Medically reviewed by Heidi Moawad, M.D. — Written by Stephanie Watson — Updated on February 23, 2026

Key takeaways

• Parkinson’s tremor is an involuntary shaking that usually happens at rest and often stops with movement. It occurs due to reduced dopamine activity in the brain.
• Dyskinesia is an involuntary writhing, twisting, or fidgeting movement that can appear after years of levodopa use. Researchers think it may be related to dopamine level fluctuations from levodopa dosing.
• Tremor can be hard to treat and may require medication changes or deep brain stimulation (DBS). Dyskinesia may improve with levodopa dose adjustments, alternate drugs like dopamine agonists, amantadine, or DBS.

Tremor and dyskinesia are both involuntary movements. However, the movements are different and occur for different reasons in Parkinson’s disease. Additionally, there are many other causes of both tremors and dyskinesia.

Here’s how to tell if the involuntary movements you’re experiencing are tremors or dyskinesia.

What is tremor?

Tremor is a neurological symptom involving involuntary shaking of your limbs or face. It’s a common symptom of Parkinson’s disease and occurs due to a lack of action of the chemical dopamine in the brain. Dopamine activity in the brain helps maintain smooth and coordinated body movements.

The exact cause of Parkinson’s disease (PD) itself is unknown. But it may result from an interaction between:

• genetic mutations
• environmental triggers, such as exposure to certain toxins
• other factors, including damage to mitochondria in the brain

Other causes of tremor

Other health conditions besides PD can cause tremor. These can include:

• multiple sclerosis (MS)
• stroke
• certain medications, including corticosteroids and some asthma medications
• caffeine
• exposure to toxins, such as heavy metals
• overactive thyroid
• liver or kidney damage
• diabetes
• stress or fatigue

About 80% of people with PD experience tremors, and for some, it is the first indicator of PD. Parkinson’s tremor can occur in any part of your body, but it often starts first in the fingers.

Tremor in different parts of the body

Parkinson’s tremor may look different, depending on the part of the body affected. For instance:

• Jaw tremor: With a jaw tremor, your chin may appear to shiver, except the movement is slower. It may be intense enough to make your teeth click together. It usually goes away when you chew, and you can eat without a problem. Chewing gum may help.
• Facial tremor: This refers to a twitching of the face, such as the lips and jaw, when you’re at rest. It’s associated with older age and a longer duration of PD. One study reported that only 1.7%Trusted Source of the participants had facial tremor at the time of PD onset, but after 9 years, 14% of people with PD had facial tremor.
• Tongue tremor: This type of tremor rarely occurs as an early symptom and often develops after tremor in the body extremities, like the hands or feet. It happens when you’re at rest. If severe, it can make your head shake.
• Finger tremor: A finger tremor looks like a “pill rolling” motion. The thumb and another finger rub together in a circular motion, making you look like you’re rolling a pill between your fingers.
• Hand and arm tremor: The hand or arm may move at rest. This typically stops if you move it.
• Foot and leg tremor: Foot tremor can happen when lying down or your foot is dangling. The movement may affect the foot or the entire leg. The shaking usually stops when you stand up and doesn’t often interfere with walking.
• Head tremor: This type affects about 1% of people with PD. Sometimes, the head doesn’t shake on its own, but rather when the tremor of an arm affects the head.

A Parkinson’s tremor happens when your body is at rest. This is what distinguishes it from other types of shaking. Moving the affected limb often stops the tremor.

The tremor might start in one limb or side of your body and can eventually progress within that limb. For example, it can progress from your hand to your arm. The other side of your body may eventually shake, or the tremor could stay on just one side.

Tremor can worsen as PD progresses.

Initiative highlights need for clearer communication across care teams

Written by Andrea Lobo | April 14, 2026

• Campaign supports earlier identification of Parkinson’s symptoms and clearer communication among care teams.
• Low symptom awareness, especially in younger people, may delay diagnosis. The campaign highlights off episodes.
• Bial is developing BIA 28-6156 for people with Parkinson’s and a GBA1 gene variation, now in a Phase 2b trial.

Bial has launched an international education campaign to support clearer communication and the early identification of symptoms among people with Parkinson’s disease, carers, and healthcare professionals.

The year-long campaign, called “Dialogues with Parkinson’s,” is being developed in collaboration with Parkinson’s Europe to mark World Parkinson’s Day, held on April 11 during Parkinson’s Awareness Month. It includes digital content and educational resources, such as guides and checklists, to help build a shared language among patients, carers, and healthcare professionals.

Company continues research into potential Parkinson’s treatment

The company is developing BIA 28-6156 for people with Parkinson’s who have a pathogenic variation in the GBA1 gene. The molecule is being evaluated in the Phase 2b ACTIVATE trial (NCT05819359). According to the company, topline results are expected by the end of the first half of this year.

23 Mar 2026

PARKINSON’S weight loss is emerging as a critical yet under-recognised feature of Parkinson’s disease, according to a new review synthesising current evidence. While the condition is best known for its motor symptoms like tremor and rigidity, non-motor features— including unintentional weight loss—may play a significant role in shaping disease progression and patient outcomes.

Parkinson’s disease is a neurodegenerative disorder marked by the gradual loss of dopaminergic neurons in the basal ganglia, leading to impaired movement and coordination. However, a growing body of research suggests that disruptions beyond dopamine systems contribute substantially to overall morbidity.

An Early and Often Missed Pattern

Weight loss appears to be both common and clinically significant in Parkinson’s. Long-term studies discussed in this review show that patients often lose significantly more weight than people without the condition, with many experiencing losses exceeding 5% of their baseline body weight. In some cases, this decline begins as early as five to seven years before diagnosis.

The trajectory is not always linear. Some individuals gain weight shortly after diagnosis, only to lose it later as the disease advances. Notably, weight loss tends to accelerate in later stages and has been linked to higher disease severity and cognitive decline.

Why Parkinson’s Weight Loss Matters

The review highlighted that weight loss in Parkinson’s disease is closely tied to poorer outcomes. Lower body weight is associated with frailty—a state of reduced physiological reserve—and increased mortality. Up to 60% of patients may be at risk of malnutrition, which in turn is linked to reduced quality of life.

Even modest changes appear relevant: each pound (0.45 kg) of weight loss has been associated with measurable declines in health-related quality of life. Patients who lose weight also tend to experience greater fatigue, reduced physical stamina and worsening mood.

Parkinson’s Disease – A Complex Biological Picture

The mechanisms driving weight loss in Parkinson’s are multifactorial. Disruptions in glucose metabolism, neuroendocrine signalling and gastrointestinal function all appear to contribute. Patients may also face challenges such as reduced appetite, cognitive impairment affecting eating behaviour, and swallowing difficulties.

Interestingly, weight loss does not always reflect reduced food intake. Some studies suggest patients maintain or even increase calorie consumption, pointing instead to altered metabolism or energy balance. Gastrointestinal dysfunction, including delayed stomach emptying, may further impair nutrient absorption.

Treatment effects add another layer of complexity. Certain dopaminergic treatments are associated with weight changes, while deep brain stimulation has been linked to significant weight gain in many patients.

Closing Gaps in Care and Future Directions

Despite its clinical impact, weight loss in Parkinson’s disease appears to remain under-recognised and lacks standardised screening guidelines. The review calls for routine monitoring of body weight and earlier nutritional interventions, particularly before cognitive decline limits patient involvement in care decisions.

Looking ahead, researchers emphasise the need for large-scale longitudinal data and targeted studies to better understand underlying mechanisms. Developing tailored, multidisciplinary strategies could offer a practical route to improving quality of life and survival in people living with Parkinson’s.

Reference

Gabriel ED et al. When the Scale Drops: Pathways to Weight Loss in Parkinson’s Disease and Future Directions. Mov Disord. 2026;DOI:10.1002/mds.70258.

This article is republished from Parkinson’s Weight Loss: A Hidden Driver of Decline? by Roli Omamuli, American Medical Journal, available at https://www.emjreviews.com/en-us/amj/neurology/news/parkinsons-weight-loss-a-hidden-driver-of-decline/
Licensed under Creative Commons Attribution-NonCommercial 4.0 (CC BY-NC 4.0): https://creativecommons.org/licenses/by-nc/4.0/
No changes were made to the original content.

10 Apr 2026  Author: Anaya Malik

PARKINSONISM trends in the UK reveal falling PD incidence, rising prevalence, and increasing recognition of vascular Parkinsonism (VP).

Parkinsonism Trends Show Diverging Patterns

A large UK cohort study found that the epidemiology of Parkinsonism subtypes has shifted over time, with Parkinson’s disease showing a slight decline in incidence but a rise in prevalence, while vascular Parkinsonism (VP) became increasingly recorded and drug induced Parkinsonism remained largely stable. The analysis used routinely collected primary care data from 2007–2021 and included adults with at least 1 year of prior observation. Annual incidence and prevalence were assessed for Parkinson’s disease, VP, and drug induced Parkinsonism, with stratification by age and sex.

From 2007 to 2019, the age standardized incidence of Parkinson’s disease fell from 35.61 to 31.27 per 100,000 person years. Over a similar period, prevalence rose from 0.21% in 2007 and peaked at 0.23% in 2016. The authors suggested that this divergence between incidence and prevalence may reflect improved survival and care. By contrast, VP diagnoses increased from 2010 onward, while drug induced Parkinsonism showed relatively stable incidence and prevalence throughout the study period.

Parkinsonism Trends Varied by Age and Sex

The burden of Parkinsonism increased with age across subtypes, although the age effect was less marked for drug induced Parkinsonism. Parkinson’s disease and VP were generally more common in males, whereas drug induced Parkinsonism was slightly more common in females. The study also found that patients with VP had the highest median age at diagnosis, while those with drug induced Parkinsonism were younger on average.

Among adults older than 70 years, incidence patterns diverged further. Parkinson’s disease incidence decreased, whereas VP incidence increased. In prevalence analyses, Parkinson’s disease rose steadily in older age groups, while drug induced Parkinsonism remained stable. These findings suggest that clinicians may increasingly encounter a more heterogeneous Parkinsonism population in older adults, with important differences in sex distribution, comorbidity patterns, and likely drivers of disease.

Clinical Relevance for Practice

The study included 20,006 patients with Parkinson’s disease, 1,126 with VP, and 809 with drug induced Parkinsonism. Patients with VP were more likely to have chronic kidney disease, dementia, stroke, and cardiovascular disease, while those with drug induced Parkinsonism more often had anxiety, depression, and prior exposure to antidepressants, antiepileptics, and psycholeptics. The authors noted that rising VP rates may reflect improved diagnostic recognition, while stable drug induced Parkinsonism rates may indicate greater awareness of causative medications and earlier review of treatment histories.

The authors also highlighted important limitations, including possible misclassification between Parkinson’s disease, VP, and drug induced Parkinsonism, as well as under recording in primary care when diagnoses made in specialist settings are not promptly captured by general practitioners. Even so, the overall message is clear: as the population ages, Parkinsonism subtypes are likely to represent an increasing clinical burden, and subtype specific recognition will matter for screening, diagnosis, and care planning.

Reference
Chen X et al. Secular trends of incidence and prevalence of Parkinsonism subtypes: a cohort study in the United Kingdom. European Journal of Public Health. 2026;36(2):ckag031.

This article is republished from How Parkinsonism Subtypes Are Changing Over Time by Anaya Malik, American Medical Journal, available at https://www.emjreviews.com/en-us/amj/neurology/news/how-parkinsonism-subtypes-are-changing-over-time/.
Licensed under Creative Commons Attribution-NonCommercial 4.0 (CC BY-NC 4.0): https://creativecommons.org/licenses/by-nc/4.0/
No changes were made to the original content.

SK-129 aims to prevent formation of toxic protein clumps

Written by Patricia Inácio, PhD | April 8, 2026

• Parkinson's and related diseases involve toxic alpha-synuclein protein clumps.
• SK-129, a lab-made molecule, reduced these toxic protein clumps and their spread.
• It crossed the blood-brain barrier, showing promise for slowing disease progression.

A small, lab-made molecule called SK-129 reduced the formation of toxic clumps of the alpha-synuclein protein, a hallmark of Parkinson’s disease, a study found.

SK-129 was able to cross the blood-brain barrier – a semipermeable membrane that protects the brain and central nervous system – and prevent damage caused by these toxic clumps, as well as their spread across the brain.

The findings may also be relevant to other Parkinson’s-like diseases characterized by abnormal clumping of the protein alpha-synuclein, including Lewy body dementia and multiple system atrophy.

“This is an important step toward developing treatments that target the root cause of these diseases,” Mazin Magzoub, PhD, associate professor of biology at NYU Abu Dhabi and a co-lead author on the study, said in a New York University press release. “Instead of only treating symptoms, we are working toward slowing or stopping the disease itself.”

The study, “Foldamers rescue synucleinopathy phenotypes in multiple in vitro and in vivo models,” was published in the journal Science Translational Medicine.

Misfolded protein forms toxic clusters

Parkinson’s disease is caused by the progressive loss of dopamine-producing neurons, a type of nerve cell important for movement control.

A hallmark of Parkinson’s and related disorders, collectively known as synucleinopathies, is the formation of toxic clumps of the protein alpha-synuclein in brain cells. In healthy neurons, alpha-synuclein normally exists in a monomeric (single-molecule) form and is involved in nerve cell communication.

But when the protein misfolds, it can assemble into small toxic clusters called oligomers, which then form larger aggregates that make up Lewy bodies, a key disease-causing feature of Parkinson’s. These clumps contribute to cell death and spread in a prion-like manner, meaning aggregates in one brain region may trigger more misfolding in nearby regions.

That means preventing alpha-synuclein from clumping and spreading is seen as a promising strategy for treating synucleinopathies.

Researchers at NYU Abu Dhabi and the University of Denver focused on the potential of foldamers, lab-made molecules designed to mimic features of natural proteins. Specifically, they investigated SK-129, a foldamer designed to inhibit alpha-synuclein aggregation.

In lab tests, they found that SK-129 blocked alpha-synuclein from clumping together and reduced disease-related effects across several lab models, including nerve cells derived from human induced pluripotent stem cells (iPSCs) and animal models such as the worm Caenorhabditis elegans and mice. iPSCs are cells that can generate almost any type of cell in the body.