Alzheimer's Disease: Definition, Molecular and Genetic Factors

Babušíková, Eva; Evinová, Andrea; Jurečeková, Jana; Jeseňák, Miloš; Dobrota, Dušan

doi:10.5772/29027

Cited by 7 publications

(7 citation statements)

References 127 publications

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“…Pathogenesis of AD is complex and involves many molecular, cellular, biochemical and physiological pathologies [9]. Alzheimer`s disease is a characteristic process with identifiable clinical state which are in a continuity with normal ageing process.…”

Section: Alzheimer`s Diseasementioning

confidence: 99%

Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

Babušíková¹,

Evinová²,

Hatok³

et al. 2013

Neurodegenerative Diseases

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Section: Alzheimer`s Diseasementioning

confidence: 99%

Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

Babušíková¹,

Evinová²,

Hatok³

et al. 2013

Neurodegenerative Diseases

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“…It covers a broad range of symptoms strictly associated with a significant decline in memory and aggravation of cognitive function [3]. Globally, 1-6% of the human population over 65 years old and 10-20% of those over 80 years old suffer from dementia [4]. The newest data have reported that due to the rapid aging of the world population, the incidence of dementia may significantly increase to approximately 65 million before 2030 and 115 million before 2050 [5].…”

Section: Introductionmentioning

confidence: 99%

The PERK-Dependent Molecular Mechanisms as a Novel Therapeutic Target for Neurodegenerative Diseases

Rozpędek‐Kamińska

Siwecka

Wawrzynkiewicz

et al. 2020

IJMS

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Higher prevalence of neurodegenerative diseases is strictly connected with progressive aging of the world population. Interestingly, a broad range of age-related, neurodegenerative diseases is characterized by a common pathological mechanism—accumulation of misfolded and unfolded proteins within the cells. Under certain circumstances, such protein aggregates may evoke endoplasmic reticulum (ER) stress conditions and subsequent activation of the unfolded protein response (UPR) signaling pathways via the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-dependent manner. Under mild to moderate ER stress, UPR has a pro-adaptive role. However, severe or long-termed ER stress conditions directly evoke shift of the UPR toward its pro-apoptotic branch, which is considered to be a possible cause of neurodegeneration. To this day, there is no effective cure for Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), or prion disease. Currently available treatment approaches for these diseases are only symptomatic and cannot affect the disease progression. Treatment strategies, currently under detailed research, include inhibition of the PERK-dependent UPR signaling branches. The newest data have reported that the use of small-molecule inhibitors of the PERK-mediated signaling branches may contribute to the development of a novel, ground-breaking therapeutic approach for neurodegeneration. In this review, we critically describe all the aspects associated with such targeted therapy against neurodegenerative proteopathies.

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“…According to reports, two types of AD exist. Sporadic AD accounts for 90–95% of all AD cases, and the familial form of AD accounts for 5–10% (Bhat, 2010 ; Babusikova et al, 2011 ). Current statistics indicate that a person in America develops AD every 67 s. By 2050, a new case of AD is expected to develop every 33 s, and nearly 1 million new cases per year is expected to arise (Alzheimer's Association, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Analyses of mRNA Profiling through RNA Sequencing on a SAMP8 Mouse Model in Response to Ginsenoside Rg1 and Rb1 Treatment

Zhang

Zhu

et al. 2017

Front. Pharmacol.

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Ginsenoside Rg1 and Rb1 are the major ingredients in two medicines called QiShengLi (Z20027165) and QiShengJing (Z20027164) approved by China. These ingredients are believed to mitigate forgetfulness. Numerous studies have confirmed that GRg1 and GRb1 offer protection against Alzheimer's disease (AD), and our morris water maze (MWM) experiment also indicated that GRg1 and GRb1 may attenuate memory deficits in the 7-month-old SAMP8 mice; however, comprehensive understanding of their roles in AD remains limited. This study systematically explored the mechanism at the genome level of the anti-AD effects of GRg1 and GRb1 in a senescence-accelerated mouse prone 8 (SAMP8) model through deep RNA sequencing. A total of 74,885 mRNA transcripts were obtained. Expression analysis showed that 1,780 mRNA transcripts were differentially expressed in SAMP8 mice compared with the SAMP8+GRg1 mice. Moreover, 1,066 significantly dysregulated mRNA transcripts were identified between SAMP8 and SAMP8+GRb1 mice. Analyses according to gene ontology and the Kyoto Encyclopedia of Genes and Genomes revealed that oral administration of GRg1 and GRb1 improved the learning performance of the SAMP8 mouse model from various aspects, such as nervous system development and mitogen-activated protein kinase signaling pathway. The most probable AD-related transcriptional responses after medication were predicted and discussed in detail. This study is the first to provide a systematic dissection of mRNA profiling in SAMP8 mouse brain in response to GRg1 and GRb1 treatment. We explained their efficacy thoroughly from the source (gene-level explanation). The findings serve as a theoretical basis for the exploration of GRg1 and GRb1 as functional drugs with anti-AD activity.

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Alzheimer's Disease: Definition, Molecular and Genetic Factors

Cited by 7 publications

References 127 publications

Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

Oxidative Changes and Possible Effects of Polymorphism of Antioxidant Enzymes in Neurodegenerative Disease

The PERK-Dependent Molecular Mechanisms as a Novel Therapeutic Target for Neurodegenerative Diseases

Analyses of mRNA Profiling through RNA Sequencing on a SAMP8 Mouse Model in Response to Ginsenoside Rg1 and Rb1 Treatment

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