Enfermedad de Alzheimer

Martínez, D. Barragán; Soldevilla, M.A. García; Santiago, A. Parra; Martínez, J.

doi:10.1016/j.med.2019.03.012

Cited by 19 publications

(7 citation statements)

References 33 publications

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“…Varios pacientes suelen permanecer con afectación de la memoria reciente por años antes de llegar a la demencia. (11,12) Posterior a la aparición de la amnesia, viene la disfunción ejecutiva y la pérdida de las habilidades…”

Section: Apoyo Social Y Educaciónunclassified

Temas Selectos en Salud Mental Tomo 2

Grijalva Andrade,

Flores Enriquez,

Ávila Fray

et al. 2023

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Section: Apoyo Social Y Educaciónunclassified

Temas Selectos en Salud Mental Tomo 2

Grijalva Andrade,

Flores Enriquez,

Ávila Fray

et al. 2023

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“…The classical neuropathological hallmarks for AD include Aβ-amyloid-containing neuritic plaques and phosphorylated Tau-containing neurofibrillary tangles (NFT) ( Karch et al, 2014 ). In addition, significant synaptic loss, selective neuronal death, neurotransmitter defects and neuroinflammation are also observed in AD ( Karch and Goate, 2015 ; Barragán Martínez et al, 2019 ). Despite the tremendous efforts and investments in the past decades, there are currently no disease-modifying therapy for effective treatments of AD ( Doody et al, 2013a ; Doody et al, 2013b ; Gauthier et al, 2016 ).…”

Section: Rin3 and Human Diseasesmentioning

confidence: 99%

Ras and Rab Interactor 3: From Cellular Mechanisms to Human Diseases

Shen

Murphy

et al. 2022

Front. Cell Dev. Biol.

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Ras and Rab interactor 3 (RIN3) functions as a Guanine nucleotide Exchange Factor (GEF) for some members of the Rab family of small GTPase. By promoting the activation of Rab5, RIN3 plays an important role in regulating endocytosis and endocytic trafficking. In addition, RIN3 activates Ras, another small GTPase, that controls multiple signaling pathways to regulate cellular function. Increasing evidence suggests that dysregulation of RIN3 activity may contribute to the pathogenesis of several disease conditions ranging from Paget’s Disease of the Bone (PDB), Alzheimer’s Disease (AD), Chronic Obstructive Pulmonary Disease (COPD) and to obesity. Recent genome-wide association studies (GWAS) identified variants in the RIN3 gene to be linked with these disease conditions. Interestingly, some variants appear to be missense mutations in the functional domains of the RIN3 protein while most variants are located in the noncoding regions of the RIN3 gene, potentially altering its gene expression. However, neither the protein structure of RIN3 nor its exact function(s) (except for its GEF activity) has been fully defined. Furthermore, how the polymorphisms/variants contribute to disease pathogenesis remain to be understood. Herein, we examine, and review published studies in an attempt to provide a better understanding of the physiological function of RIN3; More importantly, we construct a framework linking the polymorphisms/variants of RIN3 to altered cell signaling and endocytic traffic, and to potential disease mechanism(s).

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“…Alzheimer's disease (AD) is a progressive neurodegenerative disease of the brain that is characterized by memory impairment and cognitive dysfunction [1,2]. Pathological hallmarks of AD are the deposition of amyloid beta (Aβ) plaques and neurofibrillary tangles [3,4].…”

Section: Introductionmentioning

confidence: 99%

Altered Brain Leptin and Leptin Receptor Expression in the 5XFAD Mouse Model of Alzheimer’s Disease

Pratap

Holsinger

2020

Pharmaceuticals

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Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by the accumulation of amyloid plaques and neurofibrillary tangles. Interestingly, individuals with metabolic syndromes share some pathologies with those diagnosed with AD including neuroinflammation, insulin resistance and cognitive deficits. Leptin, an adipocyte-derived hormone, regulates metabolism, energy expenditure and satiety via its receptor, LepR. To investigate the possible involvement of leptin in AD, we examined the distribution of leptin and LepR in the brains of the 5XFAD mouse model of AD, utilizing immunofluorescent staining in young (10–12-weeks; n = 6) and old (48–52-weeks; n = 6) transgenic (Tg) mice, together with age-matched wild-type (WT) controls for both age groups (young-WT, n = 6; old-WT, n = 6). We also used double immunofluorescent staining to examine the distribution of leptin and leptin receptor expression in astrocytes. In young 5XFAD, young-WT and old-WT mice, we observed neuronal and endothelial expression of leptin and LepR throughout the brain. However, neuronal leptin and LepR expression in the old 5XFAD brain was significantly diminished. Reduced neuronal leptin and LepR expression was accompanied by plaque loading and neuroinflammation in the AD brain. A marked increase in astrocytic leptin and LepR was also observed in old 5XFAD mice compared to younger 5XFAD mice. We postulate that astrocytes may utilize LepR signalling to mediate and drive their metabolically active state when degrading amyloid in the AD brain. Overall, these findings provide evidence of impaired leptin and LepR signalling in the AD brain, supporting clinical and epidemiological studies performed in AD patients.

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Enfermedad de Alzheimer

Cited by 19 publications

References 33 publications

Temas Selectos en Salud Mental Tomo 2

Temas Selectos en Salud Mental Tomo 2

Ras and Rab Interactor 3: From Cellular Mechanisms to Human Diseases

Altered Brain Leptin and Leptin Receptor Expression in the 5XFAD Mouse Model of Alzheimer’s Disease

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