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=== Adults ===
Memory tends to begin to fade as when enter and go through adulthood. Ane-Victoria Idland et al.,<ref name=":0">{{Cite journal|last1=Idland|first1=Ane-Victoria|last2=Sala-Llonch|first2=Roser|last3=Watne|first3=Leiv Otto|last4=Brækhus|first4=Anne|last5=Hansson|first5=Oskar|last6=Blennow|first6=Kaj|last7=Zetterberg|first7=Henrik|last8=Sørensen|first8=Øystein|last9=Walhovd|first9=Kristine Beate|last10=Wyller|first10=Torgeir Bruun|last11=Fjell|first11=Anders Martin|date=September 2020|title=Biomarker profiling beyond amyloid and tau: cerebrospinal fluid markers, hippocampal atrophy, and memory change in cognitively unimpaired older adults|journal=Neurobiology of Aging|language=en|volume=93|pages=1–15|doi=10.1016/j.neurobiolaging.2020.04.002|pmid=32438258|s2cid=215767584|doi-access=free}}</ref> investigated the biological factors that begin to form in a person’s older life and examined biological markers that could help explain the decrease in memory. They focused on beta amyloid 1–42 (Aβ42), phosphorylated tau (P-tau), total tau, chitinase-3-like protein 1 (YKL-40), fatty acid binding protein 3 (FABP3), and neurofilament light (NFL),<ref name=":0" /> and their findings suggest that tauopathy and FABP3 tended to be associated with the most memory decline. As individuals age, the hippocampus appears to begin to lose its ability to make connections to life events and memory.<ref>{{Cite journal|last1=Dahan|first1=Lionel|last2=Rampon|first2=Claire|last3=Florian|first3=Cédrick|date=August 2020|title=Age-related memory decline, dysfunction of the hippocampus and therapeutic opportunities|journal=Progress in Neuro-Psychopharmacology and Biological Psychiatry|language=en|volume=102|pages=109943|doi=10.1016/j.pnpbp.2020.109943|pmid=32298784|s2cid=215753906}}</ref>
==Episodic Memory==
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