Alzheimer's disease and glaucoma: Is there a causal relationship?

Evidence of a link between Alzheimer's disease (AD) and glaucoma has emerged from studies showing that patients with AD may have a significantly increased rate of glaucoma occurrence. In addition, it has been reported that patients with AD exhibit optic nerve degeneration and loss of retinal ganglion cells. In spite of intensive research, the clinical and genetic relationships between AD and glaucoma remain obscure. It is unclear whether the clinical correlation between the two diseases might be due to shared risk factors or the influence of one disorder on the other. Interestingly, certain observations may provide a clue towards a better understanding of the high rate of comorbidity reported between AD and glaucoma. In this article, we hypothesise that there may be a causal relationship between AD and glaucoma that may be explained by decreased cerebrospinal fluid pressure (CSFP) in patients with AD. A very recent study reported the intriguing new observation that mean CSFP was 33% lower in subjects with primary open-angle glaucoma than that of non-glaucomatous controls. It was noted that this observation supports the concept that an abnormal high trans-lamina cribrosa pressure difference, whether the result of elevated intraocular pressure, reduced CSFP, or both, plays an important role in glaucomatous optic nerve damage. Interestingly, it was also reported that a substantial proportion of AD patients have very low CSFP. Therefore, we hypothesise that an abnormal high trans-lamina cribrosa pressure difference may explain why patients with AD have a greater risk for developing glaucoma

Neurodegeneration of the retina in mouse models of Alzheimer’s disease: what can we learn from the retina?

Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disease commonly found among elderly. In addition to cognitive and behavioral deficits, vision abnormalities are prevalent in AD patients. Recent studies investigating retinal changes in AD double-transgenic mice have shown altered processing of amyloid precursor protein and accumulation of β-amyloid peptides in neurons of retinal ganglion cell layer (RGCL) and inner nuclear layer (INL). Apoptotic cells were also detected in the RGCL. Thus, the pathophysiological changes of retinas in AD patients are possibly resembled by AD transgenic models. The retina is a simple model of the brain in the sense that some pathological changes and therapeutic strategies from the retina may be observed or applicable to the brain. Furthermore, it is also possible to advance our understanding of pathological mechanisms in other retinal degenerative diseases. Therefore, studying AD-related retinal degeneration is a promising way for the investigation on (1) AD pathologies and therapies that would eventually benefit the brain and (2) cellular mechanisms in other retinal degenerations such as glaucoma and age-related macular degeneration. This review will highlight the efforts on retinal degenerative research using AD transgenic mouse models