Long-Term Treatment with Lithium Alleviates Memory Deficits and Reduces Amyloid-β Production in an Aged Alzheimer's Disease Transgenic Mouse Model

2011 ◽  
Vol 24 (4) ◽  
pp. 739-749 ◽  
Author(s):  
Xin Zhang ◽  
Xin Heng ◽  
Ting Li ◽  
Lixi Li ◽  
Dehua Yang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Transgenic Mouse Model ◽  
Term Treatment ◽  
Long Term Treatment

scholarly journals Long-Term Pantethine Treatment Counteracts Pathologic Gene Dysregulation and Decreases Alzheimer’s Disease Pathogenesis in a Transgenic Mouse Model

2019 ◽  
Vol 16 (4) ◽  
pp. 1237-1254 ◽  
Author(s):  
Kevin Baranger ◽  
Manuel van Gijsel-Bonnello ◽  
Delphine Stephan ◽  
Wassila Carpentier ◽  
Santiago Rivera ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Transgenic Mouse Model ◽  
Disease Pathogenesis ◽  
Gene Dysregulation

scholarly journals Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 177 ◽  
Author(s):  
Natalia A. Muraleva ◽  
Oyuna S. Kozhevnikova ◽  
Anzhela Z. Fursova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Developed Countries ◽  
Term Treatment ◽  
Age Related Macular Degeneration ◽  
Eye Health ◽  
Age Related ◽  
Long Term Treatment

Age-related macular degeneration (AMD) is a major cause of irreversible visual impairment and blindness in developed countries, and the molecular pathogenesis of AMD is poorly understood. Recent studies strongly indicate that amyloid β (Aβ) accumulation —found in the brain and a defining feature of Alzheimer’s disease—also forms in the retina in both Alzheimer’s disease and AMD. The reason why highly neurotoxic proteins of consistently aggregate in the aging retina, and to what extent they contribute to AMD, remains to be fully addressed. Nonetheless, the hypothesis that Aβ is a therapeutic target in AMD is debated. Here, we showed that long-term treatment with SkQ1 (250 nmol/[kg body weight] daily from the age of 1.5 to 22 months) suppressed the development of AMD-like pathology in senescence-accelerated OXYS rats by reducing the level of Aβ and suppressing the activity of mTOR in the retina. Inhibition of mTOR signaling activity, which plays key roles in aging and age-related diseases, can be considered a new mechanism of the prophylactic effect of SkQ1. It seems probable that dietary supplementation with mitochondria-targeted antioxidant SkQ1 can be a good prevention strategy to maintain eye health and possibly a treatment of AMD.

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