WPC 2026 Update: The Current State of the Science - Why Everyone Is Talking About Alpha-Synuclein?

What alpha-synuclein is, why it matters, how it may spread through the nervous system, and why researchers believe it could hold the key to earlier diagnosis and new treatments.

If there was one scientific topic that seemed to appear in almost every lecture I attended at the World Parkinson Congress, it was alpha-synuclein.

Researchers discussed it in sessions on genetics. They discussed it in sessions on biomarkers. They discussed it in sessions on disease-modifying therapies, early diagnosis, neuroinflammation, and precision medicine.

In many ways, alpha-synuclein has become the center of modern Parkinson's disease research.

But what exactly is it, and why is everyone so interested in it?

The answer is both fascinating and surprisingly complicated.

First, What Is Alpha-Synuclein?

Alpha-synuclein is a protein that naturally exists in the brain and nervous system. In fact, it is one of the most abundant proteins found in neurons.

For many years, scientists didn't fully understand what it did. We now know that alpha-synuclein plays important roles in communication between nerve cells.

Specifically, it helps regulate the release and recycling of neurotransmitters—the chemical messengers that allow one nerve cell to communicate with another.

You can think of alpha-synuclein as one of the many workers helping to keep communication flowing smoothly at the synapse, the tiny gap where neurons exchange information.

In a healthy brain, alpha-synuclein appears to help organize synaptic activity, support dopamine signaling, and maintain efficient communication between neurons.

In other words, alpha-synuclein is not inherently "bad." It is a normal and important part of brain function.

What Happens in Parkinson's Disease?

The problem begins when alpha-synuclein changes shape.

Proteins must fold into specific three-dimensional structures to function properly. In Parkinson's disease, alpha-synuclein can misfold and begin sticking to other alpha-synuclein proteins.

Over time, these misfolded proteins clump together and form aggregates.

Eventually, these aggregates contribute to the formation of Lewy bodies—the abnormal protein deposits that are considered one of the hallmark pathological features of Parkinson's disease.

Researchers believe these protein clumps interfere with normal cellular function in several ways.

They may disrupt communication between neurons, interfere with cellular waste disposal systems, impair mitochondrial function, trigger inflammation, and contribute to eventual neuronal death.

Importantly, alpha-synuclein aggregation doesn't appear to affect only dopamine-producing neurons. It has been found throughout multiple regions of the nervous system, helping explain why Parkinson's disease involves much more than tremor and movement symptoms.

Does Alpha-Synuclein Spread?

One of the most intriguing theories discussed at the conference was the idea that alpha-synuclein may spread through the nervous system in a "prion-like" manner.

Prions are abnormal proteins capable of causing other proteins to misfold.

Researchers now believe misfolded alpha-synuclein may behave somewhat similarly.

The theory suggests that once one alpha-synuclein protein misfolds, it may encourage neighboring proteins to misfold as well. Those proteins may then spread to nearby cells and continue the process.

Over many years, this could potentially explain how pathology progresses through different regions of the nervous system.

While the exact mechanisms remain under investigation, growing evidence supports the idea that alpha-synuclein may move from cell to cell and contribute to the spread of disease.

Could Parkinson's Begin Outside the Brain?

This is where things become especially interesting.

Researchers are increasingly exploring the possibility that Parkinson's disease may not always begin in the brain itself.

Alpha-synuclein aggregates have been identified in the:

• Gut

• Enteric nervous system

• Salivary glands

• Skin

• Olfactory system

• Autonomic nervous system

Some researchers now propose that, in certain individuals, alpha-synuclein pathology may begin in the body and gradually spread toward the brain.

This concept is often referred to as the "body-first" hypothesis.

Others appear to follow a "brain-first" pattern, where pathology begins centrally and later spreads outward.

One of the major themes at WPC was that Parkinson's disease may not follow a single pathway for every individual.

Understanding these differences may eventually help explain why people experience different symptoms, progress at different rates, and respond differently to treatment.

Why Alpha-Synuclein Matters for Earlier Diagnosis

One of the biggest challenges in Parkinson's disease is that diagnosis typically occurs after substantial damage has already taken place.

Many researchers estimate that symptoms may not appear until roughly half of dopamine-producing neurons have already been lost.

This means biological changes may be occurring for years—or even decades—before diagnosis.

Because alpha-synuclein appears so early in the disease process, researchers are working intensely to develop tests capable of detecting abnormal alpha-synuclein before significant symptoms emerge.

This is where one of the most exciting developments in Parkinson's research comes in.

Seed Amplification Assays: A Potential Game Changer

Several lectures focused on a technology called a Seed Amplification Assay (SAA).

Rather than simply measuring how much alpha-synuclein is present, these tests look for whether alpha-synuclein behaves abnormally and can "seed" further aggregation.

Think of it as the difference between counting the number of people in a room versus identifying who is actively causing trouble.

Current seed amplification assays can detect abnormal alpha-synuclein in:

• Cerebrospinal fluid (CSF)

• Skin biopsy samples

Researchers are now working aggressively to develop reliable blood-based testing.

If successful, blood testing could dramatically improve screening, diagnosis, disease staging, and clinical trial recruitment.

Many speakers described blood-based alpha-synuclein testing as one of the major goals of the next decade.

But Here's the Controversy

As exciting as alpha-synuclein research has become, it is not without debate.

One of the most interesting discussions at WPC centered around a fundamental question:

Is alpha-synuclein actually causing Parkinson's disease, or is it simply a marker of broader neurodegenerative processes?

This question remains unresolved.

Researchers discussed several observations that complicate the picture:

Some individuals have positive alpha-synuclein seed amplification assays but do not have Parkinson's disease.

Some individuals with Parkinson's disease have negative alpha-synuclein testing.

Some people accumulate substantial alpha-synuclein pathology without developing symptoms.

Others develop symptoms with relatively modest pathology.

These findings suggest alpha-synuclein may be only one piece of a much larger biological puzzle.

Many researchers now believe Parkinson's disease likely results from interactions among multiple biological processes, including:

• Alpha-synuclein aggregation

• Dopamine neuron loss

• Mitochondrial dysfunction

• Neuroinflammation

• Genetic susceptibility

• Environmental influences

In other words, alpha-synuclein may be critically important without necessarily being the entire story.

What About Alpha-Synuclein Medications?

If alpha-synuclein is involved in Parkinson's disease, can we target it therapeutically?

Researchers are certainly trying.

Several strategies are currently under investigation:

• Preventing alpha-synuclein aggregation

• Breaking apart existing aggregates

• Enhancing clearance of abnormal protein

• Blocking cell-to-cell spread

• Reducing alpha-synuclein production

One of the most widely discussed therapies is Prasinezumab, an antibody designed to bind alpha-synuclein and potentially reduce its spread.

While early trials did not meet their primary endpoints, some long-term analyses suggested participants receiving the medication may have progressed more slowly over time.

This has kept the field interested and ongoing studies continue.

Importantly, many speakers reminded attendees that early trial failures are common in medicine.

In fact, several medications we now consider standard therapies initially failed early studies before later becoming successful treatments.

Research rarely moves in a straight line.

The Bigger Picture

The most important takeaway from the World Parkinson Congress wasn't that alpha-synuclein is the answer to Parkinson's disease.

It was that alpha-synuclein has become one of the most powerful tools we currently have for understanding Parkinson's disease.

Whether it ultimately proves to be the primary driver of disease, one contributor among many, or simply a valuable biomarker, it is helping researchers answer some of the biggest questions in the field.

How does Parkinson's disease begin?

Can we diagnose it earlier?

Can we identify different biological subtypes?

Can we target disease before significant neurodegeneration occurs?

And can we finally develop therapies that do more than simply treat symptoms?

Those questions remain unanswered.

But after listening to researchers from around the world discuss alpha-synuclein from every possible angle, one thing became clear:

The future of Parkinson's disease research—and perhaps the future of Parkinson's treatment—is becoming increasingly biological, increasingly personalized, and increasingly focused on understanding the role of proteins like alpha-synuclein long before symptoms ever begin.

Part 3: Is Parkinson's Genetic?

A look at the genes most strongly linked to Parkinson's disease—including LRRK2, GBA1, PINK1, and Parkin—and how genetics is driving a new era of targeted therapies.

WPC 2026 Update: The Current State of the Science - Parkinson's Research is Changing Faster Than Most People Realize

One of the biggest things I took away from the World Parkinson Congress wasn't a single study, a new medication, or a groundbreaking announcement.

It was finally understanding how all the pieces of Parkinson's research are starting to connect together.

One of the beautiful things about spending four days immersed in Parkinson's science is that you hear the same concepts repeated from different perspectives. Neurologists, neuroscientists, geneticists, rehabilitation specialists, and pharmaceutical researchers may all speak different scientific languages, but by the end of the week clear themes begin to emerge.

The biggest theme I heard over and over again was this:

Parkinson's research is rapidly moving toward earlier diagnosis, more accurate biological classification, and ultimately precision medicine.

For decades, Parkinson's disease was largely viewed as a dopamine disorder. And while the loss of dopamine-producing neurons remains central to the disease, researchers now recognize that Parkinson's is far more biologically complex than we once thought.

Across lecture after lecture, four major biological processes repeatedly emerged as key players in Parkinson's disease:

• Loss of dopamine-producing neurons
• Alpha-synuclein aggregation (Lewy body formation)
• Mitochondrial dysfunction
• Neuroinflammation

These processes do not occur independently. They interact with one another in ways we are only beginning to understand.

Even more importantly, researchers increasingly believe these biological changes may begin years—perhaps even decades—before the first tremor, shuffling gait, or diagnosis.

Many experts now estimate that a person may lose 50% or more of their dopamine-producing neurons before classic motor symptoms become noticeable. If true, Parkinson's disease may already be well underway 10–20 years before diagnosis.

This realization is changing everything.

The goal is no longer simply diagnosing Parkinson's disease after symptoms appear. The goal is identifying it earlier, understanding which biological pathways are driving disease in each individual, and eventually matching people with therapies designed for their specific disease subtype.

In other words, the future of Parkinson's care may not be one treatment for everyone. It may be the right treatment for the right person at the right stage of disease.

And that future may be closer than many people realize.

What's Next in This Series

This article is the first in a series exploring the major themes that emerged from the World Parkinson Congress and the rapidly evolving landscape of Parkinson's research.

Below, I'll take a deeper dive into some of the most important topics shaping the future of diagnosis, treatment, and ultimately disease modification. You can click each link to read the next section.

Part 2: Why Everyone Is Talking About Alpha-Synuclein

What alpha-synuclein is, why it matters, how it may spread through the nervous system, and why researchers believe it could hold the key to earlier diagnosis and new treatments.

Part 3: Is Parkinson's Genetic?

A look at the genes most strongly linked to Parkinson's disease—including LRRK2, GBA1, PINK1, and Parkin—and how genetics is driving a new era of targeted therapies.

Part 4: The New Way We Classify Parkinson's Disease

Why researchers are moving beyond symptom-based diagnosis toward biological staging systems, disease subtypes, and precision medicine.

Part 5: The Race Toward Disease-Modifying Therapies

An overview of the most promising approaches currently being tested, including alpha-synuclein therapies, LRRK2 inhibitors, anti-inflammatory treatments, mitochondrial therapies, and innovative platform trials.

Part 6: Are We Getting Closer to a Cure?

Exploring stem cells, regenerative medicine, cell replacement therapies, and the realistic possibilities—and limitations—of future curative treatments.

In Summary

The more I listened to researchers, clinicians, and people living with Parkinson's throughout the Congress, the more one thing became clear: we are entering a new chapter in Parkinson's research.

Many questions remain unanswered, and progress is rarely as fast as any of us would like. But for the first time, researchers have the tools to identify biological changes earlier, classify disease more precisely, and test therapies designed to target the underlying mechanisms of Parkinson's itself.

That's a very different place than we were even a decade ago.

And it's why there is more reason for cautious optimism today than at any point to date in the journey to better understand this complex disease.

World Parkinson’s Congress 2026: Bringing it Home

Written by: Dr. Katie Wadland, PT, DPT, Board-Certified Geriatric Clinical Specialist and Owner of Healthy Aging Physical Therapy

This summer, I’m excited to share a three-part blog series inspired by my experience attending the 7th Annual World Parkinson’s Congress. Over four days surrounded by researchers, clinicians, people living with Parkinson’s, care partners, advocates, and innovators from around the world, I filled pages and pages with notes, ideas, questions, and moments that challenged the way I think about Parkinson’s disease, rehabilitation, exercise, behavior change, and what it truly means to help people live well.

One of the most powerful parts of the conference was realizing how rapidly our understanding of Parkinson’s continues to evolve. The themes repeated throughout the week were impossible to ignore: Parkinson’s is far more complex than simply a ‘dopamine disorder’, exercise remains one of the most powerful disease-modifying tools we currently have, and long-term success depends just as much on behavior, motivation, environment, and support as it does on medications or treatment techniques.

Rather than trying to summarize an entire conference in one overwhelming post, I wanted to slow down, digest the information, and share it in a way that feels meaningful and practical — both for people living with Parkinson’s and for the clinicians and care partners supporting them.

Over the next three months, I’ll be sharing some of my biggest takeaways from the conference:

• In June, I’ll be sharing updates on The Current State of the Science of Parkinson’s — breaking down some of the most exciting and rapidly evolving research presented at the conference. We’ll explore topics like biomarkers, alpha-synuclein, neuroinflammation, gut health, exercise science, early detection, and the growing pursuit of disease-modifying treatments — along with what these discoveries may mean for the future of Parkinson’s care.

  In July, we’ll shift into Lifestyle Medicine in Parkinson’s — diving into what the evidence says about the things we CAN do right now to influence health, function, and quality of life. I’ll be exploring the research behind exercise, balance and gait training, cognitive rehabilitation, nutrition, sleep, stress management, and other lifestyle strategies that are increasingly recognized as essential components of Parkinson’s management.

  And finally, in August, we’ll focus on Making it Stick — the real-world challenge of turning recommendations into sustainable habits and habits into long-term lifestyle change. We’ll explore topics like apathy, motivation, and managing symptom fluctuation — some of the most common barriers people with Parkinson’s face when trying to consistently implement the things we know are helpful — and how science-based approaches to behavior change can help us “reverse engineer” lifestyle changes by creating systems, routines, environments, and supports that make healthy choices more realistic, sustainable, and achievable in everyday life.

My goal with this series is not just to “report back” from a conference, but to help translate complex science into real-world understanding and practical takeaways that can improve care, conversations, and quality of life.

I learned so much at WPC — and now I’m excited to bring it home to you.

From Diagnosis to Late Stage Parkinson’s Disease: How Therapy for Parkinson’s Changes Over Time

By: Dr. Katie Wadland, PT, DPT, Board-Certified Geriatric Clinical Specialist and Owner of Healthy Aging Physical Therapy

Parkinson’s disease is a progressive neurological condition that affects movement, balance, coordination, and overall function. While it is considered “progressive,” it’s important to recognize that this progression often occurs gradually—over many years, and in some cases, decades.

At Healthy Aging Physical Therapy, we understand that as the disease evolves, therapy should evolve with it. Our goal is to help our patients with Parkinson’s stay active, healthy, and safe at every stage of their journey.

In this blog, we’ll walk through the different stages of Parkinson’s disease and how therapy goals and approaches change over time to best support those evolving needs.

How Do We Define the Stages of Parkinson’s?

Clinically, Parkinson’s is often categorized using the Hoehn and Yahr Scale, which ranges from mild symptoms on one side of the body to more advanced mobility limitations.

In Stage 1, symptoms are mild and typically affect only one side of the body, often without significant impact on daily function.
In Stage 2, symptoms become more noticeable on both sides of the body, but balance is still largely intact and individuals remain independent.
In Stage 3, balance begins to decline, and fall risk increases, though individuals are usually still able to walk and perform many daily activities independently.
In Stage 4, symptoms are more advanced, and assistance is often needed for mobility and daily tasks.
In Stage 5, individuals may require a wheelchair or significant assistance with mobility and self-care.

But in real life, what matters most isn’t the number - it’s how symptoms are impacting daily movement and function. For that reason, we often think more practically in terms of early, middle, and later stages, with therapy evolving alongside those changes.

Early Stage Parkinson’s: Building the Foundation

In the early stages of Parkinson’s, changes are often subtle. Someone may notice a slight shift in posture, a reduced arm swing on one side, or that movements feel smaller or slower than they used to. Many people are still fully independent and may not feel like they “need” therapy yet.

In reality, there are some incredibly powerful things you can do early on that can help slow the progression of the disease and set you up to live well with Parkinson’s long-term—and therapy plays a key role in that education and guidance.

The focus during this stage is on building a strong foundation through exercise and movement awareness. Establishing a regular walking program is often one of the first steps, and this is something that should become part of your daily routine. Aerobic exercise is especially important, with the goal of gradually building up to 150–300 minutes per week of moderately intense activity. This level of exercise has some of the strongest evidence behind it as an effective way to help slow the progression of symptoms while also supporting overall health.

Strength training is another essential component, ideally performed two to three times per week. While strength training is important for all adults, it becomes even more critical for someone with a neuromuscular condition like Parkinson’s, where maintaining strength is key to preserving function and independence. Working with a physical or occupational therapist can help identify subtle asymmetries or early impairments—such as reduced shoulder mobility, postural changes, or decreased trunk rotation—that may not yet be limiting, but can become more impactful over time if not addressed. The benefit is that these findings can often be seamlessly incorporated into a well-rounded weekly routine that includes strength, mobility, and flexibility work.

This is also the stage when individuals are introduced to amplitude-based exercise programs, such as BIG, LOUD, or PWR! Moves. These programs focus on training larger, more intentional movements and are especially effective in Parkinson’s because they help counteract the tendency toward smaller, slower movement patterns. Starting these programs early—and continuing them consistently over time—can play a major role in maintaining your ability to move well.

At this stage, the overall goal is simple but powerful: use exercise strategically to stay ahead of the disease, rather than reacting to it later.

Middle Stage Parkinson’s: Maintaining Independence and Preventing Falls

As Parkinson’s progresses, changes become more noticeable and begin to impact daily life. Balance may feel less steady, walking may become more effortful, and challenges like freezing of gait—especially during turning or in tight spaces—can start to appear. This is often the stage when individuals first seek therapy after a fall or a noticeable decline.

At this point, the goal shifts from building capacity to maintaining independence and reducing risk.

Exercise remains a critically important part of disease management. Continuing a regular walking program is essential, though some individuals may benefit from introducing an assistive device to improve safety and efficiency. Aerobic exercise is still recommended in the 150–300 minutes per week range, but there is often a shift toward lower-risk options—such as a recumbent bike, elliptical, or NuStep—to allow for safer and more sustainable participation.

Strength training continues to play a key role, but therapy becomes more individualized and problem-focused. A physical or occupational therapist can develop a personalized balance program, address changes in gait, and help with fine motor challenges and difficulties with self-care and daily activities. Therapy at this stage also becomes increasingly focused on teaching you how to work with your body instead of against it. Simple but powerful strategies—like using external cues to improve walking—can make the difference between staying active and gradually reducing activity levels, which is something we work hard to prevent.

This is also the stage where new skills become essential—learning how to safely get up from the floor, how to manage freezing episodes, and how to navigate more complex movement challenges in daily life.

In addition, care often expands to include a broader team. Physical therapy, occupational therapy, and speech therapy may all play a role in addressing Parkinson’s-related changes, from rigidity and dyskinesia to fine motor challenges, voice changes, and swallowing difficulties.

Throughout all of this, amplitude-based programs like PWR! continue to serve as an important anchor, helping reinforce movement quality, confidence, and consistency.

At this stage, therapy becomes more about adapting, problem-solving, and preserving independence for as long as possible.

Later Stage Parkinson’s: Supporting Safety, Comfort, and Quality of Life

In the later stages of Parkinson’s, mobility becomes more limited and individuals often require increased support. Walking may become more difficult or less consistent, and caregivers frequently take on a larger role in daily care.

Even at this stage, therapy remains incredibly valuable—but the focus shifts again.

The goal is no longer just independence, but rather maximizing safety, comfort, and quality of life.

Movement is still encouraged, including walking as able, but often with modifications such as updated assistive devices or the introduction of wheeled mobility to improve safety and reduce fatigue. Aerobic activity remains important, though it is typically adapted to lower-risk formats that allow for continued participation without unnecessary strain.

Strength training continues as well, but often becomes more functional in nature—focusing on tasks like sit-to-stands, bed mobility, and transfers rather than traditional exercise formats.

A significant component of therapy at this stage involves supporting the environment and the caregiving team. This may include home modifications, equipment recommendations, and hands-on caregiver training to ensure safety with mobility and daily tasks.

Therapists also play a key role in minimizing secondary complications, such as contractures, skin breakdown, pain, and aspiration risk, while helping individuals maintain as much comfort and dignity as possible.

Even here, amplitude-based movement strategies can still be incorporated in a modified way to support engagement and movement quality.

At this stage, therapy is deeply focused on support, preservation, and quality of life—for both the individual and their caregivers.

The Common Thread Across Every Stage

While the goals of therapy evolve, a few principles remain constant.

Exercise continues to be one of the most powerful tools we have. Consistency matters. And perhaps most importantly, earlier and ongoing intervention leads to better outcomes.

Too often, therapy is only introduced after a fall or a hospitalization. But Parkinson’s is a lifelong condition—and care should evolve along with it, not stop and start during times of crisis.

Parkinsonisms: What Parkinson’s Is… and What It Isn’t

Written by: Dr. Katie Wadland, PT, DPT, Board-Certified Geriatric Clinical Specialist, Owner of Healthy Aging PT

When most people hear “Parkinson’s disease,” they picture a very specific condition—and for many, that’s accurate. But in our work at Healthy Aging Physical Therapy, we often meet patients whose symptoms look like Parkinson’s… but don’t quite follow the same rules.

These are called Atypical Parkinsonism syndromes, or simply Parkinsonisms.

As a Parkinson’s specialty practice, we’ve had the unique opportunity to work closely with individuals living with conditions like Lewy Body Dementia (LBD), Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA) and Corticobasilar Degernation (CBD). These diagnoses are less common - but incredibly important to recognize, as while there is overlap with Parkinson’s disease, the rehabilitation approach must be thoughtfully adapted for each condition.

Let’s break it down.

What Are “Parkinsonisms”?

“Parkinsonism” is a term used to describe a group of neurological conditions that share key movement features seen in Parkinson’s disease, such as:

• Slowness of movement (bradykinesia)

• Stiffness (rigidity)

• Balance and gait difficulties

However, these conditions have different underlying causes, faster progression, and often respond differently (or poorly) to typical Parkinson’s medications like levodopa.

How Are Parkinsonisms Diagnosed?

Diagnosis can be challenging and often evolves over time. Often, someone is initially diagnosed with Parkinson’s Disease, but when symptom progression is different than expected, or the individual does not respond to medications as expected, an atypical form may be suspected. Other signs might include:

• Early balance impairment or falls

• Cognitive or autonomic changes early in the disease course

• Eye movement abnormalities (especially in PSP)

• Imaging and neurological exam findings

In many cases, diagnosis is clinical and may take time, as symptoms unfold and patterns become clearer. Fortunately, we now have more concrete ways to differentiate between the different syndromes including DAT Scans and Skin Biopsies:

• DAT Scans: A DaTscan is a specialized imaging test that looks at dopamine activity in the brain. By looking at the patterns, doctors can now better identify if symptoms are coming from a neurodegenerative cause, like Parkinson’s Disease or an Atypical Parkinson’s Syndrome, or from something else, like Essential Tremor or drug-induced symptoms. It is important to be aware a DAT Scan can NOT differentiate between idiopathic Parkinson’s and Atypical Parkinson’s Disease.

• Skin Biopsies: A skin biopsy can be taken and analyzed for abnormal alpha-synuculein deposits. When these are identified in the sample, it can help differentiate between the idiopathic form of Parkinson’s and some of the atypical forms of the disease. It is important to note that while it can differentiate the two from one another, it can NOT identify which Atypical Parkinson’s disease a person may have.

As you can see, while we have many more tools at our disposal for proper diagnosis of Parkinson’s Disease and Atypical Parkinsonisms, it still remains a largely clinical diagnosis based on symptoms, progression of disease and response to medication treatment.

What are the Different Atypical Parkinson’s Diseases?

1. Lewy body Dementia (LBD)

   Lewy Body Dementia is a neurodegenerative condition characterized by a combination of:

   • Cognitive impairment

   • Parkinsonian motor symptoms

   • Fluctuations in alertness

   • Visual hallucinations

   What Makes It Different Than Parkinson’s?

   • Cognition is affected early, often before or alongside movement symptoms

   • Fluctuating attention and alertness (good days and bad days are common - and presentation may even within throughout the day)

   • Visual hallucinations are common

   • Patients may be sensitive to certain medications

   How Is Rehab Different?

   Rehabilitation for LBD requires a flexible, patient-centered approach:

   • Session-to-session variability is expected. Therapists must be prepared to adjust treatments, as needed, in real time.

   • Patients do best when care is focused on routine, familiarity, and caregiver involvement.

   • Due to the cognitive challenges, communication should be clear, calm and simple.

   • Balance and mobility training are still essential, but, patients may may need shorter sessions or breaks and should focus should focus more on compensatory strategies as it will be harder for patients to carryover instructions from session to session.

2. Progressive Supranuclear Palsy (PSP)

   PSP is a neurodegenerative condition that affects:

   • Balance and walking

   • Eye movements (especially looking down)

   • Postural control (and most notably, results in retropulsion, or the sensation of falling backwards)

   • Spinal mobility (rigidity is a marked feature in people with PSP)

   What Makes It Different Than Parkinson’s?

   • Early and frequent falls, often backward

   • Difficulty with vertical eye movements, especially downward gaze

   • Speech and swallowing issues tend to appear earlier

   • Minimal response to Parkinson’s medications

   • Axial rigidity (stiffness in the trunk more than limbs)

   How Is Rehab Different?

   Rehabilitation for PSP is very focused on safety and proactive management of symptoms:

   • Fall prevention is a #1 priority. This often involves prescribing an appropriate assistive device (we love the USTEP for our patients with PSP!), making changes to the home to make it safer and making recommendations for adequate supervision and teaching caregivers the skills they need to help their loved one move safely.

   • Therapists should assess and treat ocular coordination impairments. When patients can’t look down well, this impacts depth perception and fields of vision, making things like using stairs, curbs and navigating uneven terrain more difficult. People with PSP benefit from working on compensatory skills like visual scanning, and also on using visual exercises to maintain the ocular control they have.

   • Because of the areas impacted by PSP, people with PSP will have a more difficult time improving balance reactions and walking. They frequently do better with use of external cuing, like using targets on the floor or a laser, or by putting signs up throughout the home to remind them to use safe strategies like pushing off the chair to stand up, or holding on to a surface for support before reaching for something.

   • It is critical for someone with PSP to get therapy early! Progression of PSP is faster than in typical Parkinson’s Disease and the earlier we can address emerging changes and new symptoms, the more impact we can have on safety and quality of life.

3. Multiple Systems Atrophy (MSA)

   MSA is a progressive neurological condition that affects:

   • Movement (Parkinsonian features)

   • Posture (more rounded, head-down positions)

   • Autonomic Nervous System (causing changes in blood pressure, bladder control and breathing)

   What Makes It Different Than Parkinson’s?

   • Significant autonomic dysfunction causing frequent low blood pressure and syncope (passing out)

   • Bowel and bladder dysfunction is more common

   • Progression is faster than in typical Parkinson’s Disease

   • Minimal response to Parkinson’s medications

   • May also include cerebellar features like coordination issues

   How Is Rehab Different?

   Rehabilitation for MSA is requires careful monitoring and management of blood pressure in particular:

   • Vital sign monitoring should be completed before and during sessions and sessions may need to be modified to keep blood pressure in safe ranges.

   • Education should focus on strategies to maintain blood pressure in safe ranges throughout the day. This often requires a combination of medication management and coordination with doctors, and education for the patient and caregivers for using things like compression stockings or abdominal binders to help keep blood pressure high enough when they stand up.

   • Because orthostatic hypotension is common in MSA (drops in blood pressure with standing), it is important to include a seated warm up and slow progression to standing and walking activities during sessions.

   • Hydration is critical for patients with MSA. Being dehydrated will make the autonomic dysregulation worse and is a frequent cause of falls and hospitalizations for these patients.

4. Corticobasilar Degeneration (CBD)

   CBD Corticobasal Degeneration (CBD) is a rare neurodegenerative condition that affects both the cortex (brain) and the basal ganglia, leading to a combination of movement and higher-level motor planning difficulties. It often presents asymmetrically, meaning one side of the body is significantly more affected than the other.

   What Makes It Different Than Parkinson’s?

   CBD has several unique features that sets it apart:

   • Marked asymmetry with one side affected more than the other

   • Apraxia is a key feature, which is difficulty performing purposeful or functional movements with a limb despite having the strength and motor control to do so

   • ‘Alien Limb’ phenomenon is common - an arm or leg may seem to move involuntarily or feel disconnected from the body

   • Cortical sensory deficits make it difficult to interpret sensory information

   • Myoclonus is often present which looks like jerky or uncontrolled movements

   • Minimal to no response to Parkinson’s medications

Unlike Parkinson’s disease, where movement is primarily limited by slowness and rigidity, CBD involves a breakdown in motor planning and control at a higher neurological level.

How Is Rehab Different?

Rehabilitation for CBD Rehabilitation for CBD requires a shift in approach from “strength and movement” to motor planning, task breakdown, and functional adaptation:

• Therapy should focus on task-specific training, and patients do best when breaking down movements into smaller, step-by-step components

• Cuing should incorporate external cues, hand-over-hand support and modeling or demonstration as interpretation of body-based or sensory-cues will be very hard to understand

• Compensation with the less affected side is critical to maintaining independence as long as possible

• Consider use of adaptive strategies and equipment early on so training can be incorporated while motor control and cognition is at it’s best.

The Big Picture: Similar…But Not the Same

While all Parkinsonisms share common movement challenges, the differences between them matter—a lot. In Parkinson’s disease, we typically see a slower progression, a good response to medication (especially early on), and a rehabilitation approach that emphasizes amplitude, intensity, and long-term maintenance. In contrast, atypical Parkinsonisms often present with a faster or more complex progression and a more limited response to medication. Because of this, rehabilitation must shift—becoming more adaptive, more preventative, more caregiver-inclusive, and more medically integrated to address the broader range of symptoms these conditions can bring.

Hopefully this information has helped you better understand some of the key differences between typical, or idiopathic, Parkinson’s disease and the atypical forms of Parkinsonism. Whether you are a patient, caregiver, or therapist reading this, it is critical to recognize these differences—not only to advocate for an accurate diagnosis if things “just don’t feel right,” but also to find providers who understand these conditions and can truly individualize care.