Atherosclerosis and Alzheimer - diseases with a common cause? Inflammation, oxysterols, vasculature

Lathe, Richard; Sapronova, Alexandra; Kotelevtsev, Yuri

doi:10.1186/1471-2318-14-36

BMC Geriatrics

Table 1 Gene knockouts in mice and disease progression in ATH and AD models

From: Atherosclerosis and Alzheimer - diseases with a common cause? Inflammation, oxysterols, vasculature

Gene^a	ATH	Refs	AD	Refs
Abca1	↑↑^b	[90, 91]	↑↑	[92]
Acat1 ^c,d	↓↑	[93–96]	↓↓	[97]
Acat2 ^c,d	↓↓	[98, 99]	n/a^e
Apoe	↑↑	See text^f	↓↓	See text^e
App	↓↓	[85]; conversely, App overexpression amplifies ATH (see text)	↓↓*	*By inference; the production of Aβ (processing product of human APP) is central to AD pathology
Clu1	↓↓	[100]	↓↓↑?	[101, 102]
Cyp7b1	↑↑	[103]	↑↑**	*By inference; CYP7B1* expression is downregulated in AD patient brain [104]
Ifngr1	↓↓	[105]	↓↓	[106]
Ldlr	↑↑	[67, 68]	↑↑	[107–109]
Other immune system components	↓↓^g	See text	↓↓(↑)^f	See text

^aGene names: Apoe, apolipoprotein E; App, amyloid beta precursor protein; Abca1, ATP-binding cassette, sub-family A (ABC1), member 1 (cholesterol efflux regulatory protein); Acat1/2, acyl-CoA cholesterol acyltransferases 1/2 [SOAT1/2; see note (d) on nomenclature]; Clu1, clustered mitochondria (CluA/CLU1) homolog; Cyp7b1, cytochrome P450 7B1 (sterol and steroid 7α-hydroxylase); Ifngr1, interferon γ receptor 1; Ldlr, low density lipoprotein receptor.
^b↑↑, Increased disease development; ↓↓, reduced disease development.
^cThe biology of ACAT1 versus ACAT2 differs between mouse and human [110, 111].
^dNote concerning nomenclature: acyl-CoA cholesterol acyltransferases 1/2 (ACAT1/2) are more properly known as sterol O-acyltransferases 1/2 (SOAT1/2) and the name ACAT conflicts with the official symbol for a different enzyme (acetyl-CoA acetyltransferase 1/2; ACAT1/2); see http://www.ncbi.nlm.nih.gov/gene/6646 and http://www.ncbi.nlm.nih.gov/gene/8435. However, because the literature largely continues to use ACAT1/2 (rather than SOAT1/2) for acyl-CoA cholesterol acyltransferases 1/2 this usage is followed here.
^eData not available.
^fThe ApoE paradox. APOE4 is a risk factor for both AD and ATH, but knockout promotes ATH but reduces AD in mouse models.
^gSome data are contradictory; text for details.
*By inference; the production of Aβ (processing product of human APP) is central to AD pathology.
**By inference; CYP7B1 expression is downregulated in AD patient brain [104].

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ISSN: 1471-2318

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