Table 1Major primary abbreviations used in this book

ADAlzheimer's disease
FAD*familial AD
SAD*sporadic AD
MCImild cognitive impairment
FTDP-17front-temporal dementia with Parkinsonism linked to chromosome 17
NFTneurofibrillary tangle
ADRDAlzheimer's disease and Related Disorders (This is the title of the largest international meeting on AD held every other year. The 2002 meeting was held in Stockholm in July 20-25.)
Αβamyloid β peptide
APPamyoid precursor protein (or amyloid protein precursor)
APPs/sAPPsoluble extracellular fragment of APP
APPsα/sAPPαAPPs generated by α-secretase
APPsβ/APPsβAPPs generated by β-secretase
NTFN-terminal fragment (of APP generated by α- or β-secretase)
CTFC-terminal fragment (of APP generated by α- or β-secretase)
C83CTF generated by α secretase
C99CTF generated by β secretase
APLPAPP-like protein
NICDNotch intracellular domain
AICDAPP intracellular domain
ELISAenzyme-linked immunosorbent assay
CSFcerebrospinal fluid
ISFinterstitial fluid
BBBblood-brain barrier
KO(gene) knock-out
KI(gene) knock-in
BACEbeta-site APP cleaving enzyme
ADAMa disintegrin and metalloprotease
PKCprotein kinase C
ERendoplasmic reticulum
TGNtrans-Golgi network
IDEinsulin-degrading enzyme
ECEendothelin-converting enzyme
PDAPPAPPtransgenic mice, in which the transgene expression was driven by platelet-derived growth factor (PDGF) promoter (see ref. 5 in Chapter 11).
ApoEApolipoprotein E
CEMcholesterol-enriched (membrane) microdomain: essentially identical to LDM, DIG, or lipid raft
LDM(cholesterol-and sphingolipid-rich) low density (membrane) microdomain: essentially identical to CEM, DIG, or lipid raft
DIGdetergent-insoluble glycolipid-rich (membrane domain): : essentially identical to CEM, LDM, or lipid raft
CNScentral nervous system
CAAcerebral amyloid angiopathy

*FAD is defined as a form of AD that is inherited in an autosomal dominant manner with essentially 100% penetrance. Most FAD cases are early onset, starting between the late 20s and mid 60s. The rest that does not fulfill the definition of FAD is treated as SAD in this book unless otherwise stated. Besides, there has been no genetic risk factor identified that can be used for presymptomatic diagnosis in clinical terms.

From: Overview Αβ Metabolism: From Alzheimer Research to Brain Aging Control

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