We don’t need to tell you that Alzheimer’s is a devastating degenerative disease, one that efficiently ravages the cognitive, and eventually physical, capacity of more than five million elderly and middle-aged Americans. We also don’t need to tell you that it's a tricky disease to understand. Despite considerable money poured into research and a crop of promising findings regarding early diagnosis, the only way to certify death-by-Alzheimer’s is through posthumous identification of poisonous brian plaque.
It’s less known that patients frequently struggle with night restlessness. Their inability to wind down, say neuroscientists at the University of Bologna, may be more than a pesky side effect of the harrowing condition. In fact, nocturnal agitation could be a diagnostic blessing of sorts.
Alzheimer’s appears to damage a type of light-responsive eye cell called a melanopsin retinal ganglion cell, which senses light levels and tells the brain whether it’s day or night. The eye cells don’t affect vision in any way. Instead, they only transmit information to the suprachiasmatic nucleus, the brain region that regulates the body clock.
If the research bears out, doctors could potentially use sleep problems to gauge disease progression. The loss of these cells, study author Chiara La Morgia told Science Mag, might precede circadian dysfunction and resulting sleep disruptions.
Researchers set out to test the melanopsin-Alzheimer’s connection by using dye to mark melanopsin cells in deceased organ donors’ eyes. Donors with Alzheimer’s had almost one-quarter less melanopsin cells than those without the disease. The appearance of melanopsin cells also differed in appearance, as explained by Science Mag:
Healthy melanopsin cells have round cell bodies with many long threads criss-crossing the retina like the remnants of a spider’s abandoned web. In people with Alzheimer’s, the cells were stubbier, with thinner threads that cast a smaller network, the team will report in an upcoming issue of Annals of Neurology.
They also found amyloid beta protein — which builds up in the brains of Alzheimer’s patients — in the retinal tissue surrounding damaged melanopsin cells, a discovery that helped make sense of the degeneration. It’s not clear if melanopsin cells break down before neurodegeneration sets in, or vice versa. Regardless, the connection could prove valuable in diagnosing and treating Alzheimer’s. Easy access to the retina could help doctors keep tabs on neural degradation by monitoring melanopsin cell function or retinal amyloid beta growth.
If sleep issues and melanopsin cells can, in fact, give researchers a window into the opaque, devastating and common disease, we’d have good reason to cheer. But, researchers have to rule out other explanations for the finding. For example, per Science Mag, one cell biologist mentioned an important next step — linking melanopsin cell degradation to night restlessness in living Alzheimer’s patients, to show that eye-cell damage is causally connected to disturbed sleep and not an unrelated symptom.
Even if melanopsin cell deterioration isn’t the smoking gun doctors hope, learning how to preserve the cells could, at least, help Alzheimer’s patients sleep more soundly.