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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]
The estimate of how many people will develop dementia in their lifetimes is now higher than ever—42% for both men and women, according to a new study—with about 1 in 9 Americans 65 and older ...
The first symptoms are often mistakenly attributed to aging or stress. [34] Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of Alzheimer's disease. [35] These early symptoms can affect the most complex activities of daily living. [36]
Some plaques occur in the brain as a result of aging, but large numbers of plaques and neurofibrillary tangles are characteristic features of Alzheimer's disease. [5] The plaques are highly variable in shape and size; in tissue sections immunostained for Aβ, they comprise a log-normal size distribution curve, with an average plaque area of 400 ...
The symptoms of this dementia depend on where in the brain the strokes occurred and whether the blood vessels affected were large or small. [13] Repeated injury can cause progressive dementia over time, while a single injury located in an area critical for cognition such as the hippocampus, or thalamus, can lead to sudden cognitive decline. [75]
By the final stages of Alzheimer's, this process – called brain atrophy – is widespread, causing significant loss of brain volume. This loss of brain volume affects ones ability to live and function properly, ultimately being fatal. [33] Beta-amyloid is a small piece of a larger protein called amyloid precursor protein (APP). Once APP is ...
The hallmark symptom of LATE is a progressive memory loss that predominantly affects short-term and episodic memory. [1] This impairment is often severe enough to interfere with daily functioning and usually remains the chief neurologic deficit, unlike other types of dementia in which non-memory cognitive domains and behavioral changes might be noted earlier or more prominently. [1]
The parietal lobe is located directly behind the central sulcus, superior to the occipital lobe and posterior to the frontal lobe, visually at the top of the back of the head. [18] The make up of the parietal lobe is defined by four anatomical boundaries in the brain, providing a division of all the four lobes. [18]
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