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Review
. 2018 Feb 7:10:21.
doi: 10.3389/fnagi.2018.00021. eCollection 2018.

Use of Peptides for the Management of Alzheimer's Disease: Diagnosis and Inhibition

Mohammad H Baig  1 , Khurshid Ahmad  1 , Gulam Rabbani  1 , Inho Choi  1
Affiliations
Free PMC article
Review

Use of Peptides for the Management of Alzheimer's Disease: Diagnosis and Inhibition

Mohammad H Baig et al. Front Aging Neurosci. .
Free PMC article

Abstract

Alzheimer's disease (AD) is a form of dementia and the most common progressive neurodegenerative disease (ND). The targeting of amyloid-beta (Aβ) aggregation is one of the most widely used strategies to manage AD, and efforts are being made globally to develop peptide-based compounds for the early diagnosis and treatment of AD. Here, we briefly discuss the use of peptide-based compounds for the early diagnosis and treatment of AD and the use of peptide-based inhibitors targeting various Aβ aggregation checkpoints. In addition, we briefly discuss recent applications of peptide-based inhibitors against various AD targets including amyloid beta, β-site amyloid precursor protein cleaving enzyme 1 (BACE1), Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), tyrosine phosphatase (TP) and potassium channel KV1.3.

Keywords: Alzheimer’s disease; BACE-1; GAPDH; amyloid beta; diagnosis; inhibitors; peptides.

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Figures

Figure 1
Figure 1
Amyloidogenic amyloid precursor protein (APP) processing and the possible applications of peptide inhibitors to prevent amyloid-beta (Aβ) plaque formation at different disease stages.
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References

    1. Alexi T., Hughes P. E., van Roon-Mom W. M., Faull R. L., Williams C. E., Clark R. G., et al. . (1999). The IGF-I amino-terminal tripeptide glycine-proline-glutamate (GPE) is neuroprotective to striatum in the quinolinic acid lesion animal model of Huntington’s disease. Exp. Neurol. 159, 84–97. 10.1006/exnr.1999.7168 - DOI - PubMed
    1. Alonso De Diego S. A., Muñoz P., González-Muñiz R., Herranz R., Martín-Martínez M., Cenarruzabeitia E., et al. . (2005). Analogues of the neuroprotective tripeptide Gly-Pro-Glu (GPE): synthesis and structure-activity relationships. Bioorg. Med. Chem. Lett. 15, 2279–2283. 10.1016/j.bmcl.2005.03.015 - DOI - PubMed
    1. Alzheimer’s Association (2017). Alzheimer’s disease facts and figures. Alzheimers Dement. 13, 325–373. 10.1016/j.jalz.2017.02.001 - DOI
    1. Austen B. M., Paleologou K. E., Ali S. A., Qureshi M. M., Allsop D., El-Agnaf O. M. (2008). Designing peptide inhibitors for oligomerization and toxicity of Alzheimer’s β-amyloid peptide. Biochemistry 47, 1984–1992. 10.1021/bi701415b - DOI - PubMed
    1. Bansal S., Maurya I. K., Yadav N., Thota C. K., Kumar V., Tikoo K., et al. . (2016). C-terminal fragment, Aβ32–37, analogues protect against aβ aggregation-induced toxicity. ACS Chem. Neurosci. 7, 615–623. 10.1021/acschemneuro.6b00006 - DOI - PubMed