Protein aggregation inhibitor shows lower levels of cell death and paralysis in mice with acute strokes.
Date:
Source:
Osaka Metropolitan University
Summary:
Stroke kills millions, but Osaka researchers have unveiled GAI-17, a drug that halts toxic GAPDH clumping, slashes brain damage and paralysis in mice—even when given six hours post-stroke—and shows no major side effects, hinting at a single therapy that could also tackle Alzheimer’s and other tough neurological disorders.
FULL STORY
GAI-17 shields mouse brains from stroke damage, restores movement, works up to six hours after onset, and does so without harming heart or vessels, opening doors to treat various neurodegenerative diseases. Credit: Shutterstock
Stroke is said to be the second leading cause of death worldwide after heart disease. To prevent the death of neurons in the brain, a research group led by Osaka Metropolitan University Associate Professor Hidemitsu Nakajima of the Graduate School of Veterinary Science has developed a drug that inhibits a protein involved in cell death.
The multifunctional protein GAPDH (glyceraldehyde-3-phosphate dehydrogenase) is linked to pathogenesis in many intractable brain and nervous system diseases. The team developed GAI-17, a GAPDH aggregation inhibitor. When this inhibitor was administered to model mice with acute strokes, there was a significantly lower level of brain cell death and paralysis compared to untreated mice.
GAI-17 also showed no side effects of concern, such as adverse effects on the heart or cerebrovascular system. Furthermore, experiments using GAI-17 showed improvement in the mice even when administered six hours after a stroke.
"The GAPDH aggregation inhibitor we have developed is expected to be a single drug that can treat many intractable neurological diseases, including Alzheimer's disease," stated Professor Nakajima. "Going forward, we will verify the effectiveness of this approach in disease models other than stroke and promote further practical research toward the realization of a healthy and long-lived society."
The findings were published in iScience.
Story Source:
Materials[1] provided by Osaka Metropolitan University. Note: Content may be edited for style and length.
Journal Reference:
Masanori Itakura, Takeya Kubo, Akihiro Kaneshige, Masatoshi Nakatsuji, Naoki Harada, Ryoichi Yamaji, Takatoshi Hikida, Takashi Inui, Hidemitsu Nakajima. Inhibition of GAPDH aggregation as a potential treatment for acute ischemic stroke. iScience, 2025; 28 (6): 112564 DOI: 10.1016/j.isci.2025.112564[2]
Cite This Page:
Osaka Metropolitan University. "Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s." ScienceDaily. ScienceDaily, 15 July 2025. <www.sciencedaily.com/releases/2025/07/250715043357.htm>.
Osaka Metropolitan University. (2025, July 15). Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s. ScienceDaily. Retrieved July 15, 2025 from www.sciencedaily.com/releases/2025/07/250715043357.htm
Osaka Metropolitan University. "Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s." ScienceDaily. www.sciencedaily.com/releases/2025/07/250715043357.htm (accessed July 15, 2025).
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Nov. 17, 2023 Proteins misfolding and clumping together, a process known as aggregation, is a key feature seen in several neurological conditions, including Alzheimer's and Parkinson's diseases. These ...
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Protein aggregation inhibitor shows lower levels of cell death and paralysis in mice with acute strokes.
Date:
Source:
Osaka Metropolitan University
Summary:
Stroke kills millions, but Osaka researchers have unveiled GAI-17, a drug that halts toxic GAPDH clumping, slashes brain damage and paralysis in mice—even when given six hours post-stroke—and shows no major side effects, hinting at a single therapy that could also tackle Alzheimer’s and other tough neurological disorders.
FULL STORY
GAI-17 shields mouse brains from stroke damage, restores movement, works up to six hours after onset, and does so without harming heart or vessels, opening doors to treat various neurodegenerative diseases. Credit: Shutterstock
Stroke is said to be the second leading cause of death worldwide after heart disease. To prevent the death of neurons in the brain, a research group led by Osaka Metropolitan University Associate Professor Hidemitsu Nakajima of the Graduate School of Veterinary Science has developed a drug that inhibits a protein involved in cell death.
The multifunctional protein GAPDH (glyceraldehyde-3-phosphate dehydrogenase) is linked to pathogenesis in many intractable brain and nervous system diseases. The team developed GAI-17, a GAPDH aggregation inhibitor. When this inhibitor was administered to model mice with acute strokes, there was a significantly lower level of brain cell death and paralysis compared to untreated mice.
GAI-17 also showed no side effects of concern, such as adverse effects on the heart or cerebrovascular system. Furthermore, experiments using GAI-17 showed improvement in the mice even when administered six hours after a stroke.
"The GAPDH aggregation inhibitor we have developed is expected to be a single drug that can treat many intractable neurological diseases, including Alzheimer's disease," stated Professor Nakajima. "Going forward, we will verify the effectiveness of this approach in disease models other than stroke and promote further practical research toward the realization of a healthy and long-lived society."
The findings were published in iScience.
Story Source:
Materials[1] provided by Osaka Metropolitan University. Note: Content may be edited for style and length.
Journal Reference:
Masanori Itakura, Takeya Kubo, Akihiro Kaneshige, Masatoshi Nakatsuji, Naoki Harada, Ryoichi Yamaji, Takatoshi Hikida, Takashi Inui, Hidemitsu Nakajima. Inhibition of GAPDH aggregation as a potential treatment for acute ischemic stroke. iScience, 2025; 28 (6): 112564 DOI: 10.1016/j.isci.2025.112564[2]
Cite This Page:
Osaka Metropolitan University. "Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s." ScienceDaily. ScienceDaily, 15 July 2025. <www.sciencedaily.com/releases/2025/07/250715043357.htm>.
Osaka Metropolitan University. (2025, July 15). Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s. ScienceDaily. Retrieved July 15, 2025 from www.sciencedaily.com/releases/2025/07/250715043357.htm
Osaka Metropolitan University. "Six-hour ‘undo’ button: GAI-17 rewinds stroke damage and may beat Alzheimer’s." ScienceDaily. www.sciencedaily.com/releases/2025/07/250715043357.htm (accessed July 15, 2025).
July 15, 2025 A cutting-edge mouse study reveals that tirzepatide, the dual GLP-1/GIP drug already hailed for impressive weight loss, does more than trim fat: it slashes the growth of obesity-linked breast tumors. ...
Nov. 17, 2023 Proteins misfolding and clumping together, a process known as aggregation, is a key feature seen in several neurological conditions, including Alzheimer's and Parkinson's diseases. These ...
Mar. 10, 2022 Researchers report that they found high levels of the protein Fli-1 in the brains of deceased Alzheimer's patients. Blocking Fli-1's action in a mouse model of Alzheimer's disease ...
Oct. 5, 2021 A drug commonly used to treat cancer can restore memory and cognitive function in mice that display symptoms of Alzheimer's disease, new research has found. The drug, Axitinib, inhibits growth ...
Feb. 1, 2021 Millions of patients suffering from neurological and mental disorders such as depression, addiction, and chronic pain are treatment-resistant. New research paves the way for a promising alternative: ...
Oct. 12, 2020 Researchers building a model of muscle damage in a cultured system found that components leaking from broken muscle fibers activate ''satellite cells,'' which are muscle stem ...
