the beginning of what we call neuronal α-synuclein disease (NSD). This disease has stages that depend not only on the presence of these markers but also on how well a person is functioning in terms of their motor and cognitive skills.
According to this classification, Stage 2 is when you might have some subtle signs—like changes in smell or early cognitive issues—but you’re not yet showing significant functional impairments. Imagine that as being in a minor league for brain problems, where the game isn’t too serious yet but you can still see the cracks.
The Importance of Cognitive Assessment
In research studies, scientists need reliable ways to assess cognitive problems. A Cognitive Summary Score (CSS) can be useful as it combines results from several cognitive tests into a single score. This is like taking a report card for all your classes instead of checking each subject one by one.
Using this method, researchers have documented changes in cognition among those at risk for Parkinson’s and those newly diagnosed. This research looks to see how the cognitive abilities of these individuals compare to healthy people and if early signs of PD, like hyposmia, can lead to worse cognitive performance.
Enrollment in Studies
In studies looking at cognition in Parkinson’s, participants are carefully selected based on their health status. People who have early signs of PD, like hyposmia or iRBD, may be enrolled if they meet certain criteria, such as having motor symptoms or being free of dementia. Healthy controls (HCs), on the other hand, are individuals without any significant neurological issues and who score well on cognitive assessments.
A notable aspect is that some participants are categorized based on the presence of α-synuclein, which gives researchers more clarity about the connection between early symptoms and cognitive decline.
How the Stages Work
Participants are classified into different stages of NSD based on whether they have signs like hyposmia and whether they show any dopaminergic dysfunction (which means issues with dopamine-producing neurons).
- Stage 2A is when someone has hyposmia but no clear signs of dopamine neuron issues. They are still functioning decently.
- Stage 2B is when there’s evidence of dopamine neuron problems along with hyposmia, indicating a greater risk for cognitive decline.
Researchers are keen to understand how having these stages impacts cognitive performance and whether the presence of other symptoms like iRBD worsens cognitive issues.
Cognitive Scores Among Groups
In general, cognitive performance tends to decrease as conditions worsen. For example, both Stage 2A and Stage 2B participants scored lower on cognitive tests compared to healthy controls. This is not just a surprising twist, as we already expect groups facing challenges to perform differently.
However, the scores reveal something interesting. While the scores for Stage 2 participants (with subtle signs) are lower, they still manage to exceed certain cutoffs. This indicates that there is still some cognitive function left intact, although it might feel like running with a flat tire.
The Impact of iRBD
When you throw iRBD into the mix, the cognitive problems get a little more pronounced. It has been found that individuals with both hyposmia and iRBD show increased cognitive deficits compared to those with hyposmia alone. This suggests that iRBD could be the villain in this story of cognitive decline, making things worse as it comes into play.
The results indicate that those with hyposmia alone tend to maintain normal cognitive function, at least for a while. But once iRBD is involved, the cognitive decline becomes measurable and significant.
Dopaminergic Dysfunction and Cognition
When looking specifically at participants who have Stage 2B, meaning they exhibit dopaminergic dysfunction, the impact of hyposmia alone reveals itself in noticeable cognitive issues. Those with both hyposmia and iRBD present even greater cognitive deficits, indicating that when these symptoms stack up, they can take a toll on cognitive performance.
This leads us to think that dopamine isn’t just a chemical that helps with movement; it also plays a role in how we think. The brain is a complex system, after all, and the connections between different conditions reflect that complexity.
Why Does This Matter?
Understanding how these conditions interact and impact cognitive functions can drive future research and clinical practices. Recognizing the importance of cognition in Parkinson’s, especially in early stages, can assist in developing better treatment options and trials aimed at preventing or managing cognitive decline.
For patients and their families, this research can help establish expectations for what might come next. If you know someone with Parkinson’s, explaining that cognitive changes could be on the horizon might help them prepare for what’s to come.
Strengths and Limitations of Research
The studies conducted have a lot of strong points, such as focusing on clear early symptoms (like hyposmia and iRBD) and involving a broad group of participants. The use of reliable cognitive measures helps researchers determine how cognitive performance shifts across different stages of PD.
However, there are limitations as well. For example, the sample size of participants with iRBD without hyposmia was not large enough to draw strong conclusions. Also, the focus on just one aspect of cognitive health might overlook other factors contributing to cognitive decline.
Conclusion
In summary, the relationship between Parkinson’s disease and cognitive impairment is complex and multilayered. Early signs, such as hyposmia and iRBD, play a significant role in affecting cognitive function, especially when combined with dopamine-related issues.
The findings from these studies highlight the need for continuous evaluation of cognitive abilities in patients with Parkinson's. By understanding and addressing these early cognitive changes, people with the disease may be better equipped to manage their conditions and maintain quality of life.
So, whether it's making a joke about forgetting where you put your keys or being a little shaky in your head, it's clear that keeping an eye on cognitive function is just as important as looking at physical symptoms in the world of Parkinson’s disease. And who knows? Maybe one day, we’ll find a way to keep our brains running smoothly—just like a well-oiled machine.
Original Source
Title: Impact of dopamine deficiency and REM sleep behavior disorder on cognition in early neuronal synuclein disease with hyposmia
Abstract: ObjectivesTo determine the impact of dopamine deficiency and isolated REM sleep behavior disorder (iRBD) on cognitive performance in early neuronal alpha-synuclein disease (NSD) with hyposmia. MethodsUsing Parkinsons Progression Markers Initiative baseline data, cognitive performance was assessed with a cognitive summary score (CSS) developed by applying regression-based internal norms derived from a robust healthy control (HC) group. Performance was examined for participants with hyposmia classified as NSD-Integrated Staging System (NSD-ISS) Stage 2, either Stage 2A (CSF alpha-synuclein seed amplification assay [SAA]+, SPECT dopamine transporter scan [DaTscan]-) or 2B (SAA+, DaTscan+). ResultsParticipants were Stage 2A (N=101), Stage 2B (N=227) and HCs (N=158). Although Stage 2 overall had intact Montreal Cognitive Assessment scores (mean (SD) =27.0 (2.3)), Stage 2A had a numerically worse CSS (z-score mean difference =0.05, p-value NS; effect size=0.09) and Stage 2B had a statistically worse CSS (z-score mean difference =0.23, p-value
Authors: Daniel Weintraub, Anuprita R Nair, Ryan Kurth, Michael C. Brumm, Michele K. York, Roseanne Dobkin, Kenneth Marek, Caroline Tanner, Tanya Simuni, Andrew Siderowf, Douglas Galasko, Lana M. Chahine, Christopher Coffey, Kalpana Merchant, Kathleen L. Poston, Tatiana Foroud, Brit Mollenhauer, Ethan G. Brown, Karl Kieburtz, Mark Frasier, Todd Sherer, Sohini Chowdhury, Roy N. Alcalay, Aleksandar Videnovic
Last Update: 2024-12-13 00:00:00
Language: English
Source URL: https://www.medrxiv.org/content/10.1101/2024.12.12.24318917
Source PDF: https://www.medrxiv.org/content/10.1101/2024.12.12.24318917.full.pdf
Licence: https://creativecommons.org/licenses/by/4.0/
Changes: This summary was created with assistance from AI and may have inaccuracies. For accurate information, please refer to the original source documents linked here.
Thank you to medrxiv for use of its open access interoperability.