Detecting Alzheimer’s may soon be as easy as spotting changes in cells of the retina of the eye, according to a breakthrough study led by international researchers including one of Indian origin. The study showed that physical changes in cells of the retina can occur at the same time as brain changes found in the early stages of Alzheimer’s disease.
Researchers from Australia, Italy, and the US investigated how two proteins — beta-amyloid and tau — known to build up in the brains of Alzheimer’s patients, can also be found in the cellular tissue of the eye, often long before symptoms are apparent.
The findings, published in the peer-reviewed journal Acta Neuropathol, could potentially contribute to the future development of an imaging technique with the potential to detect Alzheimer’s disease with a non-invasive eye test.
“Researchers have recognised in recent years that there could be changes in the retina quite early in the disease process, but trying to identify these in the eyes of live patients has proved tricky,” said Professor Stuart Graham, head of Ophthalmology and Visual Science at Macquarie University.
“The accumulation of beta-amyloid and tau in the central nervous system might be a key initiating factor in the development of Alzheimer’s disease,” added Associate Professor Vivek Gupta, a visual neurobiologist who leads Macquarie`s Vision Neurodegeneration research group.
He said while the specific cause of Alzheimer’s disease remains unclear, “recent studies by our group and others have reported similar pathological processes and alterations in the retina.” The study analysed donor brain and retina tissue from 86 people.
The team developed a holistic proteome map of human retinas, and of the brains of people who had Alzheimer’s disease, showing protein changes at the molecular, cellular, and structural levels of both eye and brain and associated cell death and inflammation.
Donors included people with normal brain function, some with mild cognitive impairment, and others who were diagnosed with Alzheimer’s disease; and 39 people had donated both retina and brain tissue, so researchers could directly compare protein levels in each.
The results showed that people who had Alzheimer’s disease showed nine times the amount of beta-amyloid protein in their retinas compared to people who didn’t show any signs of cognitive impairment during their lifetime.
The study also found that these markers occurred at around five times the rate in people who had not been diagnosed with Alzheimer’s disease during their lifetime but had shown signs of mild cognitive impairment.
The researchers were also able to track patterns in the location of these markers within the retina, with higher levels found in the tissues of the retina`s inner layer.
“We don’t have a device in the clinic to identify these changes in a living eye yet; but if we can label these proteins, then develop an imaging device that can spot change at the earliest stages, we may have a way to clinically diagnose diseases such as Alzheimer’s,” Graham said.
Graham said that a range of degenerative diseases (including Alzheimer’s) share common cell deterioration pathways, and identifying patterns in the types and locations of abnormal proteins in retinal cells may also help diagnose such diseases as glaucoma.
“We can readily diagnose advanced glaucoma now by imaging the back of the eye, but we also know there are changes occurring at the molecular or cellular level, long before we can see those structural changes when nerve fibres start to drop out,” he noted.