New Treatment Target Found in Age-Related Macular Degeneration
Lower and insufficient amounts of a specific protein found in conditions such as Alzheimer's disease.
A new treatment target in age-related macular degeneration (AMD) has been found after researchers noticed a key protein involved in the body’s ability to remove waste products from the brain and retina were diminished in AMD.
This finding came in the wake of the initial discovery in a brain afflicted with Alzheimer’s disease (AD).
Normally, the brain and retina produce large amounts of waste products, which need to be cleared so it does not muck up the delicate parts of the thinking and visual system. This waste removal system consists of a waste-sensing protein in microglial cells called TREM2 protein (‘triggering receptor expressed in microglia’).
A study published in PLOS ONE examined a human AD-affected brain and an AMD-affected retina from an aging 5xFAD transgenic animals, microglial, and other retinal and brain cells in the culture.
“We have discovered that in age-related degenerative diseases of the brain, such as Alzheimer's disease, and the retina, such as age-related macular degeneration, there is a lowered and insufficient amount of TREM2 protein, and this may be in part responsible for the inability of the brain and retina to clear away their end-stage waste products,” said lead researcher Walter Lukiw, PhD.
The waste products mostly consist of amyloid: misfolded proteins; small various remnants of the innate immune system; small and sticky toxic proteins; and most prominently a 42-amino acid amyloid protein called Aβ42 peptide.
When the waste products are not removed, they accumulate in the brain and retina. This accumulation contributes to the progressive appearance of lesions called senile plaques found in the brain and drusen found in the retina.
These lesions are what contribute to the age-related inflammatory degeneration.
“We have also discovered that an excessive amount of a small piece of ribonucleic acid (RNA) called microRNA-34a, or miRNA-34a, is in part responsible for insufficient TREM2 protein,” Dr. Lukiw said. “These scientific findings further indicate that getting rid of the excessive miRNA-34a to restore normal TREM2 abundance may provide a highly effective therapeutic strategy for the treatment of both degenerative diseases of the brain, such as Alzheimer's disease, and progressive diseases of the retina, such as age-related macular degeneration.”
