| Autor: |
Baracaldo-Santamaría D; Pharmacology Unit, Department of Biomedical Sciences, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia., Avendaño-Lopez SS; Pharmacology Unit, Department of Biomedical Sciences, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia., Ariza-Salamanca DF; Medical and Health Sciences Education Research Group, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia., Rodriguez-Giraldo M; Grupo de Investigación en Neurociencias (NeURos), Centro de Neurociencias Neurovitae-UR, Instituto de Medicina Traslacional (IMT), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá 111221, Colombia., Calderon-Ospina CA; Pharmacology Unit, Department of Biomedical Sciences, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia.; Grupo de Investigación en Ciencias Biomédicas Aplicadas (UR Biomed), School of Medicine and Health Sciences, Universidad del Rosario, Bogotá 111221, Colombia., González-Reyes RE; Grupo de Investigación en Neurociencias (NeURos), Centro de Neurociencias Neurovitae-UR, Instituto de Medicina Traslacional (IMT), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá 111221, Colombia., Nava-Mesa MO; Grupo de Investigación en Neurociencias (NeURos), Centro de Neurociencias Neurovitae-UR, Instituto de Medicina Traslacional (IMT), Escuela de Medicina y Ciencias de la Salud, Universidad del Rosario, Bogotá 111221, Colombia. |
| Abstrakt: |
Alzheimer's disease (AD) is a chronic neurodegenerative disease and the most frequent cause of progressive dementia in senior adults. It is characterized by memory loss and cognitive impairment secondary to cholinergic dysfunction and N-methyl-D-aspartate (NMDA)-mediated neurotoxicity. Intracellular neurofibrillary tangles, extracellular plaques composed of amyloid-β (Aβ), and selective neurodegeneration are the anatomopathological hallmarks of this disease. The dysregulation of calcium may be present in all the stages of AD, and it is associated with other pathophysiological mechanisms, such as mitochondrial failure, oxidative stress, and chronic neuroinflammation. Although the cytosolic calcium alterations in AD are not completely elucidated, some calcium-permeable channels, transporters, pumps, and receptors have been shown to be involved at the neuronal and glial levels. In particular, the relationship between glutamatergic NMDA receptor (NMDAR) activity and amyloidosis has been widely documented. Other pathophysiological mechanisms involved in calcium dyshomeostasis include the activation of L-type voltage-dependent calcium channels, transient receptor potential channels, and ryanodine receptors, among many others. This review aims to update the calcium-dysregulation mechanisms in AD and discuss targets and molecules with therapeutic potential based on their modulation. |
