IDENTIFICATION OF DEGENERATIVE EFFECTS ASSOCIATED WITH DIET HYPERCALORIC AND HIGH IN FAT IN MICEOriginal title: IDENTIFICACIÓN DE EFECTOS DEGENERATIVOS ASOCIADOS A DIETA HIPERCALÓRICA Y ALTA EN GRASAS EN RATONES
Original title: IDENTIFICACIÓN DE EFECTOS DEGENERATIVOS ASOCIADOS A DIETA HIPERCALÓRICA Y ALTA EN GRASAS EN RATONES
- Universidad de Monterrey
Student Thesis:
Student thesis
Thesis
ABSTRACT
Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and the seventh
leading cause of death worldwide; around 800,000 older adults in Mexico suffer from
Alzheimer's, which is a neurodegenerative disorder characterized by the gradual and
progressive death of neurons. This leads to dysfunction of the nervous system in the form
of memory impairment, causing severe disability and a significant reduction in quality
and life expectancy.
The gradual cell death observed in AD has been mainly attributed to the TAU and beta
amyloid (Aβ) proteins, the aggregation of which forms neurofibrillary plaques seen in
brains with AD; which, in turn, contribute to toxicity. The transcription factor p53 shares
many characteristics with other proteins that are prone to aggregation involved in
neurodegenerative diseases. Neuronal death, reentry to the cell cycle, and dysregulation
of the response to DNA damage are associated with the pathogenesis of AD and are
controlled by P53.
The study included 19 mice, categorized as: C57 obese adults, C57 non-obese youth, and
129Sv-ebf2TGFP transgenic non-obese youth. The experiment was divided into a control
and an experimental group. The experimental group was administered a hypercaloric and
high-fat and high-carbohydrate diet in order to identify the degenerative effects that it
entails. For example, inflammation in the central nervous system.
All experimental groups underwent morphological changes seen in histological tests.
The three experimental groups with a hypercaloric diet (high in fat and carbohydrates)
were expected to have a greater weight gain than the control groups, but this was not the
case.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and the seventh
leading cause of death worldwide; around 800,000 older adults in Mexico suffer from
Alzheimer's, which is a neurodegenerative disorder characterized by the gradual and
progressive death of neurons. This leads to dysfunction of the nervous system in the form
of memory impairment, causing severe disability and a significant reduction in quality
and life expectancy.
The gradual cell death observed in AD has been mainly attributed to the TAU and beta
amyloid (Aβ) proteins, the aggregation of which forms neurofibrillary plaques seen in
brains with AD; which, in turn, contribute to toxicity. The transcription factor p53 shares
many characteristics with other proteins that are prone to aggregation involved in
neurodegenerative diseases. Neuronal death, reentry to the cell cycle, and dysregulation
of the response to DNA damage are associated with the pathogenesis of AD and are
controlled by P53.
The study included 19 mice, categorized as: C57 obese adults, C57 non-obese youth, and
129Sv-ebf2TGFP transgenic non-obese youth. The experiment was divided into a control
and an experimental group. The experimental group was administered a hypercaloric and
high-fat and high-carbohydrate diet in order to identify the degenerative effects that it
entails. For example, inflammation in the central nervous system.
All experimental groups underwent morphological changes seen in histological tests.
The three experimental groups with a hypercaloric diet (high in fat and carbohydrates)
were expected to have a greater weight gain than the control groups, but this was not the
case.