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The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy : a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain . [ 1 ]
Treatments with anticancer chemotherapeutic agents often are toxic to the cells of the brain, leading to memory loss and cognitive dysfunction that can persist long after the period of exposure. This condition, termed chemo brain, appears to be due to DNA damages that cause epigenetic changes in the brain that accelerate the brain aging process ...
Familial Alzheimer's disease mutations commonly used in animal models. Rodent animal models of Alzheimer's disease are commonly used in research as rodents and humans have many of the same major brain regions and neurotransmitter systems. [5] These models are small, easy to house, as well as breed very well. [26]
In Alzheimer’s disease, the most common form of dementia, the blood-brain barrier is disrupted. A new study has uncovered unique molecular signatures linked to the disruption of this blood-brain ...
A normal brain on the left and a late-stage Alzheimer's brain on the right. During the final stage, known as the late-stage or severe stage, there is complete dependence on caregivers. [19] [33] [41] Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech.
Brain Aβ is elevated in people with sporadic Alzheimer's disease. Aβ is the main constituent of brain parenchymal and vascular amyloid; it contributes to cerebrovascular lesions and is neurotoxic. [33] [34] [35] It is unresolved how Aβ accumulates in the central nervous system and subsequently initiates the disease of cells. Significant ...
According to the Mayo Clinic some key lifestyle changes to support brain health include the following: Avoid smoking. ... The Alzheimer’s Project, Inc, a not-for-profit group, ...
Alzheimer's disease (AD) is a chronic neurodegenerative disease that results in the loss of neurons and synapses in the cerebral cortex and certain subcortical structures, resulting in gross atrophy of the temporal lobe, parietal lobe, and parts of the frontal cortex and cingulate gyrus. [14]