Genetic Test
The OLFML3 (Olfactomedin-like 3) gene is believed to play an important role in the tissues responsible for aqueous humor outflow, such as the trabecular meshwork and the anterior chamber angle, as well as in overall ocular structure formation.
It has been studied in humans, mice, and other species for its role in intraocular pressure regulation.
In dogs, specific mutations in OLFML3 are associated with an increased risk of primary angle-closure glaucoma.
The gene influences cell-to-cell interactions and extracellular matrix (ECM) regulation in ocular tissues, affecting the morphology and function of the anterior chamber angle.
Mutations may promote narrowing or blockage of aqueous humor outflow pathways.
Disease Description
Primary angle-closure glaucoma caused by OLFML3 mutations in dogs is characterized by narrowing or blockage of the anterior chamber angle, which impedes aqueous humor drainage and leads to abnormally increased intraocular pressure (IOP).
Persistent elevated IOP causes optic nerve damage and can ultimately result in blindness.
Early stages of glaucoma may present with no symptoms or mild eye redness, but as the disease progresses, clinical signs such as vision loss, pain, and corneal opacity develop.
Primary angle-closure glaucoma is often caused by congenital or genetic structural abnormalities, and OLFML3 gene mutations have been reported to contribute to such anatomical defects (e.g., narrowing of the anterior chamber angle).
