In September 2026, PMD Alliance hosted a webinar on young-onset Parkinson’s disease (PD). Dr. Rodolfo Savica discussed the similarities and differences between typical-onset Parkinson’s disease (TOPD) and young-onset Parkinson’s disease (YOPD), possible causes of young-onset, and how symptom management could be different for those with TOPD and those with YOPD.
These are the major points from the webinar:
- The development of symptoms among those with YOPD tend to differ from those with TOPD in some specific ways. Those with YOPD tend to have more frequent and severe autonomic nervous system dysfunction, and insomnia as their most common symptom.
- The social impacts of YOPD are considerable. Those with YOPD are at a different life stage than those with TOPD, and they tend to feel isolated both from able-bodied peers and from older people with PD.
- The causes of PD are complex. Both genetics and environment play a role in whether someone develops YOPD.
- Dr. Savica encourages those with YOPD to treat their symptoms as they become bothersome, rather than seeking treatment for every symptom. A variety or combination of treatments will likely be more effective than just one.
You can find further resources for those with YOPD on the Stanford Parkinson’s website.
If you have YOPD and are lucky enough to live in the San Francisco Bay Area, see the Stanford Young-onset Parkinson’s Support Group
A recording of the webinar is available on the PMD Alliance YouTube channel.
Below are my full notes.
– Jordan
“Why Are They So Different: Young-Onset vs. Typical-Onset Parkinson’s”
Speaker: Rodolfo Savica, MD, PhD, Mayo Clinic, Rochester
Webinar Host: PMD Alliance. Part of their Young-Onset Parkinson’s Network speaker series.
Webinar Date: September 9, 2026
Summary by: Jordan Dagan, Stanford Parkinson’s Community Outreach
Editor’s note: Dr. Savica uses “young-onset” and “early-onset” interchangeably during his talk. I’ve kept it consistent, using “young-onset” and YOPD.
WHAT IS YOUNG-ONSET PARKINSON’S DISEASE?
Dr. Savica says the generally-used “cutoff” for Parkinson’s disease (PD) to be considered “young onset” (YOPD) is 50-55 years old. If someone is diagnosed with PD before age 50, this is YOPD. Having an age cutoff like this gives doctors and researchers a clear way to label the disease and research it.
The incidence of PD has increased since approximately the 1960s. Dr. Savica says there is a predicted increase of PD in future years, not only among aging individuals.
SIMILARITIES AND DIFFERENCES BETWEEN YOPD AND TYPICAL-ONSET
Dr. Savica says doctors can’t necessarily generalize knowledge between older and younger populations of people with PD.
Everyone’s presentation of PD symptoms is different. However, the development of symptoms among those with YOPD tend to differ from those with TOPD in some specific ways.
This table summarizes the similarities and differences in TOPD and YOPD as described by Dr. Savica (any errors are the editor’s, not Dr. Savica’s):
| Typical-Onset PD | Similarities | Young-Onset PD |
| Most common symptom: bradykinesia or slowness of movement. Constipation tends to occur before diagnosis. Motor symptoms happen only on one side of the body at first (called “monolateral onset”). Dyskinesia (involuntary movements) are common. | Non-motor symptoms occur years before motor symptoms occur. Motor symptoms:Bradykinesia (slowness of movement).Rigidity and stiffness.Resting tremor. Non-motor symptoms:Anosmia (loss of sense of smell).REM behavior disorders.Constipation.Anxiety.Depression.Visual symptoms. | Most common symptom: insomnia. Constipation tends to occur after diagnosis. Early in YOPD progression, dystonia (muscle cramping or spasms) only occurs in some circumstances, such as during exercise. Brain fog. More frequent and severe autonomic nervous system dysfunction, including high instances of gastroparesis (slow gastric emptying). |
The social impacts of YOPD are considerable. Those with YOPD are at a different life stage than those with TOPD, and they tend to feel isolated both from able-bodied peers and older people with PD. They are generally still employed when diagnosed, and their job will be impacted by their developing disability. There isn’t much legislation in place to protect their workplace rights.
Those with YOPD may be planning a family, or caring for children, when their symptoms begin. Dr. Savica says there is very little data on the co-occurrence of YOPD and pregnancy. That said, there does not seem to be a clear association of pregnancy and worsening of PD symptoms, or PD and complications with pregnancy.
GENETIC CAUSES OF PD
PD shows high phenotypic variability, with different individuals having different presentations of the disease. This is likely because of varying genetics between people.
In future research, we may be able to use correlations between genetic mutations and varying symptoms among those with YOPD to examine the molecular mechanisms behind the disease.
There is research done about what genetics are associated with increased risk of PD, but so far we lack information about what genes may be protective.
Dr. Savica emphasized the term “synergistic heterozygosity.” This means someone has multiple partial functional deficits across different genes and gene expressions. These deficits combine to disrupt “downstream” cell functions, including mitochondrial, lysosomal, and synaptic pathways.
There may be a few different causes converging to produce PD, including genetics and environmental factors. Dr. Savica noted that exposure to head trauma does not significantly increase PD risk, unless there is a certain gene mutation present. Women with YOPD tend to have slower symptom progression than men, suggesting that women’s second X chromosome could be protective against the decline of YOPD.
ALPHA-SYNUCLEIN AS A CAUSE OF PD
The “Braak hypothesis” refers to the theory that the buildup of misfolded alpha-synuclein protein in the brain is the primary mechanism behind PD. The mechanism behind alpha-synuclein misfolding varies. Typical Parkinsonism motor symptoms are caused by alpha-synuclein misfolding, and this is seen in PD, dementia with Lewy bodies (DLB), Parkinson’s disease dementia (PDD), and multiple system atrophy (MSA).
Trials of medications which target protein accumulation are offering those with Alzheimer’s disease better results, but the same is not true for PD treatments which target alpha-synuclein. Dr. Savica thinks this is because the underlying mechanisms behind PD are more complex than just misfolded alpha-synuclein. In addition, there are metabolic diseases associated with alpha-synuclein misfolding, not just PD. Biomarkers based on alpha-synuclein accumulation are not enough on their own to diagnose PD. This supports the idea that alpha-synuclein is not the only contributing factor to PD symptom development.
CAUSES: YOPD AND DOPAMINE TRANSMISSION DYSFUNCTION
Though PD motor symptoms are rooted in dysregulation of dopamine production and transmission, the pathology between those with TOPD and YOPD is different. When the brain is seen during autopsy, those with YOPD have few signs of an aging brain. There is a greater effect on the substantia nigra, which is where dopamine regulates motor symptoms. Those with YOPD may have a lack of misfolded alpha-synuclein buildup, or misfolded alpha-synuclein may be present in different places compared to those with TOPD.
Dopamine transporter scanning (a DaT scan) visualizes dopamine transporter levels in the brain, but data from a DaT scan cannot necessarily tell if someone has PD. This scan doesn’t allow doctors to differentiate between various parkinsonian syndromes. DaT scanning visualizes a very specific part of dopamine transmission, not the full dopamine transmission system. Young people with PD have normal DaT scans.
A positron emission tomography (PET) scan measures patterns of metabolic activity, and can be used to visualize metabolic changes in the brain and inform diagnosis. When visualized on a PET scan, diseases have specific patterns or appearances. After the PET scan data is analyzed, TOPD, YOPD, and DLB each appear different.
MANAGING YOPD
Dr. Savica encourages those with YOPD to try various treatments, since everyone’s experience and symptoms are different. L-dopa should be given as soon as symptoms become troublesome, and those with YOPD may take it as needed. Newer extended release carbidopa/levodopa formulations are available. Several non-motor symptoms are often responsive to levodopa among those with YOPD:
- Anxiety and panic attacks
- Brain fog
- Insomnia
- Pain
Regarding mucuna pruriens, Dr. Savica points out that mucuna seeds contain unpredictable concentrations of L-dopa, resulting in erratic dosing. At maximum, mucuna offers 52.1% of L-dopa given by other treatments, and mucuna doesn’t offer carbidopa.
Duopa and Vyalev are pumps which deliver carbidopa/levodopa gel directly to the small intestine. Duopa is an older model, and Vyalev is a newer model.
Among those with YOPD using dopamine agonists, Dr. Savica says common issues include taking too low a dose for the treatment to be effective, and not switching to carbidopa/levodopa when needed. Some side effects can be troublesome:
- Psychosis
- Sleepiness, which can be dangerous for driving
- Pathologically intrusive behaviors such as gambling, hypersexuality, excessive spending, excessive eating, or excessive engagement with hobbies
- Orthostatic hypotension
- Edema
The autonomic dysfunction experienced by those with YOPD can include gastroparesis, or slow gastric emptying, and poor absorption of medications. Other complications might affect the absorption of carbidopa/levodopa as well, such as gout, or competition between meals and drug absorption.
Generally, these have a positive impact on levodopa absorption:
- Caffeine
- Soy
- Fiber
- Ascorbic acid/vitamin C
- Beta-2 agonists
- Liquids/Hydration
Generally, these have a negative impact on levodopa absorption:
- Anticholinergics
- Gabapentin
- Tricyclic antidepressants
- Protein-rich food
- Hot/Hyperthermic conditions
- Methyldopa
Regarding invasive therapies like deep brain stimulation (DBS) and focused ultrasound (FUS), Dr. Savica says these are not for everyone. Among those with YOPD who choose DBS as a treatment, 57% have motor complications, and there is an increased risk of cognitive impairment compared to those with TOPD.
Research into “neuroprotective” treatments, such as stem cells, is ongoing. Stem cell treatments have been done using small sample sizes, and are not ready for general use yet. Dr. Savica urges caution when paying for experimental treatments, especially those outside of the United States; they might not be government-regulated, increasing the risks of scams and hazardous side effects.
QUESTIONS AND ANSWERS
Question: What is the cutoff age for someone to be considered YOPD vs TOPD?
Answer: Generally 50 years old is the cutoff, though 50-55 commonly used.
Question: Do you encourage the continuous pump system?
Answer: No one treatment works for everyone. Everything should be tailored to the patient’s needs. In the future, when pump systems for carbidopa/levodopa administration are more advanced, it may become a first treatment for people.
Question: Is there an association between YOPD and having gastric bypass?
Answer: Overall, there is no clear association. Studies about this are done with small sample sizes, and have not been replicable by other researchers. However, research into the gut/brain axis is very new but interesting.
Question: Is there an association between epilepsy and PD?
Answer: These diseases are very different from each other. Research is ongoing.
Question: What’s the connection between insulin resistance, hormones, and PD?
Answer: There is currently very little research on this, especially in men.
Here, Dr. Savica noted that any trial being done has assumptions built in, and those assumptions may not be true. Any treatment may work in some people, but more studies must be done to find out which people it works for.
Question: If food affects levodopa absorption, how should those with PD take their meds?
Answer: Take your meds 30 minutes apart from protein-heavy foods.
Question: Please say more about dysautonomia in YOPD.
Answer: Autonomic nervous system dysfunction can occur in PD or in other diseases. If dysautonomia is very severe, people tend to become worried they might have MSA (multiple system atrophy). Autonomic dysfunction is very disruptive to quality of life, but some people’s dysautonomia responds to dopamine therapy. It is always important to treat people as individuals and gather as much info as possible when recommending treatment.
Question: YOPD women may develop dyskinesia when they’re on levodopa, even if they’re not far into disease progression. This is concerning.
Answer: Yes, it is wrong to say that the occurrence of dyskinesia is always because of disease progression. Dyskinesia may develop even when only a bit of levodopa is being taken. This may be because of unknown genetic factors. We might see more dyskinesia affecting women taking levodopa because women have more estrogen and this displaces levodopa, so women need more medication to get the same results. My recommendation for YOPD women is to be aware of this possible complication, make sure you’re not overmedicated for your needs, and consider that different drugs you’re taking may be affecting levodopa absorption.
Question: If estrogen is amplifying levodopa uptake, should women be put on agonists instead?
Answer: Treatment should be tailored to the patient. Dopamine agonists may not work on their own. Try different combinations of treatments such as slow vs rapid release levodopa, or a pump system.