Alzheimer’s disease as a metabolic disorder
Autor: | George S. Bloom, Andrés Norambuena |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
insulin lcsh:TP670-699 Disease Mitochondrion Biology amyloid-β Biochemistry Pathogenesis 03 medical and health sciences 0302 clinical medicine medicine Extracellular tau Cognitive impairment PI3K/AKT/mTOR pathway Metabolic disorder medicine.disease mitochondria 030104 developmental biology nervous system mTOR lcsh:Oils fats and waxes Energy source Agronomy and Crop Science Neuroscience 030217 neurology & neurosurgery Food Science |
Zdroj: | Oilseeds and fats, crops and lipids, Vol 25, Iss 4, p D403 (2018) |
ISSN: | 2257-6614 2272-6977 |
Popis: | Alzheimer’s disease (AD) is defined by memory loss and cognitive impairment, along with the accumulation in brain of two types of abnormal structures, extracellular amyloid plaques and intraneuronal neurofibrillary tangles. Both plaques and tangles are composed predominantly of poorly soluble filaments that respectively assemble from amyloid-β (Aβ) peptides and the neuron-specific, microtubule-associated protein, tau. It is now widely acknowledged that soluble oligomers of Aβ and tau, the building blocks of plaques and tangles, are principal drivers of AD pathogenesis by acting coordinately to impair and destroy synapses, and kill neurons. The behavioral features of AD are a direct consequence of these attacks on synapses and neuronal viability, which in turn reflect a reduced capacity of AD neurons to utilize energy sources needed to maintain neuronal function and vitality. In other words, AD neurons are starving, even when they may be surrounded by abundant nutrients. Here, we review some of the evidence for the metabolic deficiencies of neurons in AD and how they impact neuronal health. |
Databáze: | OpenAIRE |
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