Age-related macular degeneration (AMD) is the leading cause of blindness in the aged population. The accumulation of abnormal extracellular drusen deposits between the retinal pigment epithelium (RPE) and Bruch's membrane is a significant driver of AMD pathology. Drusen deposition leads to the degeneration of RPE cells and, subsequently, photoreceptors, driving the disease to its advanced stages and ultimately resulting in complete vision loss. Although the exact mechanisms underlying the AMD pathogenesis are not fully understood, it is hypothesized that the disease begins with the dysfunction of the RPE, triggering the complement and pro-inflammatory cascade. Over the last decade, new findings have implicated the involvement of cellular senescence (CS) in the pathology of age-related disorders. Specifically for AMD, evidence suggests that the senescence of RPE cells may play a role in the pathogenesis of the disease. In this review, we discuss the potential role of senescence in the onset and progression of AMD and propose potential therapeutic interventions that could be developed by targeting senescence.
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http://dx.doi.org/10.1007/978-3-031-76550-6_6 | DOI Listing |
Aging Cell
March 2025
Department of Biochemistry and Physiology, University of Oklahoma Health Sciences, Oklahoma City, Oklahoma, USA.
Cognitive function in aging is heterogeneous: while some older individuals develop significant impairments and dementia, others remain resilient and retain cognitive function throughout their lifespan. The molecular mechanisms that underlie these divergent cognitive trajectories, however, remain largely unresolved. Here, we utilized a high-resolution home-cage-based cognitive testing paradigm to delineate mechanisms that contribute to age-related cognitive heterogeneity.
View Article and Find Full Text PDFCurr Neuropharmacol
March 2025
Laboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smętna St. 31-343 Kraków, Poland.
Introduction: Brain aging is a complex process involving genetic, neurodevelopmental, and environmental factors. Inherent features of this process are cellular senescence, the development of senescence-associated secretory phenotype (SASP), and prolonged inflammation.
Methods: Recently, progress has been made in understanding the biological roles of FPR2 receptors and their ligands in the mechanism of inflammation resolution (RoI) in the brain.
Int J Mol Sci
March 2025
Unidad Mixta de Investigación Cerebrovascular, Instituto de Investigación Sanitaria La Fe, Hospital Universitario y Politécnico La Fe, 46026 Valencia, Spain.
In recent years, evidence of the existence of cellular senescence in the central nervous system has accumulated. In ischemic stroke, cellular senescence has been suggested as an unidentified pathophysiological mechanism, prompting research into the neuroprotective potential of senolytic drugs. This study aims to provide spatio-temporal evidence of the existence of brain senescence following ischemic stroke and to elucidate the involved pathways and cell types.
View Article and Find Full Text PDFInt J Mol Sci
March 2025
Biospectrum Life Science Institute, Sinsu-ro, Suji-gu, Yongin-City 16827, Gyeonggi-Do, Republic of Korea.
The activation of hair follicle dermal papilla cells (HFDPCs), a critical target of hair loss relief, can be achieved through the upregulation of proliferation, the stimulation of hair inducibility, and the inhibition of cellular senescence. Veratric acid (VA) is a major benzoic acid found in fruits and vegetables. The biological activity of VA on HFDPCs remains to be elucidated.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Department of Biomedical and Neuromotor Sciences, University of Bologna, Piazza di Porta San Donato 2, 40126 Bologna, Italy.
deficiency disorder (CDD), a developmental encephalopathy caused by mutations in the cyclin-dependent kinase-like 5 () gene, is characterized by a complex and severe clinical picture, including early-onset epilepsy and cognitive, motor, visual, and gastrointestinal disturbances. This disease still lacks a medical treatment to mitigate, or reverse, its course and improve the patient's quality of life. Although CDD is primarily a genetic brain disorder, some evidence indicates systemic abnormalities, such as the presence of a redox imbalance in the plasma and skin fibroblasts from CDD patients and in the cardiac myocytes of a mouse model of CDD.
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