US-20260125427-A1 - METHOD FOR PREVENTING FORMATION OF AMYLOID B AGGREGATION AND TREATING AMYLOIDOSIS BY USING SYNTHETIC PEPTIDE

Abstract

The present disclosure provides a method for preventing formation of amyloid β aggregation and a method for treating amyloidosis by using a synthetic peptide. The synthetic peptide of the present disclosure achieves the effect of preventing formation of amyloid β aggregation and treating amyloidosis through various efficacy experiments.

Inventors

• Der-Yang CHO
• Shao-Chih CHIU
• Shi-Wei Huang
• Chih-Ming Pan
• Mei-Chih Chen
• Yu-Chuan Lin
• Yeh Chen
• Chung-Chun Wu

Assignees

• CHINA MEDICAL UNIVERSITY HOSPITAL

Dates

Publication Date

20260507

Application Date

20250515

Claims (11)

1. 1 . A method for preventing formation of Tau P301L protein aggregation, comprising treating to an in vitro sample an effective amount of a pharmaceutical composition comprising a synthetic peptide, wherein the synthetic peptide comprises the amino acid sequence of SEQ ID NO: 1, and the effective amount is 3.125-50 μM.
2. 2 . (canceled)
3. 3 . (canceled)
4. 4 . (canceled)
5. 5 . (canceled)
6. 6 . (canceled)
7. 7 . (canceled)
8. 8 . (canceled)
9. 9 . (canceled)
10. 10 . A method for treating amyloidosis, comprising administering the pharmaceutical composition according to claim 1 .
11. 11 . The method according to claim 10 , wherein the amyloidosis is Parkinson's disease (PD) or Alzheimer's disease (AD).

Description

STATEMENT REGARDING SEQUENCE LISTING The sequence listing associated with this application is provided in text format in lieu of a paper copy and is hereby incorporated by reference into the specification. The name of the XML file containing the sequence listing is 114F0183-IE_Sequence_listing. The XML file is 2000 bytes; was created on May 15, 2025. BACKGROUND OF THE INVENTION 1. Field of the Invention The present invention relates to a method for preventing formation of amyloid β aggregation and a method for treating amyloidosis by using a synthetic peptide. 2. The Prior Art Amyloid is an insoluble fibrous protein. Abnormal accumulation in organs can cause amyloidosis. In many neurological diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), large amounts of amyloid protein accumulation can be observed in the nervous system. Many scholars believe it may cause degeneration or dysfunction of the brain or other organs. Alzheimer's disease (AD) is characterized by the accumulation of amyloid β (Aβ) in the brain and is the leading cause of dementia worldwide, affecting an increasing number of the elderly population. According to a report by the Alzheimer's Disease International, more than 50 million people worldwide were suffering from dementia in 2020, and this number will double almost every 20 years, reaching 82 million people in 2030. In 2050, it will reach 152 million people. Unfortunately, there is currently no cure for most types of dementia. If there is one valuable lesson learned from the numerous clinical trial failures of new Alzheimer's drugs, it is that when amyloid β (Aβ) deposits and tangles have not yet caused irreversible damage to the brain, the disease should be immediately treated with early intervention. In view of the fact that current drugs for treating amyloidosis still have shortcomings of side effects, chemical synthesis and ineffective effects, in order to solve the above-mentioned problems, those skilled in the art urgently need to develop a novel and more effective medicament for treating amyloidosis for the benefit of a large group of people in need thereof. SUMMARY OF THE INVENTION A primary objective of the present invention is to provide a method for preventing formation of amyloid β aggregation, comprising administering to a subject in need thereof a pharmaceutical composition comprising a synthetic peptide and a pharmaceutically acceptable carrier, wherein the synthetic peptide comprises the amino acid sequence of SEQ ID NO:1. According to an embodiment of the present invention, the synthetic peptide prevents pan-amyloid β-sheet aggregation. According to an embodiment of the present invention, the pan-amyloid is amyloid β (Aβ) or Tau protein. According to an embodiment of the present invention, the Tau protein is recombinant Tau P301L protein. According to an embodiment of the present invention, the TTR is recombinant TTR protein (V122I). According to an embodiment of the present invention, the TTR is recombinant TTR protein (V30I). According to an embodiment of the present invention, the synthetic peptide maintains cell viability of 1-methyl-4-phenylpyridin-1-ium (MPP)+-treated SH-SY5Y-derived dopaminergic-like neurons. According to an embodiment of the present invention, the synthetic peptide prevents formation of amyloid aggregates in MPP+-treated SH-SYSY-derived dopaminergic-like neurons. According to an embodiment of the present invention, the synthetic peptide prevents formation of amyloid aggregates in Aβ-treated SH-SY SY-derived neuron-like cells. Another objective of the present invention is to provide a method for treating amyloidosis, comprising administering to a subject in need thereof the above mentioned pharmaceutical composition. According to an embodiment of the present invention, the amyloidosis is Parkinson's disease (PD) or Alzheimer's disease (AD). In summary, the present invention achieves the effect of treating amyloidosis (such as Parkinson's disease and Alzheimer's disease) through the results illustrated in the following examples. The embodiments of the present invention would be further described below. The following examples are used to illustrate the present invention and are not intended to limit the scope of the present invention. Anyone skilled in the art can make some changes and modifications without departing from the spirit and scope of the present invention. Therefore, the scope of the present invention shall be defined by the appended claims. BRIEF DESCRIPTION OF THE DRAWINGS The following drawings form part of the present specification and are included here to further demonstrate some aspects of the present invention, which can be better understood by reference to one or more of these drawings, in combination with the detailed description of the embodiments presented herein. FIG. 1 shows affinity of PAA peptide to Tau fibrils. FIG. 2 shows that PAA peptide can prevent pan-amyloid β-sheet aggregation (Aβ). FIG. 3 shows