Part of the book: Neuroscience
Part of the book: Neurochemistry
Part of the book: Neurochemistry
Part of the book: Neurochemistry
Part of the book: Neurochemistry
Part of the book: Alzheimer's Disease
Alzheimer’s disease is the most common type of dementia in occidental countries. The majority of the cases develop the disease for no genetic reasons; therefore, it is crucial to establish which environmental factors trigger the development of the disease. It has been proposed that nutritional habits, especially main components of Western countries’ diet such as saturated fat or cholesterol, increase the risk for development of Alzheimer’s disease (AD) and/or accelerate the onset of the disease, which is a big concern in countries where obesity is a public health problem. It is crucial to understand the links between alimentary habits and the development of AD and other types of dementia. A possible mechanism is the disruption of blood–brain barrier (BBB), which is the protection of the brain from circulating blood. Such disruptions can result from consuming high-fat diet (HFD) or high-cholesterol diet (HCD) and inflammation produced by alteration in brain vasculature resulted for chronic consumption of such type of diets. What has named a "Systemic view" comprises the idea that; what happens outside of the brain environment does affect brain functioning and the modifications experienced in the brain environment resulted from the influence of external factors will affect the entire body. In the current chapter, we will review the state of the art in the studies of the impact of a diet rich in fat or cholesterol on the brain and how the alterations induced in other organs can impact brain functioning increasing the susceptibility of development of dementia.
Part of the book: Update on Dementia
Alzheimer’s disease (AD) has become one of the most threatening diseases in the elderly, and type 2 diabetes mellitus (T2DM) is a major health problem in the world, representing 7.4% of the population. Several studies have produced epidemiological, clinical, and pathological evidence of the relationship between AD and T2DM. Laboratory research using animal models has identified mechanisms shared by both T2DM and AD. Particularly, there is an increase of tau phosphorylation and cleavage, which is known to be particularly toxic to neurons and to form a nucleation for neurofibrillary tangles. Also, alterations in synaptic plasticity are associated to tau pathology through the direct abnormal interaction of pathological tau with synaptic proteins and indirectly through Tau-activated neuroinflammatory processes. Many T2DM complications are potentiated or initiated by the accumulation of specific forms of advanced glycation end products (AGEs) and their interaction with its receptors (RAGE). AGEs promote β-amyloid aggregation and cytotoxicity, while glycation of tau may enhance their aggregation. Therefore, this review addresses the analysis of the common mechanisms where the major molecular players of these two diseases participate and contribute to a better understanding of these diseases in their pathogenic relationship.
Part of the book: Neurodegenerative Diseases