Mutant ubiquitin decreases amyloid β plaque formation in a transgenic mouse model of Alzheimer’s disease

2012 ◽  
Vol 61 (5) ◽  
pp. 739-748 ◽  
Author(s):  
Paula van Tijn ◽  
Frank J.A. Dennissen ◽  
Romina J.G. Gentier ◽  
Barbara Hobo ◽  
Denise Hermes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Amyloid Β ◽  
Transgenic Mouse Model ◽  
Plaque Formation ◽  
Model Of Alzheimer’S Disease

scholarly journals Tetrahydrobiopterin Improves Recognition Memory in the Triple-Transgenic Mouse Model of Alzheimer’s Disease, Without Altering Amyloid-β and Tau Pathologies

2020 ◽  
pp. 1-19
Author(s):  
Hortense Fanet ◽  
Marine Tournissac ◽  
Manon Leclerc ◽  
Vicky Caron ◽  
Cyntia Tremblay ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Metabolic Disorders ◽  
Amyloid Β ◽  
Transgenic Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Age Related ◽  
Triple Transgenic Mouse

Background: Alzheimer’s disease (AD) is a multifactorial disease, implying that multi-target treatments may be necessary to effectively cure AD. Tetrahydrobiopterin (BH4) is an enzymatic cofactor required for the synthesis of monoamines and nitric oxide that also exerts antioxidant and anti-inflammatory effects. Despite its crucial role in the CNS, the potential of BH4 as a treatment in AD has never been scrutinized. Objective: Here, we investigated whether BH4 peripheral administration improves cognitive symptoms and AD neuropathology in triple-transgenic mouse model of AD (3xTg-AD) mice, a model of age-related tau and amyloid-β (Aβ) neuropathologies associated with behavior impairment. Methods: Non-transgenic (NonTg) and 3xTg-AD mice were subjected to a control diet (5% fat – CD) or to a high-fat diet (35% fat - HFD) from 6 to 13 months to exacerbate metabolic disorders. Then, mice received either BH4 (15 mg/kg/day, i.p.) or vehicle for ten consecutive days. Results: This sub-chronic administration of BH4 rescued memory impairment in 13-month-old 3xTg-AD mice, as determined using the novel object recognition test. Moreover, the HFD-induced glucose intolerance was completely reversed by the BH4 treatment in 3xTg-AD mice. However, the HFD or BH4 treatment had no significant impact on Aβ and tau neuropathologies. Conclusion: Overall, our data suggest a potential benefit from BH4 administration against AD cognitive and metabolic symptoms accentuated by HFD consumption in 3xTg-AD mice, without altering classical neuropathology. Therefore, BH4 should be considered as a candidate for drug repurposing, at least in subtypes of cognitively impaired patients experiencing metabolic disorders.

Clioquinol Decreases Amyloid-β Burden and Reduces Working Memory Impairment in a Transgenic Mouse Model of Alzheimer's Disease

2009 ◽  
Vol 17 (2) ◽  
pp. 423-440 ◽  
Author(s):  
Cristina Grossi ◽  
Simona Francese ◽  
Angela Casini ◽  
Maria Cristina Rosi ◽  
Ilaria Luccarini ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Working Memory ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Transgenic Mouse Model ◽  
Model Of Alzheimer’S Disease
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