PSP affects approximately 5-10 per 100,000 people worldwide. Symptoms typically first appear when a person is in their 60s or 70s. It is exceedingly uncommon in individuals under the age of 50, and it affects men slightly more often than women.

The exact cause is unknown (idiopathic) in the vast majority of cases. Pathologically, it involves abnormal buildup of tau protein which helps stabilize the internal structure of nerve cells. In PSP, abnormal tau proteins clump together (forming neurofibrillary tangles), causing nerve cells in the brainstem, midbrain, and basal ganglia to malfunction and die. Because these areas control motor coordination, eye movement and executive function, their deterioration directly drives the disease's symptoms. A genetic variation in the MAPT gene (which codes for tau protein) is a known risk factor, but PSP is generally not considered directly inherited in most cases. Rare familial forms exist, but the majority of cases are sporadic with no clear family history. No definitive environmental trigger has been identified, though it has been studied in relation to toxin exposure without conclusive findings.

PSP symptoms develop gradually and generally fall into four categories:

• Movement and Balance (often the first sign): Slowed movements, a stiff, wide-based, or lurching gait. The most hallmark motor symptom is early, unexplained falls—specifically, falling backward stiffly like a tree. The natural reflexes that help a person catch their balance become severely impaired.

• Vision and Eye Movement: A classic diagnostic feature is supranuclear gaze palsy, an inability to aim the eyes properly, particularly downward. Patients often complain of blurry or double vision, difficulty reading, or trouble navigating stairs because they cannot look down at their feet.

• Cognitive and Emotional: Personality changes are common. This can include depression, apathy, loss of interest, impulsive behavior, or executive dysfunction (trouble reasoning and problem-solving). Many experience pseudobulbar affect (PBA), which involves sudden outbursts of laughing or crying that don't match how the person actually feels.

• Speech and Swallowing: As the disease advances, the muscles controlling the mouth and throat weaken, leading to slow, slurred speech and difficulty swallowing (dysphagia).

Advanced disease may include severe immobility, complete dependence, aspiration pneumonia (lung infections from material from mouth and stomach entering the lungs), weight loss, communication difficulties and dementia in some patients.

There is currently no definitive blood test or biomarker for PSP, so neurologists diagnose it clinically based on medical history and a neurological exam. Clinical features often include vertical gaze palsy, postural instability, frequent falls, poor response to Parkinson’s medications such as levodopa, speech abnormalities and cognitive impairment. To confirm the diagnosis and rule out Parkinson's disease or stroke, doctors rely heavily on a brain MRI which typically reveals midbrain atrophy and characteristic morphological features.

There is currently no cure for PSP. Treatment focuses on symptom management and multidisciplinary supportive care, focusing on maximizing quality of life. This may include:

• Medications: Doctors may trial Levodopa (the standard Parkinson's drug), though it usually provides minimal or only temporary relief for PSP. Antidepressants can help manage mood changes. Botox injections are sometimes used to treat severe eye spasms.

• Physical & Occupational Therapy: Essential for fall prevention. Therapists often recommend weighted walkers (to prevent falling backward) and home modifications.

• Speech Therapy: Help teach swallowing techniques to minimize the risk of choking, and introduces communication aids as speech becomes more difficult.

• Nutritional Support: As swallowing becomes severely impaired, a feeding tube may eventually be recommended to ensure adequate nutrition and prevent complications.

• Experimental therapies:  Studies are being done investigating the use of anti-tau monoclonal antibodies, tau aggregation inhibitors, gene-targeted therapies and neuroprotective agents, although to date, none has demonstrated clear disease-modifying benefit in phase III clinical trials.

As PSP is progressive, symptoms become more severe over time. The median survival from symptom onset is typically around 6-9 years, though this varies by subtype and individual. PSP itself is not directly fatal; rather, the complications arising from symptoms pose the greatest risk. The most common cause of death in people with PSP is aspiration pneumonia— an infection that occurs when food or liquid is accidentally inhaled into the lungs due to swallowing difficulties. Severe head injuries from backwards falls are also a major complication. Many patients eventually require wheelchairs, full-time caregiving, assisted feeding and long-term care.

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4. CurePSP:  Progressive supranuclear palsy.

5. National Institute of Neurological Disorders and Stroke:  Progressive supranuclear palsy.

6. National Organization for Rare Disorders (NORD):  Progressive supranuclear palsy.