Category: Humans

Creating Memories

Memories don’t sit in one place inside the brain—they flow through networks of regions, shifting between storage, retrieval, and reconstruction. Understanding this movement reveals how our identities, skills, and experiences are constantly being reshaped by the brain’s dynamic architecture.

The Journey of a Memory

When you recall your first day at school or the taste of a favorite meal, your brain isn’t pulling a file from a cabinet. Instead, it’s reactivating patterns of electrical and chemical activity across billions of neurons. These neurons communicate at synapses, where neurotransmitters strengthen or weaken connections depending on how often they’re used.

1. Encoding: The Birth of a Memory

  • Sensory input first enters through sensory memory, lasting only seconds.
  • If attention is given, the information moves into working memory, managed largely by the prefrontal cortex.
  • For long-term storage, the hippocampus acts as a hub, binding together sights, sounds, emotions, and context into a coherent episode.

2. Storage: Distributed Across the Brain

Memories are not stored in a single “memory bank.” Instead, they are distributed across specialized regions:

  • Hippocampus: crucial for forming new episodic memories.
  • Neocortex: long-term storage of facts and experiences.
  • Amygdala: emotional coloring of memories.
  • Basal ganglia & cerebellum: motor skills and habits.

This distribution means that remembering a song involves auditory cortex patterns, while recalling a fear involves amygdala activation.

3. Retrieval: Reconstructing the Past

When you recall, the hippocampus reactivates cortical networks, essentially replaying the original neural patterns. But retrieval is not perfect—memories are reconstructed, influenced by context, emotion, and even imagination. That’s why two people can remember the same event differently.

Movement and Transformation of Memories

Memories shift location and form over time:

  • Short-term to long-term transfer: The hippocampus gradually “teaches” the neocortex, a process called consolidation.
  • Reactivation: Each recall strengthens or alters the memory trace, sometimes introducing distortions.
  • Neuroplasticity: New connections form, allowing memories to integrate with fresh experiences.

This movement is not static—it’s a dance of signals, constantly reshaping who we are.

Why Memory Movement Matters

  • Learning: Understanding how memories move helps explain why repetition and sleep enhance retention.
  • Aging & disease: Disorders like Alzheimer’s disrupt these pathways, showing how fragile memory networks can be.
  • Identity: Since memories are reconstructed, our sense of self is fluid, shaped by how the brain replays its past.

Memories are not fixed snapshots but living patterns of activity that travel through the brain’s interconnected regions. From encoding in the hippocampus to storage in the cortex and emotional shading in the amygdala, each memory is a dynamic collaboration. Every recall reshapes the past, proving that memory is less about preservation and more about continual reinvention.

Lab Grown Brains

Lab-grown brains—known as brain organoids—are revolutionizing neuroscience, offering unprecedented insights into cognition, disease, and even the ethics of artificial intelligence. Recent breakthroughs suggest these miniature brains may soon reshape medicine and our understanding of the human mind.

In recent years, scientists have made remarkable progress in cultivating brain organoids—tiny, three-dimensional clusters of human brain cells grown from stem cells. These structures mimic the architecture and activity of early-stage human brains, and while they don’t possess consciousness, they exhibit surprising complexity.

A major milestone came in September 2025, when researchers at Johns Hopkins University demonstrated that brain organoids could replicate the fundamental building blocks of learning and memory. Their study showed that these organoids formed synaptic connections and exhibited electrical activity akin to neural circuits involved in cognition. This opens the door to studying how memory forms and how disorders like Alzheimer’s disrupt it.

Meanwhile, MIT’s Picower Institute unveiled “Multicellular Integrated Brains” (miBrains), a new generation of organoids that include all six major brain cell types, including neurons, glial cells, and vascular components. These miBrains are grown from individual donors’ stem cells, allowing for personalized models of neurological disease and drug response.

Another leap forward came from Stanford University, where researchers cultivated thousands of cortical organoids that pulse with electrical signals and develop layered structures resembling the human cortex. These models are helping scientists investigate the origins of neurodevelopmental disorders such as autism and schizophrenia.

Potential Uses:

  • Disease Modeling: Organoids allow researchers to simulate conditions like Parkinson’s, epilepsy, and ALS in a controlled environment, accelerating drug discovery and testing.
  • Personalized Medicine: By growing organoids from a patient’s own cells, doctors could predict how that individual might respond to specific treatments.
  • Developmental Biology: These models help decode how the brain forms and what goes wrong in congenital disorders.
  • Toxicology and Drug Screening: Organoids offer a human-relevant platform for testing pharmaceuticals and environmental toxins without relying on animal models.

Implications and Ethical Questions:

As organoids become more sophisticated, ethical concerns are intensifying. Could a sufficiently complex organoid develop sentience or experience pain? While current models lack the structure and input required for consciousness, the line between simulation and cognition is blurring.

Moreover, the fusion of brain organoids with AI systems or robotic interfaces raises questions about neuro-enhancement and synthetic consciousness. Some researchers envision hybrid systems where lab-grown neural tissue interfaces with machines to create bio-computers or prosthetic cognition.

There’s also the issue of identity and consent. If organoids are derived from human donors, do those donors retain rights over the research outcomes? And how should society regulate the creation of increasingly lifelike brain models?

Conclusion:

Lab-grown brains are not science fiction—they’re rapidly becoming central to neuroscience, medicine, and bioethics. As researchers push the boundaries of what these organoids can do, society must grapple with profound questions about the nature of thought, identity, and the future of human-machine integration.

Plastic Chemicals and Babies

In our modern world, plastic is everywhere—from food packaging and water bottles to cosmetics and household items. But beneath its convenience lies a growing concern: the toxic impact of plastic chemicals on pregnant women and their unborn children. Mounting scientific evidence reveals that exposure to certain compounds in plastics can disrupt hormonal systems, impair fetal development, and increase the risk of serious health complications.

At the heart of this danger are chemicals like phthalates, bisphenols (such as BPA), and benzophenones, which are commonly added to plastics to enhance flexibility, durability, and UV resistance. These substances are known endocrine disruptors, meaning they interfere with the body’s hormonal balance. For pregnant women, whose hormone systems are already in overdrive to support fetal growth, this interference can be particularly harmful.

Phthalates, often referred to as “everywhere chemicals,” are especially concerning. They leach from plastic containers into food and beverages, are absorbed through the skin from personal care products, and even contaminate indoor air and dust. Once inside the body, phthalates can cross the placenta, exposing the developing fetus to their effects. Studies have linked prenatal phthalate exposure to increased risks of preterm birth, low birth weight, and developmental disorders such as ADHD and asthma.

Bisphenols, including BPA, are another group of chemicals with alarming implications. Found in plastic bottles, food can linings, and thermal paper receipts, bisphenols mimic estrogen and can disrupt the delicate hormonal signaling crucial for fetal brain and organ development. Research suggests that exposure to BPA during pregnancy may be associated with behavioral problems, altered brain structure, and reproductive issues later in life.

The danger doesn’t stop with the products themselves. The entire lifecycle of plastic—from fossil fuel extraction to manufacturing and disposal—releases toxic byproducts like dioxins, which further contribute to hormonal disruption and immune system damage. These pollutants disproportionately affect vulnerable populations, including pregnant women and children, whose bodies are more sensitive to chemical interference.

What makes these chemicals particularly insidious is their ubiquity and persistence. Unlike some toxins that degrade over time, many plastic-related compounds linger in the environment and accumulate in human tissues. The placenta, once thought to shield the fetus from harm, offers little protection against these invaders. As Boston College pediatrician Philip Landrigan warns, “The placenta provides no protection at all”.

Despite the grim outlook, there are steps expectant mothers can take to reduce exposure. Avoiding plastic food containers, especially when heating food, choosing glass or stainless steel alternatives, and scrutinizing ingredient labels on personal care products can make a meaningful difference. Advocacy for stronger regulations and corporate accountability is also essential to protect future generations from the silent threat of plastic toxicity.

In a world saturated with synthetic materials, awareness is the first line of defense. By understanding the risks and making informed choices, pregnant women can help safeguard their health—and the health of their unborn children—from the hidden dangers lurking in plastic.

Is Aging Contagious?

Aging has long been considered a personal journey—an inevitable biological process shaped by genetics, lifestyle, and environment. But recent research suggests that aging may not be entirely solitary. In fact, it might be contagious.

A groundbreaking study published in the journal Metabolism by scientists from Korea University College of Medicine and collaborators in the U.S. has identified a molecular mechanism that allows aging signals to spread from cell to cell, like an infection. The culprit? A protein called HMGB1.

The Role of HMGB1: A Cellular Messenger

HMGB1 (High Mobility Group Box 1) is a DNA-binding protein typically found inside the nucleus, where it helps organize genetic material. However, when cells become stressed or enter a state known as senescence—where they stop dividing and begin deteriorating—they release HMGB1 into their surroundings.

Once outside the cell, HMGB1 behaves differently depending on its chemical state. The researchers discovered that the “reduced” form of HMGB1, which has been exposed to low oxygen levels, acts as a potent aging signal. When healthy cells encounter this reduced protein, they begin to show signs of aging: they stop dividing, express senescence markers, and release inflammatory molecules.

In contrast, the “oxidized” form of HMGB1, exposed to higher oxygen levels, does not trigger these aging effects. Cells exposed to oxidized HMGB1 remained healthy and continued to divide normally.

From Cells to Mice: Aging in Action

To test the theory beyond petri dishes, researchers injected reduced HMGB1 into young, healthy mice. Within a week, the mice began showing signs of premature aging, including increased inflammation and cellular senescence. Blood samples from elderly humans also revealed higher levels of reduced HMGB1 compared to younger individuals, suggesting a systemic spread of aging signals through the bloodstream.

This discovery challenges the traditional view of aging as a cell-autonomous process. Instead, it supports the idea that aging can propagate through tissues, potentially accelerating the decline of nearby healthy cells.

Implications for Anti-Aging Therapies

The study opens new avenues for therapeutic intervention. If aging can be spread via HMGB1, then blocking its reduced form—or the cellular receptors it binds to—could slow or even reverse age-related decline. Early experiments showed that inhibiting the pathways activated by reduced HMGB1 improved healing and physical performance in older animals.

Dr. Ok Hee Jeon, one of the lead researchers, emphasized the significance: “This study reveals that aging signals are not confined to individual cells, but can be systemically transmitted via the blood.”

What’s Next?

While the findings are preliminary, they offer a tantalizing glimpse into the interconnected nature of aging. Future research may explore how lifestyle factors, such as diet and oxygen exposure, influence HMGB1’s chemical state—and whether interventions can modulate its effects.

In the meantime, the idea that aging might be contagious adds a new layer of complexity to our understanding of longevity. It’s not just about how we age, but how our aging might affect others—cell by cell, molecule by molecule.

Are Human Brains Growing?

Recent studies have revealed a surprising trend: human brains are getting bigger. This discovery challenges long-held assumptions about brain evolution and opens new avenues for understanding cognitive development and neurological health.

The Evidence Behind Brain Growth

A landmark study from UC Davis Health examined brain MRIs of over 3,000 participants born between the 1930s and 1970s. The results were striking: individuals born in the 1970s had brain volumes that were 6.6% larger and cortical surface areas nearly 15% greater than those born in the 1930s. These increases were consistent across several brain structures, including white matter, gray matter, and the hippocampus—regions critical for learning, memory, and overall cognitive function.

Researchers attribute this growth to a combination of genetic and environmental factors. While genetics play a foundational role, improvements in healthcare, nutrition, education, and social conditions appear to have significantly influenced brain development across generations.

Evolutionary Insights

Complementing this generational data, a separate study led by researchers from the University of Reading, Oxford, and Durham analyzed fossil records spanning 7 million years. Their findings suggest that brain size in hominins increased gradually within species, rather than through sudden evolutionary leaps. This challenges the traditional view that major brain expansions occurred only during key evolutionary transitions.

Instead, the research points to a steady, incremental process—akin to a software update—where each species adapted over time, refining neural architecture and cognitive capacity. This gradualism underscores the complexity of evolutionary pressures and highlights how even small changes can accumulate into significant biological shifts.

Implications for Brain Health

One of the most promising aspects of this research is its potential link to dementia prevention. Larger brain structures may offer greater brain reserve, a concept referring to the brain’s ability to withstand age-related damage. As brain size increases, so does the capacity to buffer against diseases like Alzheimer’s.

Indeed, while the number of people living with dementia is rising due to aging populations, the incidence rate—the percentage of people affected—is actually declining. This suggests that improved brain health, possibly tied to increased brain size, is playing a protective role.

What This Means for the Future

These findings invite a re-evaluation of how we understand human development. They suggest that our brains are not static relics of evolution but dynamic organs shaped by both biology and environment. As we continue to improve living conditions and education worldwide, we may be nurturing not just healthier bodies—but more resilient, capable minds.

Whether this trend will continue into future generations remains to be seen. But for now, the evidence paints a hopeful picture: the human brain is still evolving, and it’s growing in ways that may help us meet the challenges of tomorrow.

Hidden Dangers in Toothpaste

Toothpaste is a daily essential, trusted for its role in maintaining oral hygiene. However, concerns have emerged regarding the presence of harmful contaminants, including lead, fluoride in excessive amounts, and other toxic substances. Understanding these risks is crucial for consumers who prioritize health and safety in their personal care routines.

The Issue of Lead Contamination 

Lead exposure is widely recognized as hazardous, even at low levels. While lead is not an intentional ingredient in toothpaste, contamination can occur through tainted raw materials or inadequate manufacturing practices. Reports have surfaced about imported toothpaste containing unsafe levels of lead, often due to the inclusion of unregulated colorants or glycerin sourced from contaminated industrial suppliers. 

Lead exposure is particularly dangerous for children, as it can result in developmental delays, neurological damage, and other systemic health issues. In adults, prolonged exposure may lead to kidney damage, cardiovascular complications, and cognitive impairments. The presence of lead in oral care products is alarming because the mucous membranes in the mouth facilitate direct absorption into the bloodstream. 

Other Harmful Contaminants 

Beyond lead, other concerning substances have been identified in toothpaste formulations. 

Excessive Fluoride: While fluoride is added to toothpaste to strengthen enamel and prevent cavities, excessive exposure can lead to dental fluorosis (discoloration and brittleness of teeth) and skeletal fluorosis (bone damage). Some regions with high natural fluoride levels in drinking water already expose populations to significant fluoride intake, making fluoride-containing toothpaste potentially problematic. 

Triclosan: Once commonly used for its antibacterial properties, triclosan has been linked to endocrine disruption and increased antibiotic resistance. Many regulatory agencies have banned its use in hygiene products, but it may still be present in older formulations or specific international brands. 

Diethylene Glycol (DEG): Found in certain counterfeit or poorly regulated toothpaste brands, DEG is a toxic substance used as an industrial solvent. It can lead to kidney damage, liver toxicity, and neurological complications upon prolonged exposure. 

Artificial Dyes and Sweeteners: Synthetic dyes, such as FD&C Blue 1, have raised concerns due to potential allergic reactions and links to hyperactivity in children. Meanwhile, sweeteners like saccharin or sodium lauryl sulfate (SLS) can cause irritation, particularly in individuals prone to ulcers or gum sensitivities. 

How to Choose a Safe Toothpaste 

Consumers can take proactive steps to ensure their toothpaste is free from harmful contaminants: 

Check for Regulatory Approval: Look for certifications from reputable health organizations or regulatory bodies such as the FDA, European Medicines Agency (EMA), or other national agencies. 

Read Ingredient Lists Carefully: Avoid products with vague ingredient disclosures or those containing known harmful substances. 

Prefer Natural Formulations: Brands emphasizing natural ingredients without artificial dyes, preservatives, or triclosan may offer a safer alternative. 

Watch for Recalls and Warnings: Stay informed about product recalls and health advisories regarding contaminated toothpaste brands, particularly when purchasing imported or discounted products. 

Conclusion 

While toothpaste is meant to promote dental health, certain formulations may pose hidden dangers. Awareness of contaminants such as lead, triclosan, and excess fluoride empowers consumers to make safer choices. By scrutinizing ingredient lists and opting for well-regulated products, individuals can maintain good oral hygiene without compromising their long-term health.