They say diamonds are produced under pressure.
So, amidst the hard pressed search for answers as to why normal tension glaucoma (NTG) happens,
brilliant gems were discovered during a session on Day 3 of the World Glaucoma e-Congress (WGC 2021)
which explored various perspectives from around the world regarding the causes. Is it in your genes?
Dr. Janey Wiggs (USA) position was: “Blame it on your parents (and their genes)!” NTG seems to be more prevalent in Asians,
she gave an example before explaining how NTG GWAS (genome-wide association studies) could find NTG in specific loci.
Two genes, OPTN and TBK1 cause familial forms of early-onset NTG. Surprisingly,
NTG may also be associated with systemic neurodegenerative disease like Alzheimer’s disease.
OPTN and TBK1 are also associated with amyotrophic lateral sclerosis (ALS) while Azheimer’s disease genes may contribute to POAG and in particular, NTG.
So far, many GWAS loci identified thus far were involved in IOP, Dr. Wiggs said.
A larger NTG GWAS and other studies to identify novel NTG genes are needed in order to better understand how genes contribute to disease.
Is it the ocular blood flow? For Dr. Yukihiro Shiga, it’s all about the ocular blood flow.
His argument was that “ocular blood flow assessment might help clinicians to predict the risk of visual function deterioration in glaucoma.”
In looking at how ocular blood flow is related to vision impairment, he and his colleagues are focusing on the model of the pericyte.
As pericytes play a role in regulating blood supply, Dr. Shiga’s colleagues at DiPolo Lab
(Quebec, Canada) have discovered its role in mediating capillary diameter regulation, thus, pericytes might be considered as a potential therapeutic target in glaucoma, he said. Is it laminar biomechanics or the optic nerve?
Dr. Crawford Downs (USA) expounded on the support system (the lamina cribrosa) for the optic nerve head.
According to him, laminar biomechanics are driven by IOP and cerebrospinal fluid pressure (CSFP) dynamics while blood flow is also thought to play a critical role in optic nerve head homeostasis.
“Laminar mechanical strains are a function of the translaminar pressure and the local structure and material properties of the laminar microstructure,” he said.
Strains can be high, even at normal levels of IOP, and the response is eye-specific.
IOP and CSFP could still be the primary drivers of glaucomatous axon damage, acting through eye-specific laminar biomechanics, even at ‘normal’ IOP levels.
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