Alzheimer's disease (AD) is a devastating neurodegenerative disorder that results in loss of memory and cognitive function, eventually leading to dementia. Fasting can be relevant since, recently, studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism, and strengthen cellular protection. Periodic Fasting Diet (PFD), characterized by fasting and re-feeding periods, promote regenerative processes and amelioration of dysfunctional neurons, leading to improvement of symptoms in mice and in humans. The absence of treatments that impact the progression of Alzheimer's disease (AD) suggest the importance of nutritional approach and lifestyle interventions that retard ageing processes and reduce disease risk. The wide-range effects of PFDs on metabolic, inflammatory, and regenerative pathways have the potential to strongly ameliorate the pathology and symptoms of AD and to prevent the pathogenesis. The aim of the project is to investigate the crosstalk between Aβ and tau that represent a crucial node in the study of the pathogenesis of Alzheimer's disease related to PFD, as well as to explore a new possibility to prevent neurodegeneration in dementia. We developed and characterized a new transgenic mouse model (5xADTg/hTauTg) that mimics the pathological evolution of AD, producing large amount of Aβ and expressing wild type human tau, to investigate the effect of PFD both at molecular and behavioral level.
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that results in loss of memory and cognitive function, eventually leading to dementia. Fasting can be relevant since, recently, studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism, and strengthen cellular protection. Periodic Fasting Diet (PFD), characterized by fasting and re-feeding periods, promote regenerative processes and amelioration of dysfunctional neurons, leading to improvement of symptoms in mice and in humans. The absence of treatments that impact the progression of Alzheimer's disease (AD) suggest the importance of nutritional approach and lifestyle interventions that retard ageing processes and reduce disease risk. The wide-range effects of PFDs on metabolic, inflammatory, and regenerative pathways have the potential to strongly ameliorate the pathology and symptoms of AD and to prevent the pathogenesis. The aim of the project is to investigate the crosstalk between Aβ and tau that represent a crucial node in the study of the pathogenesis of Alzheimer's disease related to PFD, as well as to explore a new possibility to prevent neurodegeneration in dementia. We developed and characterized a new transgenic mouse model (5xADTg/hTauTg) that mimics the pathological evolution of AD, producing large amount of Aβ and expressing wild type human tau, to investigate the effect of PFD both at molecular and behavioral level.
Role of Periodic Fasting Diet in prevention and progression of Alzheimer's disease in mouse model
MINOTTA, LORENZO
2021/2022
Abstract
Alzheimer's disease (AD) is a devastating neurodegenerative disorder that results in loss of memory and cognitive function, eventually leading to dementia. Fasting can be relevant since, recently, studies have shed light on its role in adaptive cellular responses that reduce oxidative damage and inflammation, optimize energy metabolism, and strengthen cellular protection. Periodic Fasting Diet (PFD), characterized by fasting and re-feeding periods, promote regenerative processes and amelioration of dysfunctional neurons, leading to improvement of symptoms in mice and in humans. The absence of treatments that impact the progression of Alzheimer's disease (AD) suggest the importance of nutritional approach and lifestyle interventions that retard ageing processes and reduce disease risk. The wide-range effects of PFDs on metabolic, inflammatory, and regenerative pathways have the potential to strongly ameliorate the pathology and symptoms of AD and to prevent the pathogenesis. The aim of the project is to investigate the crosstalk between Aβ and tau that represent a crucial node in the study of the pathogenesis of Alzheimer's disease related to PFD, as well as to explore a new possibility to prevent neurodegeneration in dementia. We developed and characterized a new transgenic mouse model (5xADTg/hTauTg) that mimics the pathological evolution of AD, producing large amount of Aβ and expressing wild type human tau, to investigate the effect of PFD both at molecular and behavioral level.File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.14240/6178