The DOI matches its Crossref record; 255 of the 255 references it cites were found in a registry or an index.
The Basic Biology of BACE1: A Key Therapeutic Target for Alzheimers Disease
Abstract
Alzheimer's disease (AD) is an intractable, neurodegenerative disease that appears to be brought about by both genetic and non-genetic factors. The neuropathology associated with AD is complex, although amyloid plaques composed of the beta-amyloid peptide (Abeta) are hallmark neuropathological lesions of AD brain. Indeed, Abeta plays an early and central role in this disease. beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the initiating enzyme in Abeta genesis and BACE1 levels are elevated under a variety of conditions. Given the strong correlation between Abeta and AD, and the elevation of BACE1 in this disease, this enzyme is a prime drug target for inhibiting Abeta production in AD. However, nine years on from the initial identification of BACE1, and despite intense research, a number of key questions regarding BACE1 remain unanswered. Indeed, drug discovery and development for AD continues to be challenging. While current AD therapies temporarily slow cognitive decline, treatments that address the underlying pathologic mechanisms of AD are completely lacking. Here we review the basic biology of BACE1. We pay special attention to recent research that has provided some answers to questions such as those involving the identification of novel BACE1 substrates, the potential causes of BACE1 elevation and the putative function of BACE1 in health and disease. Our increasing understanding of BACE1 biology should aid the development of compounds that interfere with BACE1 expression and activity and may lead to the generation of novel therapeutics for AD.
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“The BACE1 protein has four N‐linked glycosylation sites, which are targeted in the Golgi and facilitate pro‐peptide processing, maturation, and transportation.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [74]
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2 retracted
Puglielli, L., Ellis, B. C., Saunders, A. J., & Kovacs, D. M. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300466200 · Cited by 265
RetractedGhribi, O., Larsen, B., Schrag, M., & Herman, M. M. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2006.03.019 · Cited by 151
RetractedCorder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Inflammation and Alzheimer’s disease
Akiyama, H. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00124-x · Cited by 4,514
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
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“In 1999-2000 several groups identified a novel aspartic protease, BACE1 (also known as memapsin 2; and Asp 2) [19, 21-24] as the -secretase.”
BackgroundInfluentialSelf-citationOakley, H., Cole, S. L., Logan, S., Maus, E., Shao, P., Craft, J., Guillozet-Bongaarts, A., Ohno, M., Disterhoft, J., Van Eldik, L., et al. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.1202-06.2006 · Cited by 3,530 · cited 4×
“To address whether the BACE1 elevation observed in AD brain is merely a passive end product of advanced neurodegeneration and cell death or whether it is actively involved in disease progression, we examined BACE1 levels in two Tg models of AD [143], namely the 5XFAD mouse [60] that develops amyloid plaques at young a…”
BackgroundResultInfluentialSelf-citationAmyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921
Wolfe, M. S., Xia, W., Ostaszewski, B. L., Diehl, T. S., Kimberly, W. T., & Selkoe, D. J. (1999) · Nature · doi:10.1038/19077 · Cited by 1,916
Statins and the risk of dementia
Jick, H., Zornberg, G., Jick, S., Seshadri, S., & Drachman, D. (2000) · The Lancet · doi:10.1016/s0140-6736(00)03155-x · Cited by 1,759
Research works printed but not linked: 2
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Cited by
Circulating miRNAs as Biomarkers for Neurodegenerative Disorders
Grasso, M., Piscopo, P., Confaloni, A., & Denti, M. (2014) · Molecules · doi:10.3390/molecules19056891 · Cited by 208
The biosynthesis, signaling, and neurological functions of bile acids
Kiriyama, Y., & Nochi, H. (2019) · Biomolecules · doi:10.3390/biom9060232 · Cited by 204
BACE1: More than just a β‐secretase
Taylor, H. A., Przemylska, L., Clavane, E. M., & Meakin, P. J. (2022) · Obesity Reviews · doi:10.1111/obr.13430 · Cited by 107
Increased BACE1-AS long noncoding RNA and β-amyloid levels in heart failure
Greco, S., Zaccagnini, G., Fuschi, P., Voellenkle, C., Carrara, M., Sadeghi, I., Bearzi, C., Maimone, B., Castelvecchio, S., Stellos, K., et al. (2017) · Cardiovascular Research · doi:10.1093/cvr/cvx013 · Cited by 94
Modulation of γ- and β-secretases as early prevention against Alzheimer's disease
Voytyuk, I., De Strooper, B., & Chávez-Gutiérrez, L. (2018) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.08.001 · Cited by 67
Upregulation of APP endocytosis by neuronal aging drives amyloid-dependent synapse loss
Burrinha, T., Martinsson, I., Gomes, R., Terrasso, A. P., Gouras, G. K., & Almeida, C. G. (2021) · Journal of Cell Science · doi:10.1242/jcs.255752 · Cited by 64
Is It the Twilight of BACE1 Inhibitors?
Hrabinova, M., Pejchal, J., Kucera, T., Jun, D., Schmidt, M., & Soukup, O. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666200503023323 · Cited by 28
Hasan, N., Zameer, S., Najmi, A. K., Parvez, S., & Akhtar, M. (2022) · Neurotoxicity Research · doi:10.1007/s12640-022-00482-x · Cited by 17
RetractedMazdeh, M., Komaki, A., Omrani, M. D., Gharzi, V., Sayad, A., Taheri, M., & Ghafouri-Fard, S. (2018) · Neurological Sciences · doi:10.1007/s10072-018-3458-3 · Cited by 15
Metadata
- Authors
- Vassar, R., & Cole, S.
- Venue
- Current Genomics
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2007-12-01
- Volume
- 8
- Issue
- 8
- Pages
- 509-530
- ISSN
- 1389-2029
- PMC
- PMC2647160
- Cited by
- 84
- References
- 255
- Language
- en
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