scholarly journals Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models

2020 ◽  
Vol 21 (21) ◽  
pp. 8144
Author(s):  
Oliver Wirths ◽  
Silvia Zampar

Transgenic mouse models represent an essential tool for the exploration of Alzheimer’s disease (AD) pathological mechanisms and the development of novel treatments, which at present provide only symptomatic and transient effects. While a variety of mouse models successfully reflects the main neuropathological hallmarks of AD, such as extracellular amyloid-β (Aβ) deposits, intracellular accumulation of Tau protein, the development of micro- and astrogliosis, as well as behavioral deficits, substantial neuron loss, as a key feature of the disease, seems to be more difficult to achieve. In this review, we summarize information on classic and more recent transgenic mouse models for AD, focusing in particular on loss of pyramidal, inter-, and cholinergic neurons. Although the cause of neuron loss in AD is still a matter of scientific debate, it seems to be linked to intraneuronal Aβ accumulation in several transgenic mouse models, especially in pyramidal neurons.

2004 ◽  
Vol 25 ◽  
pp. S11
Author(s):  
Thomas A. Bayer ◽  
Oliver Wirths ◽  
Caty Casas ◽  
Patrick Benoit ◽  
Christoph Schmitz ◽  
...  

2016 ◽  
Vol 53 (3) ◽  
pp. 773-785 ◽  
Author(s):  
José Antonio Allué ◽  
Leticia Sarasa ◽  
María Izco ◽  
Virginia Pérez-Grijalba ◽  
Noelia Fandos ◽  
...  

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 870 ◽  
Author(s):  
Raluca Stefanescu ◽  
Gabriela Dumitriṭa Stanciu ◽  
Andrei Luca ◽  
Luminita Paduraru ◽  
Bogdan-Ionel Tamba

Alzheimer’s disease is a neurodegenerative disorder for which there is a continuous search of drugs able to reduce or stop the cognitive decline. Beta-amyloid peptides are composed of 40 and 42 amino acids and are considered a major cause of neuronal toxicity. They are prone to aggregation, yielding oligomers and fibrils through the inter-molecular binding between the amino acid sequences (17–42) of multiple amyloid-beta molecules. Additionally, amyloid deposition causes cerebral amyloid angiopathy. The present study aims to identify, in the existing literature, natural plant derived products possessing inhibitory properties against aggregation. The studies searched proved the anti-aggregating effects by the thioflavin T assay and through behavioral, biochemical, and histological analysis carried out upon administration of natural chemical compounds to transgenic mouse models of Alzheimer’s disease. According to our present study results, fifteen secondary metabolites from plants were identified which presented both evidence coming from the thioflavin T assay and transgenic mouse models developing Alzheimer’s disease and six additional metabolites were mentioned due to their inhibitory effects against fibrillogenesis. Among them, epigallocatechin-3-gallate, luteolin, myricetin, and silibinin were proven to lower the aggregation to less than 40%.


2014 ◽  
Vol 39 (4) ◽  
pp. 871-881 ◽  
Author(s):  
Jochim Reinert ◽  
Henrik Martens ◽  
Melanie Huettenrauch ◽  
Tekla Kolbow ◽  
Lars Lannfelt ◽  
...  

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