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neurons

Brain Cleaning Remedy: Green Tea & Vitamin B3 Boosts Alzheimer’s Risk

by Dr. Michael Lee – Health Editor August 8, 2025

written by Dr. Michael Lee – Health Editor

Brain “Cleaning” Process Revived in Lab Tests, Offering Potential Alzheimer’s Breakthrough

Irvine, CA – August 8, 2025 – Researchers at the University of California, Irvine (UCI) have announced a promising finding: a combination of Vitamin B3 (Nicotinamide) and a green tea antioxidant (Epigallocatechingallat – EGCG) can restore a key energy molecule in aging brain cells, boosting thier ability to clear out damaging metabolic waste – a process crucial in preventing neurodegenerative diseases like Alzheimer’s. The findings, published today in Gero Science, represent a potential new avenue for treating age-related cognitive decline.

The Science Behind Brain Waste removal

As we age,the brain’s natural “cleaning” system – responsible for removing cellular debris and protein build-up – becomes less efficient.This accumulation of waste products,especially amyloid proteins,is a hallmark of Alzheimer’s disease and other forms of dementia. The UCI team focused on Guanosine Triphosphate (GTP), an energy source within brain cells that powers this crucial waste removal process. They found that GTP levels decline with age, hindering the brain’s ability to function optimally.

“with increasing age,the energy of nerve cells in the brain decreases,which restricts the ability to remove unwanted proteins and damaged components,” explained lead author gregory Brewer. “We found that restoration of the energy level helps the neurons to regain this important cleaning function.”

In laboratory tests using isolated nerve cells, the combination of Nicotinamide and EGCG demonstrably reversed age-related cellular deficits and improved the cells’ capacity to eliminate harmful amyloid protein. A 24-hour treatment with the combination restored GTP levels to those typically found in younger, healthier cells. This energy boost also led to reduced oxidative stress, another key contributor to neurodegeneration.

Why GTP Matters & Future Implications

The study underscores the previously underestimated importance of GTP in maintaining healthy brain function. Researchers believe that by replenishing the brain’s energy reserves with readily available dietary supplements, a new therapeutic approach to combatting age-related cognitive decline and Alzheimer’s could be within reach.

Tho, the path to clinical application isn’t straightforward. Initial studies indicate that simply consuming Nicotinamide orally doesn’t deliver the desired effect, and drinking green tea alone is also insufficient. The team is now focused on identifying the optimal delivery method for this combination therapy. A recent clinical trial showed oral Nicotinamide was ineffective, suggesting a different administration route is necessary.

Key Details Not Explicitly Mentioned in the Original Article:

Amyloid Plaques & Tau Tangles: the article mentions amyloid proteins, but doesn’t explicitly state they form plaques. Alzheimer’s is characterized by both amyloid plaques and neurofibrillary tangles formed by the protein tau. Improving waste removal could possibly address both.
Glial Cells: While the research focuses on neurons, glial cells (astrocytes, microglia) play a critical role in brain waste clearance. The impact of Nicotinamide/EGCG on glial cell function warrants further investigation.
Blood-Brain Barrier: Successfully delivering these compounds to the brain requires overcoming the blood-brain barrier, a protective mechanism that limits the passage of substances from the bloodstream into brain tissue. This is a significant hurdle for any potential Alzheimer’s treatment. EGCG Bioavailability: EGCG has notoriously low bioavailability when ingested orally. This further complicates the challenge of achieving therapeutic levels in the brain.

This research offers a glimmer of hope in the ongoing fight against Alzheimer’s disease, highlighting the potential of harnessing the body’s natural processes to maintain brain health as we age.

August 8, 2025 0 comments

Health

Alzheimer’s Prediction: New Brainwave Biomarker Discovered

by Dr. Michael Lee – Health Editor August 5, 2025

written by Dr. Michael Lee – Health Editor

Summary of the Research on Early Alzheimer’s Detection

This article details a new method for potentially detecting Alzheimer’s disease up to two and a half years before diagnosis,using brain activity patterns. Here’s a breakdown of the key points:

New Early Marker: Researchers have identified a pattern in brain electrical signals, specifically in the beta frequency band, that predicts which patients with mild cognitive impairment will develop Alzheimer’s disease.
methodology: The study analyzed MEG (magnetoencephalography) recordings from 85 patients with mild cognitive impairment. MEG is a non-invasive technique to measure brain activity.
Spectral events Toolbox: A key tool used in the research was the “Spectral Events Toolbox,” developed at Brown University.This tool allows researchers to analyze MEG data at a neuronal level, identifying discrete brain activity events (when, how long, strength).
Key Findings: Patients who did develop Alzheimer’s within 2.5 years showed:
Lower rate of beta events
Shorter duration of beta events
Weaker power of beta events
Significance: This is the first time scientists have linked these specific beta event characteristics to Alzheimer’s disease progression. It offers a more direct way to assess neuronal response to the disease’s toxicity than current methods like spinal fluid or blood biomarkers.
Future Implications:
Early Diagnosis: The researchers hope this method can be used by clinicians for earlier diagnosis.
Treatment Monitoring: The tool could also be used to assess the effectiveness of Alzheimer’s treatments.
Understanding Mechanisms: Future research will focus on understanding why these beta event changes occur, with the goal of developing targeted therapies.In essence, this research represents a promising step towards earlier detection and potentially more effective treatment of Alzheimer’s disease.

August 5, 2025 0 comments

Health

Title=Tooth Nerves: More Than Just Pain Detectors

by Dr. Michael Lee – Health Editor August 3, 2025

written by Dr. Michael Lee – Health Editor

Tooth Nerves: Beyond Pain Detection, a Rapid Defense Mechanism

London. – Image by © Tim Sandle.

For years, it’s been understood that sensory neurons within teeth transmit pain signals to the brain. However, new research reveals these neurons have a crucial, additional function: triggering a rapid jaw-opening reflex designed to prevent tooth damage adn further injury.

While the existence of a craniofacial reflex causing the lower jaw to open suddenly was previously known, the specific cellular origins of this response remained a mystery until recently.

Researchers at the University of Michigan, spanning sensory neuroscience, dentistry, and mechanical engineering, utilized live imaging, behavioral tracking, and mouse molars to pinpoint the source of this reflex. Their work demonstrates that these neurons actively monitor both the inner tooth structure and the outer enamel.

This revelation underscores the vital role healthy, functioning nerves play in tooth preservation.

“We suspected tooth nerves had a more fundamental role than simply registering pain,” explains Joshua Emrick, senior author of the study and assistant professor at the U-M School of Dentistry. “Considering the potential for tooth pulp regeneration, restoring nerve function is paramount.”

The team observed nerve cell reactions to stimulation of mouse molars in real-time. These experiments identified a protective function for High-Threshold Mechanoreceptors (HTMRs) – specialized sensory neurons within the tooth that respond to damage. These HTMRs detect threats and quickly relay information to the brain, initiating an immediate response.

“Our study challenges the long-held belief that tooth nerves primarily exist to signal pain and prompt a dental visit,” Emrick states. “That jolt you feel when accidentally biting down on something hard, preventing a fracture? You can thank these intradental HTMRs for that.”

A Reflex Rooted in Self-Preservation

Emrick elaborates on the importance of the finding: “We believe this jaw-opening reflex, protecting teeth, is a conserved trait among mammals unable to replace teeth – like humans – and is also present in the molar teeth of mice. Furthermore, understanding these neurons’ ability to elicit pain opens avenues for developing improved toothache relief methods at the dentist’s office.”

The study details that damage to enamel or dentin triggers a response from these neurons.Subsequent experiments revealed that activating HTMRs not onyl causes acute pain, but also elicits a rapid jaw-opening reflex occurring within 5 to 15 milliseconds.

The protective capabilities of HTMRs may extend beyond teeth, perhaps safeguarding other oral and bodily structures, given the essential role sensory neurons play in tissue maintenance and protection throughout life.

The research findings are published in the journal Cell Reports under the title “Intradental mechano-nociceptors serve as sentinels that prevent tooth damage.”

August 3, 2025 0 comments

Health

Creatine may enhance neuroprotection through energy pathways

by Dr. Michael Lee – Health Editor July 27, 2025

written by Dr. Michael Lee – Health Editor

Creatine Powers More Than Muscle: Brain Boost Unveiled

New Research Illuminates Link Between Supplement and Cognitive Resilience

Creatine, long celebrated for its muscle-building prowess, is now understood to offer significant benefits to the brain, enhancing mood, cognitive function, and resilience through exercise-induced biological pathways.

The Muscle-Brain Connection

A groundbreaking review published in Frontiers in Nutrition explores how creatine impacts both muscle and brain health via the intricate muscle-brain axis. This axis involves myokines, signaling proteins released by muscle cells, which can influence brain function.

These myokines, crossing the blood-brain barrier, are believed to promote neuron growth, foster new neural connections, and improve the efficiency of existing brain circuits. This neurogenesis and neuroplasticity can sharpen cognitive performance and help protect brain cells from inflammation and oxidative stress.

The muscle-brain axis is a dynamic two-way street of communication. Key players include brain-derived neurotrophic factor (BDNF), crucial for memory and neural plasticity, alongside others like cathepsin B, IL-6, IGF-1, irisin, and lactate. BDNF levels naturally rise with exercise, supporting brain health.

Creatine, a molecule vital for energy metabolism in both muscle and brain, is showing promise beyond physical performance.

Creatine: The Energy Regulator

Creatine, a molecule derived from amino acids, is essential for rapid energy availability in the body. It plays a key role in regenerating adenosine triphosphate (ATP), the cell’s primary energy currency. This rapid energy supply is critical for high-demand tissues like muscles and the brain.

Inside cells, creatine is largely converted to phosphocreatine (PCr), which acts as an immediate phosphate reservoir for adenosine diphosphate (ADP), efficiently reforming ATP. This process is particularly vital during intense physical activity, supporting bursts of energy.

Boosting Brain Function Through Exercise

When combined with resistance training, creatine supplementation not only aids muscle growth and strength but may also trigger the release of myokines. These signaling molecules are thought to indirectly benefit the brain, potentially enhancing mood and cognitive functions.

Creatine helps regulate the body’s inflammatory and anti-inflammatory responses, which can be crucial for preventing exercise-induced injuries and maintaining stable body temperatures. Its influence extends to pathways that regulate myokines, such as the mTOR pathway.

For example, creatine supplementation has been linked to increased insulin-like growth factor-1 (IGF-1), a factor known to improve neuronal growth and synaptic plasticity. Creatine’s role in anaerobic performance may also benefit endurance athletes who require sudden power outputs.

Interestingly, lactate, a byproduct of anaerobic metabolism and a myokine, is produced during intense exercise. While creatine doesn’t directly increase lactate, its ATP-boosting effects could indirectly lead to higher BDNF levels by stimulating myokine production.

Potential Therapeutic Applications

Emerging research suggests creatine could offer neuroprotective benefits, potentially aiding in conditions like Huntington’s and Parkinson’s diseases. It may also help protect the central nervous system from concussion-related damage.

Preliminary studies hint at creatine’s positive impact on maternal health during pregnancy and a possible role in reducing the risk of depression. Its ability to combat age-related muscle weakness is another area of active investigation.

Creatine has also shown promise in mental health, influencing the exercise-dependent secretion of neurotransmitters such as serotonin and dopamine, which are vital for neural function and mood regulation. Some evidence suggests a rapid antidepressant effect, potentially enhanced when paired with cognitive behavioral therapy.

A recent pilot trial indicated that combining creatine with CBT yielded greater improvements in depression scores compared to CBT alone. However, larger-scale studies are still required to confirm these findings.

Metabolic Regulation and Beyond

Beyond its effects on energy and mood, creatine supplementation can improve glucose metabolism by enhancing insulin sensitivity. Insulin plays a role in myokine release by facilitating glucose uptake into muscle cells, potentially increasing myokine signaling in response to exercise.

Future Outlook

The link between creatine supplementation, exercise, and increased myokine production highlights a multifaceted impact on both physical performance and brain health. While current research is promising, particularly regarding its anti-inflammatory and mood-boosting potential, further clinical studies are essential.

Researchers are exploring how creatine might directly influence BDNF and other myokine levels, examining pathways like increased phosphocreatine availability and the upregulation of PGC-1α in muscle tissue during exercise. Understanding these intricate connections could solidify creatine’s role in supporting overall physical and mental well-being.

July 27, 2025 0 comments

Health

New research identifies critical gene for treatment

by Dr. Michael Lee – Health Editor July 26, 2025

written by Dr. Michael Lee – Health Editor

ALS Breakthrough Pinpoints Common Weakness

New Research Identifies UNC13A Gene as Key Target for Treatment

Scientists have uncovered a unifying molecular mechanism in Amyotrophic Lateral Sclerosis (ALS), a devastating neurodegenerative disease. This discovery centers on the gene UNC13A, crucial for nerve cell communication, offering a promising new avenue for developing effective therapies.

Unraveling ALS Complexity

For years, the genetic diversity of ALS has complicated the search for a single effective treatment. Different genetic mutations, such as those affecting TDP-43, FUS, MATR3, and hnRNPA1, lead to varied pathological pathways. This heterogeneity makes it challenging to find a common therapeutic target.

“Scientists still don’t fully understand the process behind the loss of motor neurons in ALS. ALS is known for its genetic heterogeneity – meaning that there are numerous possible combinations of genes and factors that could lead to ALS. This makes it difficult to develop a singular treatment that works for everyone.”

—Yasuaki Watanabe, Assistant Professor, Tohoku University

A research team from Tohoku University and Keio University aimed to bridge this gap. They generated neural cell lines where key ALS-related RNA-binding proteins were depleted. Consistently, they observed a significant reduction in UNC13A expression across all tested cell lines.

Two Paths to UNC13A Deficiency

The study identified two distinct molecular routes leading to lower UNC13A levels. One pathway involves the insertion of a cryptic exon into the UNC13A transcript, destabilizing the messenger RNA. The second, novel finding revealed that the loss of FUS, MATR3, or hnRNPA1 triggers the overexpression of REST, a known transcriptional repressor.

REST actively suppresses UNC13A gene transcription. This increased REST activity may be the underlying cause of the motor neuron damage seen in ALS patients. The researchers validated these findings by examining motor neurons from ALS patient iPS cells and post-mortem spinal cord tissues, confirming elevated REST levels.

UNC13A: A Central Hub for Therapy

This convergence of diverse ALS-causing mutations on UNC13A deficiency provides critical insights into the disease. It highlights UNC13A as a central player in ALS pathology. Strategies aimed at preserving UNC13A expression or modulating REST activity could offer broad-spectrum therapeutic benefits.

“This study provides a valuable framework for developing broad-spectrum treatments that target shared molecular vulnerabilities in ALS,” stated **Keiko Nakayama**, Professor at Tohoku University.

With an estimated 30,000 people living with ALS in the United States alone, the potential to slow or halt the progression of muscle wasting and loss of function in a wider patient population would represent a monumental advancement in patient care (ALS Association).

July 26, 2025 0 comments

Health

Gut bacteria send direct signals to the brain to stop you from overeating

by Dr. Michael Lee – Health Editor July 24, 2025

written by Dr. Michael Lee – Health Editor

Gut Bacteria Signal Brain to Curb Appetite

New Study Reveals Direct Microbial Feedback Loop

A groundbreaking study has unveiled a direct communication pathway from gut microbes to the brain, influencing our decision to stop eating. This discovery opens exciting new avenues for understanding appetite and metabolic health.

The Neurobiotic Sense Uncovered

Researchers have identified a novel gut-brain sensory mechanism, dubbed the “neurobiotic sense.” This system allows the body to interpret microbial patterns, directly impacting feeding behavior. The findings, published in the journal Nature, suggest a sophisticated interplay between our internal microbiome and our brain’s satiety signals.

Gut bacteria send direct signals to the brain to curb appetite, a new study reveals.

While the gut’s neural network for sensing nutrients is known, a direct neural circuit for microbial signals remained elusive. This new research pinpoints specific cells in the small intestine, known as PYY-labeled neuropod cells, which express Toll-like receptor 5 (TLR5). This receptor is crucial for detecting bacterial flagellin, a common component of bacterial flagella.

Flagellin: The Microbial Signal

Flagellin levels have been observed to increase in stool after meals. The study demonstrated that these PYY-labeled cells, rather than vagal neurons themselves, utilize TLR5 to sense flagellin. This sensing triggers the release of peptide YY (PYY), a satiety-inducing protein.

When researchers genetically removed TLR5 from these PYY-labeled cells in mice, the animals exhibited increased meal sizes and longer feeding durations. This weight gain was observed independently of immune responses or metabolic disruptions, highlighting the specific role of this microbial sensing pathway.

Experiments confirmed that higher colonic flagellin levels correlate with feeding, and this signal is transmitted via the PYY-labeled cells to the vagus nerve. Blocking the PYY receptor (Y2R) on vagal neurons abolished this nerve activity in response to flagellin, confirming the signaling cascade.

Real-Time Appetite Regulation

Further investigation into real-time feeding behavior showed that administering flagellin via enema significantly reduced food intake in mice within 20 minutes. This effect was absent in mice lacking TLR5 in their PYY-labeled cells, proving the pathway’s direct impact.

Even in germ-free mice, flagellin alone was sufficient to suppress food intake, indicating that the sensing of this specific microbial pattern can regulate appetite without the presence of a full microbiome. This suggests that flagellin sensing is a potent, standalone signal for satiety.

The findings are particularly relevant given that obesity rates continue to rise globally. In the United States, over 42% of adults aged 20 and over have obesity, according to the CDC’s latest available data (CDC 2024).

This discovery of the “neurobiotic sense” provides a critical insight into how our gut microbiome directly communicates with our brain to regulate fundamental behaviors like eating. Future research may explore how manipulating this pathway could offer novel therapeutic strategies for appetite control and metabolic disorders.

July 24, 2025 0 comments

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