Animal models of neurodegenerative diseases

Ribeiro, Fabíola M.; Camargos, Elizabeth Ribeiro da Silva; Souza, Leonardo Cruz de; Teixeira, Antônio Lúcio

doi:10.1590/1516-4446-2013-1157

Cited by 45 publications

(22 citation statements)

References 118 publications

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“…Several animal models were generated to recapitulate hyperphosphorylation of tau and the formation of NFTs as key aspects of tauopathies (Ribeiro et al, 2013). Some studies showed that the overexpression of human mutant tau in transgenic mice led to increased phosphorylation of tau and the formation of tau inclusions, aggregates, and fibrils.…”

Section: Tau Phosphorylation In Alzheimer's Disease and Other Tauopatmentioning

confidence: 99%

Protein phosphorylation in neurodegeneration: friend or foe?

Tenreiro¹,

Eckermann

Outeiro

2014

Front. Mol. Neurosci.

205

194

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Protein misfolding and aggregation is a common hallmark in neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), and fronto-temporal dementia (FTD). In these disorders, the misfolding and aggregation of specific proteins occurs alongside neuronal degeneration in somewhat specific brain areas, depending on the disorder and the stage of the disease. However, we still do not fully understand the mechanisms governing protein aggregation, and whether this constitutes a protective or detrimental process. In PD, alpha-synuclein (aSyn) forms protein aggregates, known as Lewy bodies, and is phosphorylated at serine 129. Other residues have also been shown to be phosphorylated, but the significance of phosphorylation in the biology and pathophysiology of the protein is still controversial. In AD and in FTD, hyperphosphorylation of tau protein causes its misfolding and aggregation. Again, our understanding of the precise consequences of tau phosphorylation in the biology and pathophysiology of the protein is still limited. Through the use of a variety of model organisms and technical approaches, we are now gaining stronger insight into the effects of phosphorylation in the behavior of these proteins. In this review, we cover recent findings in the field and discuss how targeting phosphorylation events might be used for therapeutic intervention in these devastating diseases of the nervous system.

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Section: Tau Phosphorylation In Alzheimer's Disease and Other Tauopatmentioning

confidence: 99%

Protein phosphorylation in neurodegeneration: friend or foe?

Tenreiro¹,

Eckermann

Outeiro

2014

Front. Mol. Neurosci.

205

194

View full text Add to dashboard Cite

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“…In mammalian models, genetically modified rodents have proven critical to the understanding of PD pathology and the exploration of new therapeutic strategies (Ribeiro et al, 2013). Rodent models display many of the clinical features of PD such as the loss of dopaminergic neurons (Meredith and Rademacher, 2011; Thiele et al, 2012; Torres and Dunnett, 2012), neurochemical changes in dopamine transmission and signaling, motor dysfunction, and non-motor symptoms including cognitive decline, autonomic dysfunction, depression, and hyposmia (Taylor et al, 2010; Schirinzi et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

“…Rodent models display many of the clinical features of PD such as the loss of dopaminergic neurons (Meredith and Rademacher, 2011; Thiele et al, 2012; Torres and Dunnett, 2012), neurochemical changes in dopamine transmission and signaling, motor dysfunction, and non-motor symptoms including cognitive decline, autonomic dysfunction, depression, and hyposmia (Taylor et al, 2010; Schirinzi et al, 2016). However, these models do not mimic some important pathological hallmarks of the disease (Fleming and Chesselet, 2006; Visanji et al, 2016) such as the gradual neurodegenerative process, gross morphological abnormalities and overt motor alterations (Yue and Lachenmayer, 2011; Ribeiro et al, 2013; Schirinzi et al, 2016). Moreover, gene editing techniques in rodents involve complex experimental design, significant time investment and considerable expense.…”

Section: Introductionmentioning

confidence: 99%

Behavioral Phenotyping and Pathological Indicators of Parkinson's Disease in C. elegans Models

et al. 2017

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Parkinson's disease (PD) is a neurodegenerative disorder with symptoms that progressively worsen with age. Pathologically, PD is characterized by the aggregation of α-synuclein in cells of the substantia nigra in the brain and loss of dopaminergic neurons. This pathology is associated with impaired movement and reduced cognitive function. The etiology of PD can be attributed to a combination of environmental and genetic factors. A popular animal model, the nematode roundworm Caenorhabditis elegans, has been frequently used to study the role of genetic and environmental factors in the molecular pathology and behavioral phenotypes associated with PD. The current review summarizes cellular markers and behavioral phenotypes in transgenic and toxin-induced PD models of C. elegans.

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“…With the advancement of understanding of the pathogenesis of AD, a series of animal models of dementia have been developed (Ribeiro et al, 2013;Neha et al, 2014). An ideal animal model should exhibit all AD features in animals (Neha et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia

Liu

Zhu

Feng

et al. 2015

J. Zhejiang Univ. Sci. B

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Senile dementia (SD) is a syndrome characterized by progressive neurological deterioration. Treatment for the disease is still under investigation. Bamboo leaf extract (B-extract) has been known for its biological efficacy in anti-oxidant and anti-cancer activities. However, study on B-extract for its protection against dementia is very limited. The effect of B-extract on a rat model with SD was examined. B-extract improved spatial learning ability of the dementia rats. The hippocampus of dementia model rats showed reduced levels of acetylcholine (ACh), epinephrine (E), norepinephrine (NE), and dopamine (DA), and increased activities of acetylcholine esterase (AChE) and monoamine oxidase (MAO). Treatment with B-extract 20 mg/(kg·d) for 7 weeks significantly inhibited the enzyme activity compared with untreated dementia rats, and raised the levels of ACh, E, and DA in the hippocampus. In addition, treatment with B-extract elevated the level of γ-aminobutyric acid (GABA), but reduced the level of glutamate (Glu) in the brain. These data suggest that B-extract might be a potential drug in treating impairment of spatial memory in dementia rats by regulating the central neurotransmitter function.

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Animal models of neurodegenerative diseases

Cited by 45 publications

References 118 publications

Protein phosphorylation in neurodegeneration: friend or foe?

Protein phosphorylation in neurodegeneration: friend or foe?

Behavioral Phenotyping and Pathological Indicators of Parkinson's Disease in C. elegans Models

Bamboo leaf extract improves spatial learning ability in a rat model with senile dementia

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