What genes have been linked to Parkinson’s disease? 

For most individuals, Parkinson’s disease is sporadic, meaning it occurs due to a combination of environmental triggers and aging. However, research confirms that genetics play a role in approximately 10 to 15 percent of cases. Scientists have identified specific genes that either directly cause the condition or significantly increase a person susceptibility to it. Understanding these genetic links is more than just academic; it is now the foundation for precision medicine, where new clinical trials target the specific biological pathways affected by these mutations. Whether a gene causes Parkinson’s depends on its inheritance pattern, some require only one copy from one parent, while others require a copy from both. 

What we will discuss in this article 

• The role of LRRK2 and GBA as major genetic risk factors 

• SNCA and the first discovered genetic link to alpha synuclein 

• PRKN and PINK1 mutations in young onset Parkinson’s 

• Autosomal dominant versus autosomal recessive inheritance patterns 

• The impact of genetic mutations on disease progression and symptoms 

• Availability of genetic testing and counselling in the UK 

• Emergency guidance for families with suspected hereditary syndromes 

Major risk genes: LRRK2 and GBA 

The two most common genetic contributors to Parkinson’s are LRRK2 and GBA. These are often referred to as risk variants because having the mutation does not guarantee you will develop the disease, but it increases the probability. 

LRRK2 (Leucine rich repeat kinase 2) 

LRRK2 is one of the most studied genes in Parkinson’s research. Mutations in this gene account for about 1 percent of all cases and up to 5 percent of familial cases. In certain ethnic groups, such as those of Ashkenazi Jewish or North African Berber descent, LRRK2 mutations are much more common. LRRK2 is an autosomal dominant gene, meaning only one copy is needed to increase risk. LRRK2 associated Parkinson’s often progresses more slowly than the sporadic form, and new drugs targeting this specific protein are currently in advanced clinical trials. 

GBA (Glucocerebrosidase beta) 

GBA is the most common genetic risk factor, found in 5 to 10 percent of all people with Parkinson’s. This gene provides instructions for an enzyme that helps cells break down waste. When it is mutated, toxic proteins can build up more easily. People with a GBA mutation may experience symptoms at an earlier age and may have a higher risk of cognitive changes. If a person inherits two mutated GBA genes, they develop Gaucher disease, a different metabolic disorder. 

The SNCA gene and alpha synuclein 

The SNCA gene was the first ever genetic link discovered in Parkinson’s and remains central to our understanding of the disease biology. 

SNCA provides the instructions for making a protein called alpha synuclein. In all forms of Parkinson’s, this protein misfolds and clumps together to form Lewy bodies, which damage neurons. Mutations in SNCA, such as duplications or triplications of the gene, cause the brain to produce too much alpha synuclein. This is an autosomal dominant condition that typically leads to an earlier onset of symptoms and a faster progression. Because alpha synuclein is the hallmark of the disease, many experimental therapies are focused on stopping the SNCA gene from overproducing this protein. 

Genes linked to young onset Parkinson’s 

When Parkinson’s is diagnosed before the age of 50, genetic factors are often the primary cause. These are typically autosomal recessive, meaning a person must inherit a mutated copy from both parents. 

• PRKN (Parkin): Mutations in the PRKN gene are the most common cause of juvenile and young onset Parkinson’s. The Parkin protein normally helps recycle damaged mitochondria. Without it, cells become stressed and die. 

• PINK1: Similar to PRKN, PINK1 helps protect mitochondria. Mutations in this gene lead to early onset symptoms, often including slow movement and balance issues in a person 30s or 40s. 

• PARK7 (DJ-1): A rare mutation that also leads to early onset disease by failing to protect cells from oxidative stress. 

Inheritance patterns at a glance 

Understanding how these genes are passed down helps families assess their own risk and the likelihood of passing the condition to children. 

Gene	Inheritance Pattern	Typical Onset	Note
LRRK2	Autosomal Dominant	Late (50+)	Most common dominant gene
SNCA	Autosomal Dominant	Early to Middle	Leads to high alpha synuclein
GBA	Risk Factor	Variable	Increases risk of cognitive changes
PRKN	Autosomal Recessive	Young (Under 50)	Most common young onset cause
PINK1	Autosomal Recessive	Young (Under 50)	Linked to mitochondrial health

Genetic testing in the UK 

In 2026, genetic testing for Parkinson’s is becoming more accessible, but it should always be accompanied by professional counselling. 

The NHS Genomic Medicine Service provides specific gene panels for individuals with young onset Parkinson’s or those with a very strong family history. Furthermore, research initiatives like PD Frontline in the UK offer free genetic testing to people with Parkinson’s to help identify candidates for gene targeted clinical trials. Knowing your genetic status can be empowering, as it may qualify you for trials testing new treatments specifically for GBA or LRRK2 carriers. However, a positive test for a risk gene like GBA does not mean you will definitely get the disease, which is why counselling is essential to help interpret the results. 

Emergency guidance 

Genetic forms of Parkinson’s usually progress at a predictable rate, but certain rare genetic syndromes can lead to acute crises. 

If a family member with a known genetic movement disorder experiences a sudden, total inability to swallow, acute respiratory distress, or a rapid onset of severe confusion, seek medical help immediately. 

Seek urgent medical advice if you notice: 

• High fever combined with lead pipe muscle rigidity 

• Sudden, severe falls resulting in head injury or loss of consciousness 

• Acute psychiatric changes or distressing hallucinations in a young person 

• Rapid worsening of physical symptoms over just a few days 

• Signs of a stroke, such as facial drooping or one sided weakness 

To summarise 

Genetics provide a crucial map for understanding why some people develop Parkinson’s and how the disease might progress. While the majority of cases are not directly inherited, mutations in genes like GBA and LRRK2 act as significant risk factors. In younger patients, autosomal recessive genes like PRKN and PINK1 are the primary drivers. As we move through 2026, the discovery of these genes is fuelling a revolution in treatment, moving us away from one size fits all approaches and toward precision therapies that target the underlying genetic cause of the condition. 

Authority Snapshot 

This article was reviewed by Dr. Rebecca Fernandez, a UK trained physician with an MBBS and extensive experience in internal medicine, surgery, and psychiatry. Her background includes working with complex neurodegenerative and psychiatric disorders using evidence based clinical approaches. Dr. Fernandez is dedicated to integrating the latest genomic research with compassionate patient care to help families navigate the complexities of hereditary neurological conditions.