Editing Dementia (section)

=== Alzheimer's disease ===
{{Main|Alzheimer's disease}}
[[File:Alzheimers brain.jpg|thumb|Brain [[atrophy]] in severe Alzheimer's]]

Alzheimer's disease accounts for 60–70% of cases of dementia worldwide. The most common symptoms of Alzheimer's disease are [[short-term memory loss]] and [[Anomic aphasia|word-finding difficulties]]. Trouble with [[visuospatial function]]ing (getting lost often), reasoning, judgment and [[insight]] fail. Insight refers to whether or not the person realizes they have memory problems.

The part of the brain most affected by Alzheimer's is the [[hippocampus]]. Other parts that show [[atrophy]] (shrinking) include the [[Temporal lobe|temporal]] and [[parietal lobe]]s. Although this pattern of brain shrinkage suggests Alzheimer's, it is variable and a brain scan is insufficient for a diagnosis.

Little is known about the events that occur during and that actually cause Alzheimer's disease. This is due to the fact that, historically, brain tissue from people with the disease could only be studied after the person's death. Brain scans can now help diagnose and distinguish between different kinds of dementia and show severity. These include magnetic resonance imaging (MRI), computerized tomography (CT), and positron emission tomography (PET).  However, it is known that one of the first aspects of Alzheimer's disease is overproduction of [[amyloid]]. Extracellular senile plaques (SPs), consisting of beta-amyloid (Aβ) peptides, and intracellular [[neurofibrillary tangle]]s (NFTs) that are formed by hyperphosphorylated tau proteins, are two well-established pathological hallmarks of AD.<ref>{{cite journal | vauthors = Abyadeh M, Gupta V, Chitranshi N, Gupta V, Wu Y, Saks D, Wander Wall R, Fitzhenry MJ, Basavarajappa D, You Y, Salekdeh GH, Haynes PA, Graham SL, Mirzaei M | display-authors = 6 | title = Mitochondrial dysfunction in Alzheimer's disease – a proteomics perspective | journal = Expert Review of Proteomics | volume = 18 | issue = 4 | pages = 295–304 | date = April 2021 | pmid = 33874826 | doi = 10.1080/14789450.2021.1918550 | s2cid = 233310698 }}</ref> Amyloid causes [[inflammation]] around the [[Amyloid plaques|senile plaques of the brain]], and too much buildup of this inflammation leads to changes in the brain that cannot be controlled, leading to the symptoms of Alzheimer's.<ref>{{cite journal | vauthors = Wenk GL | title = Neuropathologic changes in Alzheimer's disease | journal = The Journal of Clinical Psychiatry | volume = 64 | issue = Suppl 9 | pages = 7–10 | date = 2003 | pmid = 12934968 | url = http://www.psychiatrist.com/jcp/article/pages/2003/v64s09/v64s0902.aspx }}</ref>

Several articles have been published on a possible relationship (as an either primary cause or exacerbation of Alzheimer's disease) between general [[anesthesia]] and Alzheimer's in specifically [[the elderly]].<ref>{{cite journal | vauthors = Papon MA, Whittington RA, El-Khoury NB, Planel E | title = Alzheimer's disease and anesthesia | journal = Frontiers in Neuroscience | volume = 4 | page = 272 | date = 2011 | pmid = 21344011 | pmc = 3034231 | doi = 10.3389/fnins.2010.00272 | doi-access = free }}</ref>