Marcaje colinérgico en la corteza cerebral y el hipocampo en algunas especies animales y su relación con la enfermedad de Alzheimer

Orta‐Salazar, Erika; Cuellar-Lemus, C.A.; Dı́az-Cintra, Sofı́a; Feria‐Velasco, Alfredo

doi:10.1016/j.nrl.2012.10.007

Cited by 26 publications

(4 citation statements)

References 36 publications

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“…Cumulative evidence has suggested that cognitive dysfunction in AD is the result of impaired neurogenesis in the hippocampus of the adult brain, and it is crucial to identify novel drugs that can be used for the treatment of AD [27,28]. The cholinergic function is reduced in the forebrain, especially in the hippocampus, and a change in AChE activity in the hippocampus is usually a biomarker for diagnosing AD [29]. SCO impairs memory in rodents and humans, which interferes with the cholinergic system, including ACh, and causes oxidative stress, leading to cognitive dysfunction [30,31,32].…”

Section: Discussionmentioning

confidence: 99%

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Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

Sohn

Lim

Kim

et al. 2019

IJMS

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We explored the preventative effect of Annona atemoya leaf (AAL) extract on memory impairment in a scopolamine (SCO)-induced cognitive deficit mouse model. Fifty-eight mice were randomly divided into six groups and orally treated with AAL extract at (50, 100, or 200 mg/kg) or tacrine (TAC) for 21 days. Memory deficits were induced by a single injection of 1 mg/kg SCO (i.p.) and memory improvement was evaluated by using behavioral tests such as the passive avoidance task and Y-maze test. The levels of cholinergic functions, neuronal cell death, reactive oxygen species, and protein expression related to hippocampal neurogenesis were examined by immunohistochemical staining and western blotting. The administration of AAL extract improved memory impairment according to increased spontaneous alternation in the Y-maze and step-through latency in passive avoidance test. AAL extract treatment increased the acetylcholine content, choline acetyltransferase, and acetylcholinesterase activity in the hippocampus of SCO-stimulated mice. In addition, AAL extract attenuated oxidative stress-induced neuronal cell death of hippocampal tissue. In terms of the regulatory mechanisms, AAL extract treatment reversed the SCO-induced decreases in the expression of Akt, phosphorylation of cAMP response element binding protein, and brain-derived neurotrophic factor. Our findings demonstrate that AAL extract has the ability to alleviate memory impairment through preventative effect on cholinergic system dysfunction and oxidative stress-related neuronal cell death in a SCO-induced memory deficit animal model. Overall, AAL may be a promising plant resource for the managing memory dysfunction due to neurodegenerative diseases, such as Alzheimer’s disease (AD).

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Section: Discussionmentioning

confidence: 99%

“…AD is highly related to cholinergic system impairment and intracellular oxidative stress [7,29]. Hippocampal cholinergic dysfunction has been identified in neurodegenerative diseases that are characterized by memory impairment, including AD, and in animal experiments [33,34].…”

Section: Discussionmentioning

confidence: 99%

Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

Sohn

Lim

Kim

et al. 2019

IJMS

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“…At the same time, ChAT can help to catalyze the biosynthesis of acetylcholine [29]. Thus changes in AChE and ChAT activities are often used as cholinergic biomarkers for diagnose AD [30]. In this study, walnut oil treatment significantly inhibited AChE activity and promoted ChAT activity in the brain of cognitive deficient mice.…”

Section: Discussionmentioning

confidence: 71%

Walnut Oil Prevents Scopolamine-Induced Memory Dysfunction in a Mouse Model

Liao

Nai

et al. 2020

Molecules

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For thousands of years, it has been widely believed that walnut is a kind of nut that has benefits for the human body. Walnut oil, accounting for about 70% of walnut, mainly consists of polyunsaturated fatty acids. To investigate the effect of walnut oil on memory impairment in mice, scopolamine (3 mg/kg body weight/d) was used to establish the animal model during Morris Water Maze (MWM) tests. Walnut oil was administrated orally at 10 mL/kg body weight/d for 8 consecutive weeks. The results showed that walnut oil treatment ameliorated the behavior of the memory-impaired mice in the MWM test. Additionally, walnut oil obviously inhibited acetylcholinesterase activity (1.26 ± 0.12 U/mg prot) (p = 0.013) and increased choline acetyltransferase activity (129.75 ± 6.76 U/mg tissue wet weight) in the brains of scopolamine-treated mice (p = 0.024), suggesting that walnut oil could prevent cholinergic function damage in mice brains. Furthermore, walnut oil remarkably prevented the decrease in total superoxide dismutase activity (93.30 ± 5.50 U/mg prot) (p = 0.006) and glutathione content (110.45 ± 17.70 mg/g prot) (p = 0.047) and the increase of malondialdehyde content (13.79 ± 0.96 nmol/mg prot) (p = 0.001) in the brain of scopolamine-treated mice, indicating that walnut oil could inhibit oxidative stress in the brain of mice. Furthermore, walnut oil prevented histological changes of neurons in hippocampal CA1 and CA3 regions induced by scopolamine. These findings indicate that walnut oil could prevent memory impairment in mice, which might be a potential way for the prevention of memory dysfunctions.

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“…Una de las funciones elementales de la vía colinérgica se basa en la regulación del ciclo de vigilia y sueño, así como en la modulación de los procesos de aprendizaje y memoria, de forma que la disfunción de la neurotransmisión colinérgica supone una hipótesis explicativa sobre la aparición de los déficits cognitivos y de la gravedad de la EA (Orta-Salazar, Cuellar-Lemus, Díaz-Cintra & Feria-Velasco, 2014). Datos recientes apuntan a una redefinición de la hipótesis colinérgica en la que el déficit colinérgico impide al cerebro la capacidad de compensación frente a otros factores de riesgo neuropatológicos concomitantes (Craig, Hong & McDonald, 2011) y es susceptible de ser investigada mediante la pupilometría (Fotiou, Kaltsatou, Tsiptsios, Nakou, 2015).…”

Section: Hipótesis Colinérgicaunclassified

Sinopsis Del Alzheimer

2020

EDITORIAL

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A pesar de que la Enfermedad de Alzheimer (EA) supone la primera causa de demencia (Alzheimer`s Association, 2015; García-Alberca et al., 2008) su etiología sigue siendo de naturaleza desconocida y multifactorial, por lo que algunas de las principales líneas de investigación actuales se han basado en el estudio de los factores epidemiológicos, genéticos, neuropatológicos, así como en diferentes métodos de análisis orientados al diagnóstico precoz de la enfermedad. A pesar de la ausencia de un biomarcador completamente fiable para diagnosticar in vivo la EA, existen múltiples manifestaciones clínicas como la presencia de sintomatología cognitiva, neuroconductual y funcional que siguen constituyendo la tríada fundamental para describir tanto el diagnóstico como el curso evolutivo de la enfermedad. Se puede conceptualizar la EA como una enfermedad neurodegenerativa, cortical, primaria, de inicio insidioso, curso lento, progresivo e irreversible, producida por la acumulación de proteína beta- amiloide y que genera una serie de alteraciones cognitivas cuyo síntoma nuclear es la pérdida de memoria. En el desarrollo de la misma, surgen otras alteraciones afásico-práxico-gnósicas junto con alteraciones neuropsiquiátricas como presencia de síntomas de ansiedad y depresión, y afectación en la esfera funcional para la realización de actividades de la vida diaria como el manejo de asuntos económicos. Los datos epidemiológicos apuntan a que la demencia causada por EA se está convirtiendo en una epidemia a nivel mundial, puesto que se estima que, en la década del 2020, las cifras puedan alcanzar casi los 70 millones de personas. Uno de los principales factores de riesgo que afectan sobre la incidencia de la EA es la edad, ya que a partir de los 65 años se multiplica la probabilidad de desarrollarla, factor que ha aumentado durante el último siglo por el enorme progreso en el sector sanitario. De manera similar, la prevalencia tiende a ser de 10 a 20% entre los 80 a los 90 años, lo que sugiere que sigue una relación de carácter exponencial.

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Marcaje colinérgico en la corteza cerebral y el hipocampo en algunas especies animales y su relación con la enfermedad de Alzheimer

Abstract: This paper reviews the main immunomorphological studies of the cerebral cortex and hippocampus in some animal species with particular emphasis on the cholinergic system and its relationship with the AD.

Cited by 26 publications

References 36 publications

Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

Annona atemoya Leaf Extract Improves Scopolamine-Induced Memory Impairment by Preventing Hippocampal Cholinergic Dysfunction and Neuronal Cell Death

Walnut Oil Prevents Scopolamine-Induced Memory Dysfunction in a Mouse Model

Sinopsis Del Alzheimer

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