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Kai Kaarniranta
Department of Ophthalmology, University of Eastern Finland, Kuopio, Finland
Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland
Age-related macular degeneration (AMD) is a late-onset, neurodegenerative retinal disease that shares several clinical and pathological features with Alzheimer's disease (AD), including stress stimuli such as oxidative stress and inflammation. In both diseases, the detrimental intra- and extracellular deposits have many similarities. Aging, hypercholesterolaemia, hypertension, obesity, arteriosclerosis, and smoking are risk factors to develop AMD and AD. Cellular aging processes have similar organelle and signaling association in the retina and brain tissues. However, it seems that these diseases have a different genetic background.
Michał Bogocz
Department of Ophthalmology, Professor K. Gibinski University Clinical Center, Medical
University of Silesia, Katowice, Poland
Retinal imaging methods have shown promise as potential tools for identifying markers of neurodegenerative diseases. Some of the key markers and features observed in retinal imaging that may be indicative of neurodegenerative conditions, such as Retinal Nerve Fiber Layer (RNFL) and Ganglion Cell Layer (GCL) thinning, retinal microvascular changes, retinal Amyloid Beta (Aβ) deposits, vascular changes in the retina, changes in the optic nerve head. All of these have been linked with various neurodegenerative diseases, including Alzheimer’s disease, multiple sclerosis and Parkinson’s disease. Aβ plaques are characteristic of Alzheimer’s disease, and their presence in the retina may provide a non-invasive method for early detection. Its important to note that while these markers show promise, they are not definitive diagnostic tools on their own. Research in this field is ongoing, and further studies are needed to validate the reliability and specificity of these retinal
imaging markers for different neurodegenerative diseases.
Piotr Rodak
Department of Physiology, Faculty of Medical Sciences in Katowice, Medical University of
Silesia in Katowice, Katowice, Poland
Department of Paediatric Neurology, Faculty of Medical Sciences in Katowice, Medical
University of Silesia, Katowice, Poland
The relationship between menopause and neurodegeneration is an area of ongoing research. Menopause is a natural biological process that marks the end of a woman's reproductive years and is associated with hormonal changes, particularly a decline in estrogen levels. Estrogen receptors are found in various tissues throughout the body, including the brain, and estrogen has been shown to have neuroprotective effects. Therefore, the hormonal changes during menopause may influence brain health and potentially contribute to neurodegeneration. Researchers have paid particular attention to age-related neurodegenerative diseases because of the overlap of endocrine and neuronal dysfunction observed during aging. Hormonal decline (especially a lack of estrogens during the perimenopausal period) is an important risk factor for ocular neurodegenerative diseases, such as glaucoma, ischemic optic neuropathy and retinopathy, age-related macular degeneration, and diabetic retinopathy. On the other hand, population-based studies highlighted a substantial difference in the prevalence of dementia between men and women, with Alzheimer-associated dementia being more prevalent in women, indicating that estrogen deficiency might be a risk factor for neurodegenerative diseases.
Funding: National Science Centre (Poland) grant: NCN PRELUDIUM 2021/41/N/NZ4/01271.
Anna Pacwa
Department of Physiology, Faculty of Medical Sciences in Katowice, Medical University of Silesia in Katowice, Katowice, Poland
The decline of Retinal Ganglion Cells (RGC) is a gradual process that occurs slowly over time and is associated with the aging process. External factors, such as ischemia, elevated intraocular pressure, or inflammation, may expedite this age-related cell deterioration, ultimately resulting in blindness by impairing RGC function. Neuroprotective mechanisms aim to mitigate the adverse chain reactions triggered by such insults, thereby extending the survival of RGC. Remarkably, one of the RNA-binding proteins, the ELAVL1 has been identified as a regulatory factor for many stress response-related proteins, positioning it as a crucial element in the network of neuroprotective pathways. It has been demonstrated that silencing the HuR gene accelerates retinal aging in healthy conditions and leads to significant RGC loss in a glaucoma model. Furthermore, it has been shown that functional level of the ELAVL1 protein is pivotal for efficient activity of neuroprotection therapies. Similarly as in the retina, the ELAVL1 has been studied in the context of Alzheimer’s disease due to its role in post-transcriptional regulation of gene expression.
