Various Products / Alzheimer's Disease

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CAT# Product Name M.W Molecular Formula Inquiry
10-101-317 Galanin, human 3157.4 C139H210N42O43 Inquiry
A13004 Amyloid Toxicity Inhibitor Peptide 110 1018.2 Inquiry
A13119 Beta-Amyloid/A4 Protein Precursor (APP) (96-110) 1918.2 Inquiry
A13180 Humanin, human 2687.3 C119H204N34O32S2 Inquiry
A13208 Non-beta-Amyloid Component of Alzheimer.s Disease (NAC) 3373.8 Inquiry
A13355 Serum Amyloid P-Component 786 Inquiry
A13365 Amyloid Toxicity Inhibitor Peptide 13 872.0 Inquiry
A13374 Amyloid Toxicity Inhibitor Peptide 11 940.1 Inquiry
A13376 Amyloid Toxicity Inhibitor Peptide 111 972.1 Inquiry
C07001 Acetyl-Calpastatin (184-210) (human) 3177.6 C142H230N36O44S Inquiry
C29004 CRF (6-33) (human, rat) 3220.70 C141H231N41O43S Inquiry
CAD-074 Abz-Gly-Ala-Lys(Ac)-Ala-Ala-Dap(Dnp)-NH₂ Inquiry
CAD-075 Abz-Gly-Ile-Val-Arg-Ala-Lys(Dnp)-OH 928.02 C₄₁H₆₁N₁₃O₁₂ Inquiry
CAD-076 Amyloid Bri Protein Precursor₂₇₇ (244-266) 2627.99 C₁₁₆H₁₇₅N₃₁O₃₅S₂ Inquiry
CAD-077 Amyloid Bri Protein Precursor₂₇₇ (244-277) (reduced) 3937.52 C₁₇₃H₂₇₅N₄₉O₅₂S₂ Inquiry
CAD-078 Amyloid Dan Protein Precursor₂₇₇ (244-277) 4044.59 C₁₈₅H₂₆₈N₄₈O₅₁S₂ Inquiry
CAD-079 Amyloid P Component (27-38) amide 1494.78 C₆₈H₁₀₇N₁₉O₁₇S Inquiry
CAD-080 Tyr-Amyloid P Component (27-38) amide 1657.96 C₇₇H₁₁₆N₂₀O₁₉S Inquiry
CAD-081 Amyloid P Component (33-38) amide 784.98 C₃₇H₅₆N₁₀O₇S Inquiry
CAD-082 (Asp(4-aminobutylamide)¹·⁷·²³,Glu(4-aminobutylamide)³·¹¹·²²)-Amyloid β-Protein (1-40) 4750.69 C₂₁₈H₃₅₅N₆₅O₅₂S Inquiry

Introduction

Alzheimer's disease (AD) is the most common fatal neurodegenerative disease (ND),) characterized by loss of neuronal structure and function. Over the past few decades, AD and its associated risk factors have become a major health care problem in most developed countries. In addition, Alzheimer's disease is reported to be the fifth leading cause of death among people over 65 years of age, with an incidence of more than 5 million cases per year in the United States (Alzheimer's Association, 2017). The World Health Organization (WHO) estimates that the prevalence of Alzheimer’s disease worldwide will quadruple to about 114 million people by 2050 (Alzheimer's Association, 2017).

Pathogenesis

The pathological features of AD include extracellular plaques (extracellular amyloid plaques) and neurofibrillary tangles within neurons (hyperphosphorylated tau protein accumulation; Vanitallie, 2015). These pathological changes gradually lead to loss of neurons, and ultimately lead to neuron death. Although the etiology and pathogenesis of AD is still unclear, the amyloid cascade theory has been widely accepted and supported by some studies (Drachman, 2014; Herrup, 2015). A protective mutation of amyloid precursor protein (APP) (APP) was found near the β -cleavage site of amyloid precursor protein (APP), which could prevent the development of late-onset dementia (Jonsson et al., 2012). This assumption is further reinforced.

Application of Peptide in Alzheimer's disease

In the past few years, the applicability of several Aβ aggregation peptide inhibitors as new therapeutic lead compounds has been studied. In conclusion, very few IA β5, Aβ 12-28P, LPYF Da, Trp-Aib, D-4F and D3 are effective in rodent models. It is not clear whether peptide inhibitors should target Aβ, oligomeric Aβ or Aβ fibrils deposited in plaques. It is not clear whether Aβ 1-40 or Aβ 1-42 should be treated, and weather compounds need to pass through BBB to be effective. More work needs to be done to elucidate the properties of the most synaptotoxic Aβ species in the genesis and development of AD. The ongoing studies on the peptides of different Aβ species and their effects on the aggregation and toxicity of Aβ will provide a basis for further understanding the molecular mechanism of AD.

References

  1. Hilbich, C., Kisters-Woike, B., Reed, J., Masters, C. L., & Beyreuther, K. (1991). Aggregation and secondary structure of synthetic amyloid βA4 peptides of Alzheimer’s disease. Journal of molecular biology, 218(1), 149-163.
  2. Roberts, B. R., Ryan, T. M., Bush, A. I., Masters, C. L., & Duce, J. A. (2012). The role of metallobiology and amyloid‐β peptides in Alzheimer’s disease. Journal of neurochemistry, 120, 149-166.
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