Alström syndrome (AS), also called Alström–Hallgren syndrome, is a very rare autosomal recessive genetic disorder characterised by childhood obesity and multiple organ dysfunction. Symptoms include early-onset type 2 diabetes, cone-rod dystrophy resulting in blindness, sensorineural hearing loss and dilated cardiomyopathy. Endocrine disorders typically also occur, such as hypergonadotrophic hypogonadism and hypothyroidism, as well as acanthosis nigricans resulting from hyperinsulinemia. Developmental delay is seen in almost half of people with Alström syndrome.

It is caused by mutations in the gene ALMS1, which is involved in the formation of cellular cilia, making Alström syndrome a ciliopathy. At least 239 disease-causing mutations in ALMS1 have been described as of 2015^[update]. Alström syndrome is sometimes confused with Bardet–Biedl syndrome, another ciliopathy which has similar symptoms, but Bardet–Biedl syndrome tends to have later onset in its symptoms, includes polydactyly and is caused by mutations in BBS genes.

There is no cure for Alström syndrome. Treatments target the individual symptoms and can include diet, corrective lenses, hearing aids, medications for diabetes and heart issues and dialysis and transplantation in the case of kidney or liver failure. Prognosis varies depending on the specific combination of symptoms, but individuals with Alström syndrome rarely live beyond 50.

At least 900 cases have been reported. Prevalence is fewer than 1 in 1,000,000 individuals in the general population, but the disorder is much more common in Acadians, both in Nova Scotia and Louisiana. It was first described by Swedish psychiatrist Carl-Henry Alström and his three associates, B. Hallgren, I. B. Nilsson and H. Asander, in 1959.

Symptoms for Alström syndrome generally appear during infancy with great variability in age. Some of the symptoms include:^{[medical citation needed]}

Alström syndrome is caused by a mutation in the ALMS1 gene, located on the short arm of chromosome 2 (2p13.2). The gene mutation is inherited as an autosomal recessive trait. This means both parents have to pass a defective copy of the ALMS1 gene in order for their child to have the syndrome, even though the parents may not show signs or symptoms of the condition.

The ALMS1 gene contains instructions to encode a specific protein known as ALMS1. The protein then is involved in ciliary function, cell cycle control and intracellular transport. In addition, the protein is expressed in all organ tissues of the body. It has a role in the proper function, maintenance and formation of cilia, which are found in all types of cells in the body. At least 239 disease-causing mutations in ALMS1 have been described as of 2015^[update]. Most of these mutations have led to the production of a dysfunctional version of the ALSM1 protein which are present in tissues, but at low levels.

It is possible to clinically detect Alström syndrome in infancy, but more frequently, it is detected much later, as doctors tend to detect symptoms as separate problems. Currently, Alström syndrome is often diagnosed clinically, since genetic testing is costly and only available on a limited basis.