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Alexander disease
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Condition

Alexander disease

Alexander disease is a rare, progressive disorder of the nervous system that involves the destruction of myelin and the formation of abnormal protein deposits called Rosenthal fibers.

Overview

Alexander disease is a rare disorder of the nervous system and is part of a group of conditions called leukodystrophies. These disorders involve the destruction of myelin, the fatty covering that insulates nerve fibers and promotes the rapid transmission of nerve impulses. As myelin deteriorates, nervous system functions are impaired.

Symptoms

The disease is categorized by the age of onset:

  • Infantile form: Most cases begin before age 2. Symptoms include an enlarged brain and head size (megalencephaly), seizures, stiffness in the arms and/or legs (spasticity), intellectual disability, and developmental delay.
  • Juvenile and adult forms: Onset occurs later in childhood or in adulthood. Common problems include speech abnormalities, swallowing difficulties, seizures, and poor coordination (ataxia).
  • Neonatal form: Rarely occurs within the first month of life, associated with severe intellectual disability, developmental delay, a buildup of fluid in the brain (hydrocephalus), and seizures.

The disease is also characterized by abnormal protein deposits known as Rosenthal fibers, which are found in specialized cells called astroglial cells.

Causes

Mutations in the GFAP gene cause Alexander disease. This gene provides instructions for making glial fibrillary acidic protein. Mutations lead to the production of a structurally altered protein that impairs the formation of normal intermediate filaments, causing the accumulation of Rosenthal fibers, which impair cell function.

Inheritance

This condition is inherited in an autosomal dominant pattern, meaning one copy of the altered gene in each cell is sufficient to cause the disorder. Most cases result from new (de novo) mutations in the gene in people with no family history of the disorder.

Frequently Asked Questions

Early multidisciplinary intervention is crucial: regular physiotherapy to maintain joint range of motion, occupational therapy for feeding and positioning, and respiratory support (e.g., cough assist devices) when bulbar weakness develops. Nutritional support via gastrostomy may be needed, and antispasticity medications (baclofen, diazepam) can reduce rigidity. Pain management and family psychosocial support are also essential components of care.
Typical findings include extensive, symmetric white‑matter abnormalities with frontal predominance, a markedly enlarged ventricles (hydrocephalus ex vacuo), and periventricular Rosenthal fiber‑like signal changes. The presence of a “tadpole” or “butterfly” pattern of frontal white‑matter loss is especially suggestive.
Currently no cure exists; management focuses on supportive care. Anticonvulsants control seizures, physiotherapy addresses spasticity and ataxia, and speech therapy helps with dysarthria. Experimental approaches such as gene‑silencing or small‑molecule chaperones are under investigation but are not yet clinically available.
Each child of an affected individual has a 50 % chance of inheriting the pathogenic GFAP variant. Predictive genetic testing is offered to at‑risk adult relatives, and prenatal or pre‑implantation genetic diagnosis can be considered for couples who wish to avoid transmission. Genetic counseling should cover variable expressivity, as disease severity can differ even within families.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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