=== Sygdomsmekanisme ===
Det vides ikke præcis, hvordan forstyrrelser i produktion og aggregering af betaamyloid-peptid fører til AD's patologi.<ref name="pmid17622778">{{vcite journal | vauthors = Van Broeck B, Van Broeckhoven C, Kumar-Singh S | title = Current Insights into Molecular Mechanisms of Alzheimer Disease and Their Implications for Therapeutic Approaches | journal = Neuro-Degenerative Diseases | volume = 4 | issue = 5 | pages = 349–65 | year = 2007 | pmid = 17622778 | doi = 10.1159/000105156 }}</ref><ref>{{vcite journal | vauthors = Huang Y, Mucke L | title = Alzheimer Mechanisms and Therapeutic strategies | journal = Cell | volume = 148 | issue = 6 | pages = 1204–22 | year = 2012 | pmid = 22424230 |doi=10.1016/j.cell.2012.02.040 }}</ref> Ophobning af aggregerede amyloid-[[fibril]]ler medfører [[programmeret celledød]] ([[apoptose]]).<ref name="pmid2218531">{{vcite journal | vauthors = Yankner BA, Duffy LK, Kirschner DA | title = Neurotrophic and Neurotoxic Effects of Amyloid Beta Protein: Reversal by Tachykinin Neuropeptides | journal = Science | volume = 250 | issue = 4978 | pages = 279–82 | year = 1990 | pmid = 2218531 | doi = 10.1126/science.2218531 | month = October }}</ref> Det vides også, at A<sub>β</sub> opbygges selektivt i cellernes [[mitokondrie]]rne i hjernen hos mennesker med Alzheimers, samt at det hæmmer visse [[enzym]]funktioner og neuronernes anvendelse af [[glukose]].<ref name="pmid17424907">{{vcite journal | vauthors = Chen X, Yan SD | title = Mitochondrial Abeta: A Potential Cause of Metabolic Dysfunction in Alzheimer's Disease | journal = IUBMB Life | volume = 58 | issue = 12 | pages = 686–94 | year = 2006 | pmid = 17424907 | doi = 10.1080/15216540601047767 | month = December }}</ref>
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