In the present analysis, we aim at probing into many important mechanisms
that serve to bridge conceptual gaps to fill up the mosaic of a picture revealing that
glaucoma indeed is brain specific diabetes and more appropriately “Diabetes Type 4”.
Based on this conceptual substance, we weave a novel idea of insulin being a potential
remedy for glaucoma. This analysis synthesizes upon the published literature on brain
changes in glaucoma, possibility of isolated brain diabetes, insulin signaling glitches in
glaucoma pathology, mitochondrial dysfunction and insulin resistance in glaucomatous
eyes, insulin mediated regulation of intraocular pressure and its dysregulation in
mitochondrial dysfunction. We also look into the role of amyloidopathy and taupathy in
glaucoma pathogenesis vis-à-vis insulin signaling. At every step, the discussion reveals
that insulin and other allied moieties are a sure promise for glaucoma treatment and
management. In this article, we aim at synthesizing a persuasive and all inclusive picture
of glaucoma etiopathomechanism centered on “insulin-hypofunctionality” in the central
nervous system (i.e. brain specific diabetes). We start with considering the possibility of
neurodegenerative diabetes that exists independent of the peripheral diabetes. Once
that condition is met, then a metabolic conglomeration of this brain specific diabetes is
deliberated upon leading us to understand the development of retinal ganglion cell
apoptosis, intraocular pressure elevation, optic cupping and mitochondrial dysfunction.
All these are the hallmarks and sufficient conditions to satisfy the diagnostic criteria for
glaucoma. Immediate application of this analysis points towards glaucoma therapy
centered upon improving what we have termed insulin-hypofunctionality.
Keywords: Alzheimer's disease, brain, central nervous system, diabetes, glaucoma, inflammation, insulin, insulin
resistance, intraocular pressure, mitochondria, neurodegeneration, neuron, optic nerve, retina.
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