★Half of America Has This 'Hidden' Brain Problem
★ TOP STORY
Half of America Has This ‘Hidden’ Brain Problem
A major analysis exposes the true scale of brain-related disorders in the US. The findings raise uncomfortable questions about why survival is improving - but quality of life is not.
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Breaking News: What You Need to Know
Up-to-date info on the latest health-related news happening in the world.
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Mercury exposure causes protein degradation, increased reactive oxygen species, and enzyme inhibition. It is suggested that neurodegenerative disorders occur due to defective protein degradation and aggregation, mitochondrial dysfunction related to oxidative stress and free radical formation, and the metal's toxicity. There is considerable evidence that mercury and its compounds cause neurodegenerative diseases. Toxic effects such as DNA fragmentation and impaired neuronal integrity can be observed due to mercury exposure. Severe neuronal damage results in neuronal loss, which in turn makes neurodegenerative diseases inevitable. In this review, we summarize studies on Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis, which are the main neurodegenerative diseases related to mercury exposure.
http://193.140.108.196:8080/handle/20.500.11851/11515 (2024).--- Aluminum is the most abundant neurotoxic metal in the Earth's crust. It accumulates semi-permanently in neuronal foci susceptible to Alzheimer's disease (AD) through the blood-brain barrier and the intracellular transferrin transport pathway, and is involved in the induction of oxidative stress, upregulation of the APP gene, and amyloid-β conformational changes. Some studies have reported increased morbidity or mortality from AD in areas with high Al exposure, suggesting that chronic Al exposure contributes to AD. Arsenic (As) is neurotoxic and impairs cognitive and memory functions. Exposure to As and its metabolites leads to the formation of reactive oxygen species (ROS), inflammation, mitochondrial dysfunction, and disruption not only of protein homeostasis but also of calcium signaling. Furthermore, As is a known cardiovascular toxin. The vascular hypothesis of Alzheimer's disease (AD) suggests that AD results from vascular damage that reduces cerebral blood perfusion rates and, therefore, indirectly damages neurons.
Magnesium (Mg) is the second most abundant intracellular divalent cation and a cofactor for more than 300 metabolic reactions in the body. It is neuroprotective, interacting with the N-methyl-D-aspartate (NMDA) receptor and blocking the calcium channel at the NMDA receptor, preventing oxidative stress and neuronal cell death due to excitotoxicity. Mg is also involved in normal neuronal maturation, neuromuscular transmission, and maintaining the integrity of the blood-brain barrier. Because the blood-brain barrier keeps daily fluctuations of blood Mg in check in brain tissue, cerebrospinal fluid appears to be a more representative biomaterial for analyzing Mg homeostasis in patients with AD. A systematic review of magnesium (Mg) levels in Alzheimer's disease (AD) patients found that Mg concentrations were significantly lower in the cerebrospinal fluid and hair of AD patients, but no differences were observed in serum and plasma. Lead (Pb) has complex and numerous mechanisms of neurotoxicity and is a known neurotoxin that causes nonspecific brain damage. Approximately 95% of the human lead burden is in bone. Bone lead has a half-life of 20 to 30 years, while the average turnover period for blood lead is approximately 30 days, and circulating lead levels are associated with acute exogenous exposures. Lead binds to divalent metal transporter proteins, crosses the blood-brain barrier in place of calcium (Ca), and accumulates in the brain. It causes oxidative stress by depleting thiols and impairing antioxidant defenses, leading to endoplasmic reticulum stress, mitochondrial damage, and neuronal apoptosis. In older populations, lead exposure is associated with lower cognitive status and longitudinal cognitive decline, but further prospective evidence from human clinical samples is needed.
https://link.springer.com/article/10.1186/s12302-024-00980-z (2024).--
Ginkgo biloba extract is widely used for its neuroprotective properties, which include improving cognitive function and memory, especially in age-related diseases such as Alzheimer's. Ascorbic acid is vital for collagen synthesis, tissue repair, and the enzymatic production of certain neurotransmitters. As a powerful antioxidant, ascorbic acid helps protect cells from damage caused by free radicals. The present study aimed to evaluate the effects of Ginkgo biloba and L-ascorbic acid on mercury-induced oxidative stress and neuroinflammation.
https://www.irrespub.com/biolsciences/index.php/1/article/view/197 (2024).
Midwestern Doctor's research on DMSO is extraordinary. An interesting piece of news:
A NEW FINDING ABOUT A NATURAL COMPOUND OPENS THE DOOR TO INNOVATIVE THERAPIES FOR ALZHEIMER'S.
Scientists at the National University of Singapore have identified a metabolite present in the body as a potential tool to restore neuronal functions affected by the disease and delay cognitive decline.
According to a new study published in Aging Cell, calcium alpha-ketoglutarate (CaAKG), a metabolite naturally produced by the human body, has been identified as a potential tool to restore brain functions impaired by Alzheimer's.
This advance opens the door to potentially safer and more accessible therapeutic strategies to combat age-related cognitive decline.
A medicinal plant with ancestral uses in Brazil has shown effectiveness against arthritis in scientific research.
The study demonstrated that a natural metabolite can restore synaptic plasticity, key to memory and learning (Illustrative Image Infobae).
Brian K. Kennedy, from the Department of Biochemistry and chair of the Translational Research Program on Healthy Longevity (TRP), stated: “The research suggests that safe, natural compounds like CaAKG could one day complement existing approaches to protecting the brain and slowing memory loss.”
“Since AKG is already present in our bodies, focusing on these pathways could offer fewer risks and greater accessibility. This could provide us with a powerful new strategy to delay cognitive decline and promote healthy brain aging,” he noted.
The research team from the Yong Loo Lin School of Medicine at the National University of Singapore demonstrated that CaAKG can restore functionality to key neuronal processes altered in patients with Alzheimer's disease.
The compound, previously studied for its role in healthy aging, showed positive results in restoring synaptic plasticity, considered fundamental for learning and memory formation, a function severely impaired in this disease.
CaAKG allowed for the recovery of associative memory, one of the first abilities typically lost in the early stages of Alzheimer's, and restored synaptic retrieval, a mechanism that enables the brain to link events and form complex memories. Furthermore, it enhanced autophagy, the brain's natural system for eliminating harmful proteins, crucial for maintaining neuronal health.
The research indicates that CaAKG promotes the strengthening of connections between neurons by activating L-type calcium channels and calcium-permeable AMPA receptors, which are important for neuronal flexibility.
It also prevents the overload of NMDA receptors, frequently affected by the accumulation of amyloid protein, a hallmark of the disease. This multifaceted action suggests that CaAKG contributes both to maintaining basic memory function and to supporting more complex learning abilities.
Since AKG levels naturally decline with age, replenishing this metabolite could be a less risky and more accessible way to promote healthy brain aging.
https://www.infobae.com/salud/ciencia/2025/12/30/alzheimer-un-nuevo-hallazgo-sobre-un-compuesto-natural-abre-la-puerta-a-terapias-innovadoras/