Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level

Molecular Neurodegeneration

Volumn 10, Issue 1, 2015, Pages

  Sadleir, Katherine R ^a   Eimer, William A ^a,b   Cole, Sarah L ^a,c   Vassar, Robert ^a  

^a NORTHWESTERN UNIVERSITY   (United States)

^b MASSACHUSETTS GENERAL HOSPITAL   (United States)

^c Neurodegeneration Group   (United Kingdom)

Author keywords

5XFAD; Alzheimer's disease; Amyloid; Amyloid precursor protein; APP transgenic mouse models; A ; BACE1 heterozygous; Dot blot; Estrogen response element; secretase

Indexed keywords

AMYLOID BETA PROTEIN[1-42]; AMYLOID PRECURSOR PROTEIN; BETA SECRETASE 1; AMYLOID BETA PROTEIN; ASPARTIC PROTEINASE; BACE1 PROTEIN, HUMAN; BACE1 PROTEIN, MOUSE; SECRETASE;

ARTICLE; CONTROLLED STUDY; COST EFFECTIVENESS ANALYSIS; DOT HYBRIDIZATION; ENZYME INHIBITION; ENZYME LINKED IMMUNOSORBENT ASSAY; ESTROGEN RESPONSIVE ELEMENT; FEMALE; HETEROZYGOTE; MALE; MEASUREMENT ACCURACY; MOUSE; NONHUMAN; PROTEIN CLEAVAGE; PROTEIN EXPRESSION; PROTEIN FUNCTION; SEX DIFFERENCE; STEADY STATE; ALZHEIMER DISEASE; AMYLOID PLAQUE; ANIMAL; BRAIN; DISEASE MODEL; GENETICS; HUMAN; KNOCKOUT MOUSE; MEMORY; METABOLISM; PHYSIOLOGY; TRANSGENIC MOUSE;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; AMYLOID PRECURSOR PROTEIN SECRETASES; ANIMALS; ASPARTIC ACID ENDOPEPTIDASES; BRAIN; DISEASE MODELS, ANIMAL; HETEROZYGOTE; HUMANS; MEMORY; MICE, KNOCKOUT; MICE, TRANSGENIC; PLAQUE, AMYLOID;

EID: 84988600875     PISSN: None     EISSN: 17501326     Source Type: Journal    
DOI: 10.1186/1750-1326-10-1     Document Type: Article

References (42)

1. Haass C, Kaether C, Thinakaran G, Sisodia S. Trafficking and proteolytic processing of APP. Cold Spring Harb Perspect Med. 2012;2(5):a006270.
2. Tanzi RE. The genetics of Alzheimer disease. Cold Spring Harb Perspect Med. 2012;2(10):a006296.
3. Cai H, Wang Y, McCarthy D, Wen H, Borchelt DR, Price DL, et al. BACE1 is the major beta-secretase for generation of Abeta peptides by neurons. Nat Neurosci. 2001;4(3):233-4.
4. Luo Y, Bolon B, Damore MA, Fitzpatrick D, Liu H, Zhang J, et al. BACE1 (beta-secretase) knockout mice do not acquire compensatory gene expression changes or develop neural lesions over time. Neurobiol Dis. 2003;14(1):81-8.
5. Luo Y, Bolon B, Kahn S, Bennett BD, Babu-Khan S, Denis P, et al. Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. Nat Neurosci. 2001;4(3):231-2.
6. Ohno M, Cole SL, Yasvoina M, Zhao J, Citron M, Berry R, et al. BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice. Neurobiol Dis. 2007;26(1):134-45.
7. Ohno M, Sametsky EA, Younkin LH, Oakley H, Younkin SG, Citron M, et al. BACE1 deficiency rescues memory deficits and cholinergic dysfunction in a mouse model of Alzheimer's disease. Neuron. 2004;41(1):27-33.
8. Vassar R, Kuhn PH, Haass C, Kennedy ME, Rajendran L, Wong PC, et al. Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects. J Neurochem. 2014;130(1):4-28.
9. Yan R, Vassar R. Targeting the beta secretase BACE1 for Alzheimer's disease therapy. Lancet Neurol. 2014;13(3):319-29.
10. Roberds SL, Anderson J, Basi G, Bienkowski MJ, Branstetter DG, Chen KS, et al. BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics. Hum Mol Genet. 2001;10(12):1317-24.
11. Dominguez D, Tournoy J, Hartmann D, Huth T, Cryns K, Deforce S, et al. Phenotypic and biochemical analyses of BACE1-and BACE2-deficient mice. J Biol Chem. 2005;280(35):30797-806.
12. Hitt BD, Jaramillo TC, Chetkovich DM, Vassar R. BACE1-/- mice exhibit seizure activity that does not correlate with sodium channel level or axonal localization. Mol Neurodegener. 2010;5:31.
13. Hu X, Hicks CW, He W, Wong P, Macklin WB, Trapp BD, et al. Bace1 modulates myelination in the central and peripheral nervous system. Nat Neurosci. 2006;9(12):1520-5.
14. Laird FM, Cai H, Savonenko AV, Farah MH, He K, Melnikova T, et al. BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J Neurosci Off J Soc Neurosci. 2005;25(50):11693-709.
15. Rajapaksha TW, Eimer WA, Bozza TC, Vassar R. The Alzheimer's beta-secretase enzyme BACE1 is required for accurate axon guidance of olfactory sensory neurons and normal glomerulus formation in the olfactory bulb. Mol Neurodegener. 2011;6:88.
16. Savonenko AV, Melnikova T, Laird FM, Stewart KA, Price DL, Wong PC. Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice. Proc Natl Acad Sci U S A. 2008;105(14):5585-90.
17. Willem M, Garratt AN, Novak B, Citron M, Kaufmann S, Rittger A, et al. Control of peripheral nerve myelination by the beta-secretase BACE1. Science. 2006;314(5799):664-6.
18. Hitt B, Riordan SM, Kukreja L, Eimer WA, Rajapaksha TW, Vassar R. Beta-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects. J Biol Chem. 2012;287(46):38408-25.
19. Kuhn PH, Koroniak K, Hogl S, Colombo A, Zeitschel U, Willem M, et al. Secretome protein enrichment identifies physiological BACE1 protease substrates in neurons. EMBO J. 2012;31(14):3157-68.
20. Zhou L, Barao S, Laga M, Bockstael K, Borgers M, Gijsen H, et al. The neural cell adhesion molecules L1 and CHL1 are cleaved by BACE1 protease in vivo. J Biol Chem. 2012;287(31):25927-40.
21. Devi L, Ohno M. Genetic reductions of beta-site amyloid precursor proteincleaving enzyme 1 and amyloid-beta ameliorate impairment of conditioned taste aversion memory in 5XFAD Alzheimer's disease model mice. Eur J Neurosci. 2010;31(1):110-8.
22. Devi L, Ohno M. Phospho-eIF2alpha level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice. PLoS One. 2010;5(9):e12974.
23. Kimura R, Devi L, Ohno M. Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice. J Neurochem. 2010;113(1):248-61.
24. McConlogue L, Buttini M, Anderson JP, Brigham EF, Chen KS, Freedman SB, et al. Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. J Biol Chem. 2007;282(36):26326-34.
25. Pastorino L, Ikin AF, Lamprianou S, Vacaresse N, Revelli JP, Platt K, et al. BACE (beta-secretase) modulates the processing of APLP2 in vivo. Mol Cell Neurosci. 2004;25(4):642-9.
26. Rabe S, Reichwald J, Ammaturo D, de Strooper B, Saftig P, Neumann U, et al. The Swedish APP mutation alters the effect of genetically reduced BACE1 expression on the APP processing. J Neurochem. 2011;119(1):231-9.
27. Oakley H, Cole SL, Logan S, Maus E, Shao P, Craft J, et al. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci Off J Soc Neurosci. 2006;26(40):10129-40.
28. Zhao J, Fu Y, Yasvoina M, Shao P, Hitt B, O'Connor T, et al. Beta-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis. J Neurosci Off J Soc Neurosci. 2007;27(14):3639-49.
29. Sadleir KR, Bennett DA, Schneider JA, Vassar R. Elevated Abeta42 in aged, non-demented individuals with cerebral atherosclerosis. Curr Alzheimer Res. 2013;10(8):785-9.
30. Kandalepas PC, Sadleir KR, Eimer WA, Zhao J, Nicholson DA, Vassar R. The Alzheimer's beta-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques. Acta Neuropathol. 2013;126(3):329-52.
31. Moechars D, Lorent K, De Strooper B, Dewachter I, Van Leuven F. Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice. EMBO J. 1996;15(6):1265-74.
32. Ingraham HA, Evans GA. Characterization of two atypical promoters and alternate mRNA processing in the mouse Thy-1.2 glycoprotein gene. Mol Cell Biol. 1986;6(8):2923-31.
33. Gruber CJ, Gruber DM, Gruber IM, Wieser F, Huber JC. Anatomy of the estrogen response element. Trends Endocrinol Metab: TEM. 2004;15(2):73-8.
34. Games D, Adams D, Alessandrini R, Barbour R, Berthelette P, Blackwell C, et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein. Nature. 1995;373(6514):523-7.
35. Fukumoto H, Cheung BS, Hyman BT, Irizarry MC. Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. Arch Neurol. 2002;59(9):1381-9.
36. Holsinger RMD, McLean CA, Beyreuther K, Masters CL, Evin G. Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease. Ann Neurol. 2002;51:783-6.
37. Citron M, Oltersdorf T, Haass C, McConlogue L, Hung AY, Seubert P, et al. Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production. Nature. 1992;360(6405):672-4.
38. Callahan MJ, Lipinski WJ, Bian F, Durham RA, Pack A, Walker LC. Augmented senile plaque load in aged female beta-amyloid precursor protein-transgenic mice. Am J Pathol. 2001;158(3):1173-7.
39. Hirata-Fukae C, Li HF, Hoe HS, Gray AJ, Minami SS, Hamada K, et al. Females exhibit more extensive amyloid, but not tau, pathology in an Alzheimer transgenic model. Brain Res. 2008;1216:92-103.
40. Sierksma AS, Prickaerts J, Chouliaras L, Rostamian S, Delbroek L, Rutten BP, et al. Behavioral and neurobiological effects of prenatal stress exposure in male and female APPswe/PS1dE9 mice. Neurobiol Aging. 2013;34(1):319-37.
41. Overk CR, Lu PY, Wang YT, Choi J, Shaw JW, Thatcher GR, et al. Effects of aromatase inhibition versus gonadectomy on hippocampal complex amyloid pathology in triple transgenic mice. Neurobiol Dis. 2012;45(1):479-87.
42. Hy LX, Keller DM. Prevalence of AD among whites: a summary by levels of severity. Neurology. 2000;55(2):198-204.