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WhatIsLCA
Hope Through Science

Understanding Leber Congenital Amaurosis

A comprehensive resource for patients and families navigating LCA — from diagnosis to the latest gene therapy breakthroughs.

0-3per 100,000 newborns
0+Known Genes
0%of childhood blindness
0FDA-Approved Gene Therapy
Understanding the Condition

What is LCA?

Leber Congenital Amaurosis (LCA) is a group of inherited retinal dystrophies that cause severe vision loss or blindness from birth or within the first few months of life. It is one of the most common causes of inherited childhood blindness.

Named after Theodor Leber, the German ophthalmologist who first described the condition in 1869.

Key Facts

Inherited Condition

LCA is primarily autosomal recessive — both parents carry one copy of the mutated gene without being affected.

Early Onset

Visual impairment is typically present at birth or within the first 6 months of life.

Retinal Disease

The condition affects the retina — the light-sensitive tissue at the back of the eye responsible for converting light into neural signals.

Treatable Forms

Luxturna, the first FDA-approved gene therapy for an inherited disease, treats RPE65-related LCA.

The Genetic Basis

Genetics of LCA

LCA is caused by mutations in at least 25 different genes. Each gene plays a crucial role in retinal function — from photoreceptor development to the visual cycle.

How LCA is Inherited

Most forms are autosomal recessive: each parent carries one copy of the mutation without symptoms. Each child has a 25% chance of inheriting both copies and being affected.

Carrier Father
x
Carrier Mother
25% Unaffected
25% Carrier
25% Carrier
25% Affected

Rare dominant forms exist (CRX, IMPDH1, OTX2) where only one copy is needed.

Source: GeneReviews — Leber Congenital Amaurosis / EOSRD, MedlinePlus Genetics

Most Common Gene Mutations

CEP290
15-20%
GUCY2D
10-20%
CRB1
~10%
RDH12
~10%
RPE65
5-10%
RPGRIP1
~6%
IMPDH1
~5%

Source: GeneReviews, MedlinePlus Genetics

Clinical Signs

Signs & Symptoms

LCA presents with characteristic signs that are typically noticed in infancy.

Severe Vision Loss

Visual acuity typically 20/400 or worse from birth

Nystagmus

Involuntary, rhythmic eye movements

Sluggish Pupil Response

Absent or slow pupillary light reflexes

Photophobia

Increased sensitivity to light

Eye Poking (Oculo-Digital Sign)

Children press their eyes to stimulate light flashes — a hallmark of LCA

Absent ERG

Electroretinogram shows severely reduced or no electrical response

Therapeutic Advances

Treatments & Hope

The field of LCA treatment has seen revolutionary progress. From the first FDA-approved gene therapy to cutting-edge CRISPR approaches, the future is brighter than ever.

FDA Approved

Luxturna (Voretigene Neparvovec)

First FDA-approved gene therapy for an inherited disease (2017). Treats RPE65-related LCA by delivering a functional gene via subretinal injection.

Phase 1-3

Gene Therapy Trials

Multiple clinical trials are underway for GUCY2D (LCA1), AIPL1 (LCA4), LCA5, and other subtypes.

Phase 1/2

CRISPR Gene Editing

EDIT-101, the first in vivo CRISPR therapy in humans, targets the CEP290 mutation in LCA10.

Phase 3

RNA Therapies

Sepofarsen targets CEP290 mutations via antisense oligonucleotide, administered by intravitreal injection.

Supporters & Partners

Together for LCA Families

We are building this resource with the support of organizations and individuals dedicated to the LCA community.

Take the First Step

Genetic testing can identify the specific gene causing LCA, determine eligibility for treatments and clinical trials, and guide family planning.

Learn About Genetic Testing

This website provides educational information only and is not a substitute for professional medical advice.