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- W2896688167 abstract "Alzheimer’s disease (AD) is the most common form of dementia affecting 40% of the population over 80 years old. Reflecting an ageing population and lack of effective therapies, AD is estimated to double the number of cases in 30 years, becoming a major health and economic burden. Clinically, AD is defined by a progressive loss of cognitive functions that lead to dementia and death. Neuropathologically, signs such as neuroinflammation, oxidative stress and neuronal death are prominent. The Metallothionein family (MT), is formed by low molecular weight, cysteine rich proteins with high metal content, which are subdivided in four subfamilies (MT-1 to MT-4). Although the primary function of MTs remains unknown, they are involved in antioxidant, anti-inflammatory and anti-apoptotic processes, conferring survival advantage under stress or tissue injury. MT-1/2 isoforms, ubiquitously expressed in all tissues, are upregulated in several neurodegenerative diseases such as AD. In this thesis we intend to further characterise the role of the MT-1, by crossing Mt1 overexpressing mice with the Tg2576 mouse model of AD, which expresses the human amyloid-β protein precursor (hAβPP) with the Swedish K670N/M671L mutations. In old mice, MT-1/2 protein levels were significantly increased by Mt1 overexpression throughout the cortex, which exhibited a marked caudal-frontal gradient, and the hippocampus. MT-1/2 immunostaining tended to increase in hAβPP compared to wild type mice. In contrast, when comparing TgMT and AβPPTgMT mice, MT-1/2 immunostaining tended to decrease in the latter. Mt1 overexpression protected from hAβPP-induced mortality at perinatal stages but did not affect survival in adult mice. Mt1 overexpression ameliorated the effects of hAβPP on exploration in young females, exacerbated those on anxiety in old males, and improved spatial memory and learning in young females. Amyloid plaque burden in old mice was increased by Mt1 overexpression in the hippocampus, but not in the cortex, in both sexes. However, oligomeric and monomeric forms of Aβ, which are reported to contribute more to toxicity, were decreased in the hippocampus of females and increased in males. Mt1 overexpression decreased the inflammatory response in the hippocampus of young males, before the deposit of amyloid plaques but increased microgliosis in old male mice. Hippocampal CA1 neuronal loss was found in Tg2576 mice, but was unaffected by Mt1 overexpression. Aging increased Zn and Cu levels differently depending on brain area, sex and genotype, and were barely affected by Mt1 overexpression. These results suggest that MT-1 can modulate some traits of the Tg2576 phenotype, highlighting the relevance of these studies in the development of human therapies." @default.
- W2896688167 created "2018-10-26" @default.
- W2896688167 creator A5072296986 @default.
- W2896688167 date "2017-01-01" @default.
- W2896688167 modified "2023-09-28" @default.
- W2896688167 title "Metallothionein family: influence of Metallothionein-1 in the Tg2576 mouse model of Alzheimer's disease / the multipurpose protein :" @default.
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