Category: News

DEAR MAYO CLINIC: I’ve recently been diagnosed with inflammatory bowel disease. I’m trying to understand what IBD is and how it will affect me. Will I need surgery?

ANSWER: Inflammatory bowel disease, or IBD, is an umbrella term for a group of chronic conditions that cause inflammation and swelling in the digestive tract. It primarily includes two conditions: ulcerative colitis and Crohn’s disease. While both involve inflammation, they affect different parts of the gastrointestinal (GI) tract and behave differently over time.

Symptoms of both categories of IBD usually include belly pain, diarrhea, rectal bleeding, extreme fatigue colitis typically affects the colon and rectum, and it leads to the development of sores called ulcers. On the other hand, Crohn’s disease primarily affects the small intestine and often involves deeper and weight loss. Some people experience mild illness, while in others, the disease can be debilitating and lead to life-threatening complications.

Diagnosing IBD

Diagnosing IBD involves a combination of tests and procedures. Your care team will begin by taking a detailed medical history and asking about your symptoms. To confirm the diagnosis, your care team may recommend:

• Blood tests to check for signs of inflammation, anemia or infection.
• Stool studies to rule out infections and detect markers of inflammation.
• Endoscopic procedures, such as:
  • Colonoscopy, which allows doctors to view the entire colon and take biopsies.
  • Flexible sigmoidoscopy, used when the colon is too inflamed for a complete colonoscopy.
  • Upper endoscopy, if symptoms involve the upper GI tract.
  • Capsule endoscopy, where you swallow a small camera to examine the small intestine.
  • Balloon-assisted enteroscopy, which is used to explore deeper parts of the small bowel.

A biopsy, a small tissue sample taken during endoscopy, is essential to confirm the diagnosis and distinguish IBD from other causes of inflammation.

Understanding the role of surgery

Most people with IBD are treated first with medications. These include anti-inflammatory drugs, immune system suppressors and biologics that target specific pathways in the immune response. However, surgery can become necessary when medications are no longer effective, not well tolerated or when complications arise.

In ulcerative colitis, a colectomy is performed when medications fail or when complications like perforation, obstruction, or cancerous changes occur. A colectomy is when the surgeon removes the entire colon and rectum. An internal pouch is then made and surgically attached to the anus to allow passing waste without an external bag. Sometimes, an internal pouch isn’t possible. In these cases, a permanent opening is surgically created in the abdomen, called an ileostomy.

Up to two-thirds of people with Crohn’s disease will require at least one surgery in their lifetime. During this operation, the surgeon removes the damaged part of the digestive tract and reconnects the healthy sections. Surgeons aim to preserve as much of the healthy intestine as possible. Surgery also may be needed for issues such as fistulas, bowel obstructions or perforations.

Surgical decisions are highly individualized and should be made in collaboration between the patient, gastroenterologist and surgeon. Factors that influence the decision include:

• Severity and location of disease.
• Response to medications.
• Overall health and nutritional status.
• Quality of life and personal preferences.

In urgent situations, such as a perforated bowel or severe bleeding, surgery may be performed immediately. But in most cases, there’s time for thoughtful discussion and planning.

What to expect moving forward

If you’re facing surgery for IBD, know that you’re not alone — and you’re not without options. The goal of surgery is always to improve your quality of life, reduce symptoms and prevent complications. Seek care from centers like Mayo Clinic that are well versed in IBD treatment and that approach care in a collaborative, compassionate way, tailoring the treatment plan to your unique needs.

Patients should feel empowered to ask questions and be part of the decision-making process. When surgery isn’t urgent, your team will work with you to ensure you’re in the best possible health before the operation and choose the approach to support long-term success.

Kellie Mathis, M.D., Colon and Rectal Surgery, Mayo Clinic, Rochester, Minnesota

The post Mayo Clinic Q&A: What does an IBD diagnosis mean for me? appeared first on Mayo Clinic News Network.

On this week’s episode of Tomorrow’s Cure, we explore brain-computer interfaces (BCIs), cutting-edge technologies that create direct communication pathways between the human brain and external devices. Once considered science fiction, BCIs are now transforming lives. 

The podcast episode features Dr. Jonathon Parker, epilepsy and functional neurosurgeon, assistant professor of neurosurgery and neuroscience, and director of the Neuroelectronics Research Lab at Mayo Clinic; and Dr. Allen Waziri, neuroscientist and neurosurgeon, and CEO and co-founder of iCE Neurosystems. Together, they discuss the science behind BCIs, current medical applications and the transformative possibilities they hold for the future.

BCIs offer groundbreaking possibilities in the treatment of neurological disorders, with the potential to restore mobility, communication and independence to people affected by severe neurologic injuries or conditions. Already, this technology is enabling users to control prosthetic limbs and digital interfaces through brain activity.

“The brain is a piece of hardware; the brain-computer interface is another piece of hardware we are connecting to the brain,” says Dr. Parker. “We are used to communicating through speech, movement, understanding other sensory inputs, right? So this is digitizing those inputs to solve a problem.” 

“BCIs, for several decades, is the translation of those electrical potentials that are coming off of the brain into something that we can understand on a computer side that will then functionalize whatever device — a robotic arm, a cursor on a screen, drive a wheelchair, so on and so forth,” says Dr. Waziri.

BCIs are being used to assist people with neurological injuries that impair speech or movement. However, experts believe this technology has far greater potential. Beyond restoring motor function, BCIs could pave the way for continuous neurological monitoring and new forms of intervention, opening doors to transformative applications in brain health.

Dr. Parker emphasizes the broader clinical implications of the technology. “When delivered to clinicians so they can just monitor the brain signals overtime, (it) could have tremendous impact for epilepsy, depression, Alzheimer’s — these conditions which are affecting huge swaths of our population. That’s the future of this technology,” he says. 

Don’t miss this thought-provoking conversation on the evolving science of BCIs and the remarkable innovations that could redefine human-machine interaction. Listen to the latest episode of Tomorrow’s Cure, and explore the full library of episodes and guests at tomorrowscure.com.

The post Tommorow’s Cure: Mind meets machine — the future of neurological care appeared first on Mayo Clinic News Network.

On this week’s episode of Tomorrow’s Cure, we explore brain-computer interfaces (BCIs), cutting-edge technologies that create direct communication pathways between the human brain and external devices. Once considered science fiction, BCIs are now transforming lives. 

The podcast episode features Dr. Jonathon Parker, epilepsy and functional neurosurgeon, assistant professor of neurosurgery and neuroscience, and director of the Neuroelectronics Research Lab at Mayo Clinic; and Dr. Allen Waziri, neuroscientist and neurosurgeon, and CEO and co-founder of iCE Neurosystems. Together, they discuss the science behind BCIs, current medical applications and the transformative possibilities they hold for the future.

BCIs offer groundbreaking possibilities in the treatment of neurological disorders, with the potential to restore mobility, communication and independence to people affected by severe neurologic injuries or conditions. Already, this technology is enabling users to control prosthetic limbs and digital interfaces through brain activity.

“The brain is a piece of hardware; the brain-computer interface is another piece of hardware we are connecting to the brain,” says Dr. Parker. “We are used to communicating through speech, movement, understanding other sensory inputs, right? So this is digitizing those inputs to solve a problem.” 

“BCIs, for several decades, is the translation of those electrical potentials that are coming off of the brain into something that we can understand on a computer side that will then functionalize whatever device — a robotic arm, a cursor on a screen, drive a wheelchair, so on and so forth,” says Dr. Waziri.

BCIs are being used to assist people with neurological injuries that impair speech or movement. However, experts believe this technology has far greater potential. Beyond restoring motor function, BCIs could pave the way for continuous neurological monitoring and new forms of intervention, opening doors to transformative applications in brain health.

Dr. Parker emphasizes the broader clinical implications of the technology. “When delivered to clinicians so they can just monitor the brain signals overtime, (it) could have tremendous impact for epilepsy, depression, Alzheimer’s — these conditions which are affecting huge swaths of our population. That’s the future of this technology,” he says. 

Don’t miss this thought-provoking conversation on the evolving science of BCIs and the remarkable innovations that could redefine human-machine interaction. Listen to the latest episode of Tomorrow’s Cure, and explore the full library of episodes and guests at tomorrowscure.com.

The post Tommorow’s Cure: Mind meets machine — the future of neurological care appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.

Changes in how brain cells generate energy may drive the development of Alzheimer’s disease and influence how patients respond to therapy, according to a new study from Mayo Clinic researchers. The findings, published in the journal Alzheimer’s & Dementia, spotlight mitochondrial complex I — a critical component of cellular energy production — as both a contributor to disease progression and a promising target for new treatments.

Led by senior author Eugenia Trushina, Ph.D., the Mayo Clinic team found that disruptions in complex I activity can trigger gene expression patterns commonly observed in Alzheimer’s disease. The researchers demonstrated that using small molecules to gently adjust how complex I functions can help activate protective mechanisms in brain cells.

“This research offers new clues about how Alzheimer’s begins and shows a promising new path for developing better, more personalized treatments,” says Dr. Trushina, a researcher who studies neurodegenerative diseases.

Mitochondria, often described as the powerhouse of the cell, produces the energy necessary for proper cellular function. In neurons, which have especially high energy demands, mitochondrial dysfunction can have devastating consequences. The Mayo Clinic researchers found that when complex I is not working properly, it disrupts how brain cells manage energy and respond to stress — changes that resemble those seen in the brains of people with Alzheimer’s disease.

Using experimental models and advanced molecular and computational tools, the team showed that mild modulation of complex I activity with specially designed small molecules helped neurons launch protective responses, such as reducing inflammation and improving energy balance.

Interestingly, they found that males and females responded differently to these treatments, suggesting a need for sex-specific approaches to therapy. “This sex-dependent effect is intriguing,” says Dr. Trushina. “It suggests that future therapies could be tailored by sex, especially for a disease like Alzheimer’s that affects men and women differently.”

Current Alzheimer’s treatments mostly focus on managing symptoms or targeting hallmark brain changes such as amyloid plaques and tau tangles. However, these approaches have seen limited success in halting disease progression. The new study points to mitochondrial dysfunction as a possible upstream trigger — one that may begin long before cognitive symptoms emerge.

“This study gives us a deeper understanding of the cellular events that spark Alzheimer’s and, more importantly, how we might intervene to slow or prevent its progression,” says Dr. Trushina. “Our results open the door to a new class of drugs that work by protecting the brain’s energy supply and buffering it against early disease-related changes.”

The research is part of a larger effort at Mayo Clinic called the Precure initiative, focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions. In the future, the team plans to further investigate the safety and effectiveness of complex I modulators in preclinical models, with the goal of advancing into clinical trials.

The post Mitochondrial dysfunction linked to Alzheimer’s onset and treatment response appeared first on Mayo Clinic News Network.