Aging is a biological process that no one can avoid. Ideally, growing old should be a time to relax and enjoy the fruits of your labor. Aging also has a darker side, however, often linked to disease.

Every second, your cells perform billions of biochemical reactions that fuel essential functions for life, forming a highly interconnected metabolic network. This network enables cells to grow, proliferate and repair themselves, and its disruption can drive the aging process.

But does aging cause metabolic decline, or does metabolic disruption accelerate aging? Or both?

To address this chicken-or-egg question, you first need to understand how metabolic processes break down during aging and disease. I am a scientist and researcher, and my lab focuses on exploring the complex relationship between metabolism, stress and aging. Ultimately, we hope this work will provide strategies to promote healthier aging and more vibrant lives.

Link between metabolism and aging

Aging is the most significant risk factor for many of society’s most common diseases, including diabetes, cancer, cardiovascular disease and neurodegenerative disorders. A key factor behind the onset of these health issues is the disruption of cellular and metabolic homeostasis, or balance. Disrupting homeostasis destabilizes the body’s internal environment, leading to imbalances that can trigger a cascade of health issues, including metabolic disorders, chronic diseases and impaired cellular functions that contribute to aging and other serious conditions.

Disrupted metabolism is linked to many hallmarks of aging cells, such as telomere shortening, which is damage to the protective ends of chromosomes, and genomic instability, the tendency to form genetic mutations.

A dysfunctional metabolism is also linked to poorly functioning mitochondria; cellular senescence, or when cells stop dividing; imbalances in gut microbes; and cells’ reduced ability to detect and respond to different nutrients.

Neurological disorders, such as Alzheimer’s disease, are prime examples of age-related conditions with a strong link between dysregulated metabolism and functional decline. For example, my research team previously discovered that in aging mice, the ability of bone marrow cells to produce, store and use energy is suppressed due to increased activity from a protein that modulates inflammation. This energy-deficient state leads to an increase in inflammation that’s worsened by these aging cells’ reliance on glucose as their main fuel source.

Experimentally inhibiting this protein in the bone marrow cells of aging mice, however, revitalizes the cells’ ability to produce energy, reduces inflammation and improves plasticity of an area of the brain involved in memory. This finding suggests that some cognitive aging could be reversed by reprogramming the glucose metabolism of bone marrow cells to restore immune functions.

Repurposing drugs to treat Alzheimer’s

In our newly published research, my team and I discovered a new connection between disrupted glucose metabolism and neurodegenerative disease. This led us to identify a drug originally designed for cancer that could potentially be used to treat Alzheimer’s.

We focused on an enzyme called IDO1 that plays a critical role in the first step of breaking down amino acid tryptophan. This pathway produces a key compound called kynurenine, which fuels additional energy pathways and inflammatory responses. However, excessive kynurenine can have detrimental effects, including increasing the risk of developing Alzheimer’s.

We found that inhibiting IDO1 can recover memory and brain function in a range of preclinical models, including in cell cultures and mice. To understand why, we looked at the metabolism of brain cells. The brain is one of the most glucose-dependent tissues in the body. An inability to properly use glucose to fuel critical brain processes can lead to metabolic and cognitive decline.

High levels of IDO1 reduce glucose metabolism by producing excess kynurenine. So IDO1 inhibitors – originally designed to treat cancers such as melanoma, leukemia and breast cancer – could be repurposed to reduce kynurenine and improve brain function.

Using a range of lab models, including mice and cells from Alzheimer’s patients, we also found that IDO1 inhibitors can restore glucose metabolism in brain cells. Furthermore, we were able to restore glucose metabolism in mice with both amyloid and tau accumulation – abnormal proteins involved in many neurodegenerative disorders – by blocking IDO1. We believe repurposing these inhibitors could be beneficial across various neurodegenerative disorders.

Promoting healthier cognitive aging

The effects of neurological disorders and metabolic decline weigh heavily on individuals, families and the economy.

While many scientists have focused on targeting the downstream effects of these diseases, such as managing symptoms and slowing progression, treating these diseases earlier can improve cognition with aging. Our findings suggest that targeting metabolism has the potential to not only slow neurological decline but also to reverse the progression of neurodegenerative diseases such as Alzheimer’s, Parkinson’s and dementia.

Discovering new insights at the intersection of stress, metabolism and aging can pave the way for healthier aging. More research can improve our understanding of how metabolism affects stress responses and cellular balance throughout life.

Melanie R. McReynolds, Assistant Professor of Biochemistry, Penn State

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Eating the seaweed Ecklonia cava may be able to slow down or prevent Parkinson’s disease, according to a 2024 study.

Researchers found that antioxidants in the seaweed – which is often used in soups and salads in Asian cuisine – may protect our neurons from free radicals to prevent this debilitating disease.

Parkinson’s is a condition that affects the nervous system, causing symptoms like shaking, stiffness and difficulty moving. It happens when neurons that produce dopamine – a chemical that helps control movement – start to die off in the brain. While Parkinson’s is not itself fatal, it causes serious complications that can lead to death. Unfortunately, there is no cure yet.

But researchers have previously found links between dietary antioxidants and Parkinson’s prevention. For example, research has found that resveratrol – which is in many plants and fruits including red grapes, berries and peanuts – protected the neurons producing dopamine in the brain from death in several mouse models of Parkinson’s disease.

Ellagic acid, α-lipoic acid and myrtenal all improved learning and memory performance as well as neuromuscular coordination in mouse models of Parkinson’s. Ellagic acid is found in many fruits and vegetables including grapes, pomegranates, berries and nuts.

Myrtenal is found in various plants, such as hyssop and sage. And α-lipoic acid is found in red meat, spinach and broccoli.

Several studies have suggested that drinking tea can help prevent Parkinson’s disease. Although we don’t really know how it works, some research suggests it is due to the antioxidants that tea contains.

Fighting free radicals

Our body produces harmful free radicals in response to environmental insults such as ultraviolet rays and air pollution. Free radicals are also a natural byproduct of normal processes in cells.

Antioxidants are like bodyguards, protecting cells from the damage caused by free radicals. Our body naturally produces antioxidants but some foods, like Ecklonia cava, are rich in antioxidants and can supplement our naturally produced antioxidants to help our bodies battle free radical damage.

For the most recent study, based in Japan, researchers induced Parkinson’s disease in mice using the pesticide rotenone. Rotenone kills the neurons that produce dopamine in the brain, which causes the mice to develop a disease that looks like Parkinson’s, with similar symptoms, such as slower movement and impaired gastrointestinal motility (when there are problems moving food and waste through the digestive tract).

Once the researchers induced Parkinson’s in the mice, they fed some with antioxidants from Ecklonia cava and some with a regular diet. They found that the neurons producing dopamine in the brain of the mice fed with antioxidants seemed to be protected. Also, those mice had fewer Parkinson’s symptoms than the mice fed with the regular diet.

The researchers also looked at the effect of antioxidants in cells grown in a dish and exposed to rotenone. Rotenone increases the production of free radicals, killing the cells.

The researchers found that antioxidants decreased the production of free radicals induced by rotenone in the cells, preventing cell death. This research opens up the possibility of using Ecklonia cava polyphenols – plant compounds with antioxidant properties – to develop new treatments and prevention methods for Parkinson’s.

Lost in translation?

Unfortunately, results from studies on animal models and cells are not always translatable to humans. For example, despite the protective action of another antioxidant, vitamin C, found in cells and animal models to protect against Parkinson’s, it does not seem to have the same effect in humans.

This is because animal and cell models do not completely mimic Parkinson’s disease in humans. Animals have different brain structures and functions compared to humans, which means the way the disease develops and progresses can be different. On the other hand, cell models, even if researchers use human cells, lack complexity.

Swimming, sailing, even just building a sandcastle - the ocean benefits our physical and mental wellbeing. Curious about how a strong coastal connection helps drive marine conservation, scientists are diving in to investigate the power of blue health.

This article is part of a series, Vitamin Sea, exploring how the ocean can be enhanced by our interaction with it.

Parkinson’s disease affects the entire brain and body, involving many different types of cells and interactions. Cell models usually focus on a single type of cell, missing out on this complexity.

Parkinson’s disease develops over many years, with symptoms changing over time. Cell and animal models cannot easily replicate this long-term progression. For example, the maximum lifespan of most laboratory mice is two years, whereas Parkinson’s is thought to develop over decades.

In conclusion, robust large-scale clinical trials are needed to validate the efficacy of Ecklonia cava in preventing or slowing down Parkinson’s. However, because Ecklonia cava is already available in food supplements, it probably does no harm to take it on a regular basis.

Will it prevent you from getting Parkinson’s? Maybe, but so does regular exercise.

Marine Krzisch, Lecturer in Neuroscience, University of Leeds

This article is republished from The Conversation under a Creative Commons license. Read the original article.