Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease

Daniela Baracaldo-Santamaría; Sara Sofía Avendaño-López; Daniel Felipe Ariza Salamanca; Mateo Rodríguez-Giraldo; Carlos Alberto Calderon Ospina; Rodrigo Esteban Gonzalez Reyes; Mauricio Orlando Nava Mesa

doi:10.3390/ijms24109067

Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease

Título traducido de la contribución: Papel de la modulacion de calcio en la fisiopatología y el tratamiento de la enfermedad de Alzheimer

Daniela Baracaldo-Santamaría
, Sara Sofía Avendaño-López
, Daniel Felipe Ariza Salamanca
, Mateo Rodríguez-Giraldo
, Carlos Alberto Calderon Ospina
, Rodrigo Esteban Gonzalez Reyes
, Mauricio Orlando Nava Mesa

Producción científica: Contribución a revista › Artículo de revisión › revisión exhaustiva

59 Citas (Scopus)

132 Descargas (Pure)

Resumen

La enfermedad de Alzheimer (EA) es una enfermedad neurodegenerativa crónica y la más frecuente causa de demencia progresiva en adultos mayores. Se caracteriza por la pérdida de la memoria y la capacidad cognitiva, deterioro secundario a disfunción colinérgica y mediado por N-metil-D-aspartato (NMDA) y neurotoxicidad, ovillos neurofibrilares intracelulares, placas extracelulares compuestas de amiloide-β (Aβ) y la neurodegeneración selectiva son las características anatomopatológicas de esta enfermedad. La desregulación del calcio puede estar presente en todas las etapas de la EA y se asocia con otros mecanismos fisiopatológicos, como insuficiencia mitocondrial, estrés oxidativo y
neuroinflamación. Aunque las alteraciones del calcio citosólico en la EA no están del todo aclaradas, se ha demostrado que algunos canales permeables al calcio, transportadores, bombas y receptores están involucrados a nivel neuronal y glial. En particular, la relación entre el NMDA glutamatérgico la actividad del receptor (NMDAR) y la amiloidosis ha sido ampliamente documentada. Los mecanismos involucrados en la dishomeostasis del calcio incluyen la activación de tipo L dependiente de voltaje, canales de calcio, canales de potencial receptor transitorio y receptores de rianodina, entre muchos otros. Esta revisión tiene como objetivo actualizar los mecanismos de desregulación del calcio en la EA y discutir los objetivos y moléculas con potencial terapéutico en función de su modulación.

Título traducido de la contribución	Papel de la modulacion de calcio en la fisiopatología y el tratamiento de la enfermedad de Alzheimer
Idioma original	Inglés estadounidense
Número de artículo	9067
Páginas (desde-hasta)	1-42
Número de páginas	42
Publicación	International Journal of Molecular Sciences
Volumen	24
DOI	https://doi.org/10.3390/ijms24109067
Estado	Publicada - may. 22 2023

ODS de las Naciones Unidas

Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

ODS 3: Salud y bienestar

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Neurociencias General
Neurociencia (miscelánea)

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2023 (Baracaldo-Santamaria D) - Role of calcium modulation in the pathophysiology and treatment of Alzheimer´s disease (Review)Versión de la editorial, 2,14 MB

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Baracaldo-Santamaría, D., Avendaño-López, S. S., Ariza Salamanca, D. F., Rodríguez-Giraldo, M., Calderon Ospina, C. A., Gonzalez Reyes, R. E., & Nava Mesa, M. O. (2023). Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease. International Journal of Molecular Sciences, 24, 1-42. Artículo 9067. https://doi.org/10.3390/ijms24109067

@article{89039c31a2c34a2db94239ae1f04ebb0,

title = "Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer{\textquoteright}s Disease",

abstract = "Alzheimer{\textquoteright}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.",

author = "Daniela Baracaldo-Santamar{\'i}a and Avenda{\~n}o-L{\'o}pez, \{Sara Sof{\'i}a\} and \{Ariza Salamanca\}, \{Daniel Felipe\} and Mateo Rodr{\'i}guez-Giraldo and \{Calderon Ospina\}, \{Carlos Alberto\} and \{Gonzalez Reyes\}, \{Rodrigo Esteban\} and \{Nava Mesa\}, \{Mauricio Orlando\}",

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month = may,

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doi = "10.3390/ijms24109067",

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Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease. / Baracaldo-Santamaría, Daniela; Avendaño-López, Sara Sofía; Ariza Salamanca, Daniel Felipe et al.
En: International Journal of Molecular Sciences, Vol. 24, 9067, 22.05.2023, p. 1-42.

Producción científica: Contribución a revista › Artículo de revisión › revisión exhaustiva

TY - JOUR

T1 - Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease

AU - Baracaldo-Santamaría, Daniela

AU - Avendaño-López, Sara Sofía

AU - Ariza Salamanca, Daniel Felipe

AU - Rodríguez-Giraldo, Mateo

AU - Calderon Ospina, Carlos Alberto

AU - Gonzalez Reyes, Rodrigo Esteban

AU - Nava Mesa, Mauricio Orlando

PY - 2023/5/22

Y1 - 2023/5/22

N2 - 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.

AB - 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.

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DO - 10.3390/ijms24109067

M3 - Review article

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SN - 1661-6596

VL - 24

SP - 1

EP - 42

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

M1 - 9067

ER -

Role of Calcium Modulation in the Pathophysiology and Treatment of Alzheimer’s Disease

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