(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, this time focusing on osteoclasts: the specialized bone-resorbing cells responsible for breaking down bone as part of the continuous process of skeletal remodeling.

While bone is often thought of as permanent and unchanging, it is actually one of the most dynamic tissues in the body. Osteoclasts play an essential role in maintaining that balance by removing old or damaged bone, releasing stored minerals, and creating the foundation for new bone formation. Without carefully regulated bone resorption, the skeleton cannot properly repair itself or adapt throughout life.

In this piece, I explore how osteoclasts form from immune cell precursors, create their specialized ruffled border to dissolve bone, and coordinate with osteoblasts to regulate bone remodeling. I also dive into the signaling pathways that drive osteoclast differentiation, including the RANK/RANKL and NFATc1 pathways, and discuss how hormones, mechanical loading, inflammation, and epigenetic regulation influence their activity.

One of the most fascinating aspects of osteoclast biology is that these cells are far more than simple “bone destroyers.” They are highly specialized cells that integrate immune, hormonal, and mechanical signals to precisely regulate when and where bone should be resorbed, ensuring the skeleton remains strong while constantly renewing itself.

At the core of this story is another theme I love exploring through science communication: biology depends on balance. Even processes that appear destructive often serve an essential purpose, working in harmony with other cells to maintain health. Osteoclasts remind us that breaking down is sometimes the first step toward rebuilding.

🔗 Read the full feature below:
👉 Breaking Down and Balancing Bone

Credits

Art by Alexandra Banbanaste | Animation by Dr. Emanuele Petretto
Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Maksymowicz-Trivedi
Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series

The League of Extraordinary Cell Types

The teams at Sci-Illustrate and Endosymbiont bring you an ongoing series exploring the remarkable cell types that make our bodies function, combining scientific rigor, storytelling, and visual science communication to make complex biology more accessible and engaging. ❤

Subscribe now

(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, this time focusing on osteoblasts: the specialized bone-forming cells responsible for building, repairing, and maintaining the skeletal system throughout life.

Most people think of bone as static, but bone is actually one of the most dynamic and metabolically active tissues in the body. Osteoblasts sit at the center of that process, continuously responding to mechanical stress, hormonal signaling, inflammation, injury, and aging to help shape and reinforce the skeleton.

In this piece, I explore how osteoblasts produce and mineralize bone matrix, communicate with osteoclasts and osteocytes during remodeling, and respond to signaling pathways like Wnt/β-catenin, BMP, and IGF-1. I also dive into their emerging roles beyond structural support, including their involvement in endocrine signaling, metabolism, fracture repair, and systemic health.

One of the most fascinating aspects of osteoblast biology is that these cells are not simply passive “builders.” They are adaptive, highly responsive cells constantly integrating environmental, immune, and mechanical signals to maintain skeletal integrity.

At the core of this story is a broader theme I love exploring through science communication: biology is rarely static. Even tissues we think of as rigid and permanent are constantly sensing, adapting, communicating, and remodeling beneath the surface.

🔗 Read the full feature below:
👉 Building Bones and Shaping Strength

🖋️ Credits

Art by Alexandra Banbanaste | Animation by Dr. Emanuele Petretto
Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Małgorzata Maksymowicz-Trivedi
Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series:

The League of Extraordinary Cell Types

The teams at Sci-Illustrate and Endosymbiont bring you an ongoing series exploring the remarkable cell types that make our bodies function; combining scientific rigor, storytelling, and visual science communication to make complex biology more accessible and engaging ❤

(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, this time focusing on osteogenic cells: the stem-like progenitors responsible for building, maintaining, and repairing our skeletal system.

Often overlooked, these cells are the foundation of bone biology. Residing in the periosteum, endosteum, and bone marrow, osteogenic cells remain quiet until activated by growth, mechanical stress, or injury, then rapidly differentiate into osteoblasts to drive bone formation and regeneration.

This piece explores how osteogenic cells integrate mechanical, hormonal, and molecular signals, such as the BMP and Wnt pathways, to regulate bone homeostasis. I also dive into their emerging roles in metabolism, aging, and immune signaling, highlighting how disruptions in these processes contribute to conditions like osteoporosis and impaired fracture healing.

At the core of this story is a powerful shift in perspective: bone is not just structural, it’s dynamic, communicative, and deeply integrated with systemic health.

🔗 Read the full feature:
👉 Fueling Formation and Healing Fractures

🖋️ Credits

Art by Alexandra Banbanaste | Animation by Dr. Emanuele Petretto
Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Małgorzata Maksymowicz-Trivedi
Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series:

The League of Extraordinary Cell Types

The team at Sci-Illustrate and Endosymbiont bring you an ongoing series exploring the remarkable cell types that make our bodies function - combining scientific rigor with visual storytelling to make complex biology accessible and engaging ❤

Subscribe now

Your dreams aren’t trying to send you a secret message.

They’re your brain processing what you didn’t fully deal with during the day.

During sleep, especially REM sleep, your brain is actively:

• integrating memories

• regulating emotions

• reorganizing recent experiences

That’s why dreams can feel intense, emotional, or even bizarre.

But despite popular belief, there’s no consistent scientific evidence that dreams follow a universal symbolic language.

They’re not a hidden code you need to decode.

They’re a byproduct of your brain doing essential overnight maintenance.

References/PMIDs: 19702380, 20079677, 21570

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This felt like a full-circle moment for me.

My neuroscience expert profile is now live on Liven, where I contribute as a consultant and science communicator focused on making brain science actually make sense.

It’s honestly a little surreal seeing everything in one place… from my years in research studying neuroinflammation and the brain’s immune response, to building Brain & Beyond, to now working with digital health platforms.

For a long time, my work lived almost entirely in academic spaces. Publications, lab work, experiments, data. And while that work mattered, it didn’t always reach the people it could actually help.

That’s a big part of why I started Brain & Beyond.

I wanted to take what I had spent years learning and make it clear, accessible, and genuinely useful for everyday life. Not oversimplified. Not sensationalized. Just accurate science, explained in a way people can actually understand.

Now, through my work with platforms like Liven, I get to do that at a different scale. I work with teams to make sure the science behind their content is accurate, current, and trustworthy… especially in a space where misinformation spreads fast.

A lot of what I care about comes down to this:

We don’t need more content.
We need better science communication.

And we need it to be clear, honest, and grounded in real evidence.

If you’re curious, you can view my full Liven expert profile here:
[Liven profile]

Subscribe now

I’m a neuroscientist and neuroimmunologist with over a decade of experience studying how the brain and immune system interact in health and disease.

I earned my PhD in neuroimmunology at the Medical University of South Carolina, where I studied the role of the complement system in stroke and traumatic brain injury. I went on to complete postdoctoral research in oncology, focusing on therapeutic development in pancreatic cancer.

After years in academic research, I realized something surprising: the biggest gap wasn’t in the science; it was in how we communicate it.

That’s why I created Brain & Beyond: to translate complex neuroscience into evidence-based explanations that are accurate, accessible, and genuinely useful.

My goal is simple: make complex brain science clear, accurate, and actually useful in everyday life.

What I Do

Through my platform Brain & Beyond, I translate peer-reviewed research into engaging, evidence-based content across social and digital platforms. My work focuses on:

• Neuroscience & neuroimmunology

• Brain health and behavior

• Scientific literacy & misinformation

• Translating primary research

• Evidence-based health communication

My Work

• PhD in Neuroimmunology (Medical University of South Carolina)

• Postdoctoral training in oncology and drug development

• 9 peer-reviewed publications and 14 published science communication articles

• Founder of Brain & Beyond (55,000+ people across platforms)

• Published by MedEvidence, Science Spectrum, and Endosymbiont (The League of Extraordinary Cell Types)

• Featured by Harvard LabXchange, Humans of Academia, Built By Girls, and MUSC Alumni

Why I Do This

I believe everyone deserves access to science they can understand and trust.

There has never been more access to health information, or more misinformation. My mission is to bridge that gap by translating complex neuroscience and immunology into evidence-based explanations that are accurate, accessible, and grounded in the primary literature.

Science doesn’t have to be oversimplified to be understandable.

Work With Me

I partner with biotech companies, digital health platforms, academic institutions, media organizations, and healthcare brands to make complex science accurate, engaging, and accessible.

Areas of collaboration include:

• Scientific consulting

• Speaking engagements

• Science communication

• Educational content development

• AI-assisted scientific workflows and research translation

If you’re interested in working together:
👉 [Work with Me]

Follow My Work

If you’re interested in neuroscience, brain health, and evidence-based science communication, you can follow my work on Substack.

Subscribe now

(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, this time spotlighting one of the most misunderstood yet powerful cell types in the body: adipocytes.

Often reduced to the label of “fat cells,” adipocytes are anything but passive. These metabolically active cells sit at the center of energy balance, thermogenesis, inflammation, and systemic metabolic regulation. Through their ability to store fuel, generate heat, secrete hormones, and adapt their identity, adipocytes play a defining role in metabolic health, and disease.

This piece explores the three major adipocyte populations: white, brown, and beige, and how their structure, plasticity, and signaling functions shape physiology. I also unpack how adipocyte dysfunction contributes to conditions such as obesity, insulin resistance, type 2 diabetes, and cardiovascular disease, while highlighting emerging therapeutic strategies that harness adipocyte adaptability.

At the core of this story is a simple but powerful idea: understanding adipocytes is key to understanding metabolism itself.

🔗 Read the full feature:
👉 The Metabolic Marvels: Adipocytes

🖋️ Credits
Art by Nelli Aghekyan | Animation by Dr. Emanuele Petretto
Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Małgorzata Maksymowicz-Trivedi
Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series:

The League of Extraordinary Cell Types

The team at Sci-Illustrate and Endosymbiont bring you an ongoing series that dives deep into the remarkable cell types that make our bodies work - combining scientific rigor with visual storytelling to make biology accessible and engaging. ❤

(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, this time exploring the powerhouse cells at the center of ovarian biology: granulosa cells.

Often overshadowed by the oocyte they support, granulosa cells are anything but passive. These somatic support cells orchestrate every stage of follicle development, decode hormonal cues, fuel estrogen and progesterone synthesis, and ultimately help determine fertility outcomes. Their coordination with the oocyte and responsiveness to FSH and LH shape the entire reproductive timeline — from follicle recruitment all the way to ovulation and luteinization.

This piece breaks down how granulosa cells develop, specialize, communicate, and transform, while also highlighting what happens when their finely tuned machinery goes awry in conditions like PCOS, premature ovarian insufficiency, and granulosa cell tumors. I also spotlight several leading labs whose work continues to expand our understanding of these remarkable cells.

🔗 Read the full feature on Medium:
👉 Granulosa Cells — Fueling Fertility, Balancing Hormones

🖋️ Credits:
Art by Olga Kurkina | Animation by Dr. Emanuele Petretto | Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Małgorzata Maksymowicz-Trivedi | Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series:

The League of Extraordinary Cell types

The team at Sci-Illustrate and Endosymbiont bring to you an exciting series where we dive deep into the wondrous cell types in our body, that make our hearts tick ❤.

Sci-Illustrate, Endosymbiont

Each disorder looks distinct on the surface, yet beneath the symptoms lies a shared biological storm: neuroinflammation.

Across these conditions, the brain’s immune cells, microglia and astrocytes, play a double-edged role. In small doses, inflammation helps repair damage. But when it persists, it turns destructive, releasing toxic molecules that erode neurons and fuel a vicious cycle of degeneration. Misfolded proteins like α-synuclein, β-amyloid, and tau only add fuel to the fire, keeping these immune cells locked in overdrive.

Together, chronic inflammation and protein misfolding form a molecular feedback loop that slowly dismantles the brain from within a shared mechanism linking diseases once thought worlds apart.

The Brain’s Immune Landscape

The brain has its own immune ecosystem, an intricate network of microglia and astrocytes that balance defense with delicate control.
Microglia are sentinels: in their resting state, they prune synapses, clear debris, and keep neurons healthy. But when injury or misfolded proteins appear, they release cytokines and chemokines meant to contain damage. If the alarm stays on too long, those same molecules become toxic, fueling oxidative stress and neuronal loss.

Astrocytes, the most abundant glial cells, maintain the blood–brain barrier, regulate nutrient exchange, and communicate with neurons. Under stress, though, they turn reactive, producing inflammatory mediators that amplify damage. Their dialogue with microglia forms a feedback loop, activated microglia push astrocytes into neurotoxic “A1” states, while astrocytes sustain microglial activation. When this loop persists, inflammation shifts from protective to pathological.

Chronic activation of these glial partners is now recognized as a core feature of diseases like Alzheimer’s and multiple sclerosis, where signals meant to heal instead erode myelin and neurons. The challenge for modern neuroscience is to harness their protective power without letting the fire burn unchecked. When microglia and astrocytes stay in balance, they sustain life. When they don’t, they light the match for neurodegeneration.

When Proteins Go Rogue

At the heart of many brain disorders lies a molecular misstep: a protein that loses its shape. When β-amyloid, tau, or α-synuclein misfold, they clump into toxic aggregates that the brain struggles to clear. These tangled proteins aren’t passive by-products, they spark an immune alarm that recruits microglia and astrocytes into action.

In Alzheimer’s, β-amyloid plaques disrupt synapses and trigger microglial activation; in Parkinson’s, α-synuclein aggregates form Lewy bodies that provoke the same immune cascade. What begins as cleanup soon becomes self-defeating: microglia release cytokines and reactive oxygen species to destroy debris, but the response damages nearby neurons and fuels even more misfolding.

This feedback loop, misfolding begets inflammation, and inflammation drives further misfolding, creates a slow-burning fire in the brain. Emerging research suggests that modulating this immune response or enhancing aggregate clearance may interrupt the cycle. The goal isn’t to silence the immune system but to retrain it, restoring the balance between protection and precision that defines a healthy brain.

Shared Pathways Across Disorders

Though Parkinson’s, Alzheimer’s, multiple sclerosis, and epilepsy appear distinct, they converge on the same cycle: protein misfolding leads to immune activation, which leads to neurodegeneration.

In Parkinson’s disease, misfolded α-synuclein aggregates into Lewy bodies that alarm microglia, prompting the release of TNF-α, IL-1β, and other inflammatory mediators that accelerate dopaminergic neuron loss in the substantia nigra. Alzheimer’s follows a similar pattern, β-amyloid plaques and tau tangles provoke a prolonged microglial response. Variants in TREM2 impair microglial clearance of these aggregates, linking genetic risk to chronic inflammation and synaptic decline.

In multiple sclerosis, misfolded myelin basic protein acts as a neoantigen, triggering autoimmune activation that strips myelin and injures neurons. Epilepsy reveals the feedback from the opposite direction: recurrent seizures induce microglial and astrocytic cytokine release that heightens neuronal excitability, lowers seizure thresholds, and remodels synapses.

Across these conditions, the pattern repeats, misfolded proteins or hyperactive neurons awaken immune cells that, when left unchecked, erode the very networks they were meant to protect. Understanding this shared inflammatory language offers a roadmap for therapies that calm, rather than silence, the brain’s defenses.

The Cycle of Destruction

Inflammation and protein aggregation feed each other in a destructive loop that underpins many neurodegenerative diseases. Misfolded proteins like β-amyloid in Alzheimer’s and α-synuclein in Parkinson’s activate microglia and trigger the release of TNF-α and IL-1β, generating reactive oxygen species (ROS) that damage neurons and promote further misfolding. Rising oxidative stress impairs mitochondrial function, depleting the energy neurons need to survive. Meanwhile, disrupted proteostasis, the balance between protein synthesis, folding, and degradation, prevents the brain from clearing these aggregates, overwhelming chaperone proteins and perpetuating cellular stress.

As inflammation persists, the blood–brain barrier (BBB) begins to weaken. Once compromised, it allows peripheral immune cells and cytokines to flood the brain, amplifying local inflammation and neuronal injury. The result is a self-reinforcing storm: inflammation drives misfolding, misfolding fuels oxidative stress, and a leaky BBB ensures the cycle continues unchecked. Breaking this loop, by stabilizing mitochondria, restoring proteostasis, or reinforcing BBB integrity represents a critical frontier in neurodegenerative research.

Calming the Fire Within

Across Parkinson’s, Alzheimer’s, multiple sclerosis, and epilepsy, the same biological fault lines appear: misfolded proteins, hyperactive immune cells, and chronic inflammation that erode the brain from within. What was once seen as coincidence now reads as convergence, variations of the same cellular war, fought between the brain’s need for protection and its struggle for balance.

Yet this shared biology also offers shared opportunity. By targeting the inflammatory feedback loop, restoring proteostasis, and modulating microglial activation, researchers are beginning to chart a new course. The goal isn’t to silence the brain’s defenses, but to re-educate them, transforming destructive inflammation back into repair.

Neuroinflammation, once viewed as a side effect, is now recognized as a central driver and potentially the key to prevention. The challenge for the next decade is not simply to understand these shared mechanisms, but to translate that understanding into interventions that protect the brain before damage becomes irreversible. The path forward lies in calming the fire, not extinguishing it.

(Originally published on Medium by Sci-Illustrate Stories: The League of Extraordinary Cell Types)

I’m excited to share my latest article with Sci-Illustrate Stories, a deep dive into the unsung heroes of male fertility: Sertoli cells.

Far more than “nurse cells,” Sertoli cells are the architects and guardians of the testis, orchestrating the entire process of spermatogenesis while shielding developing germ cells from immune attack. From building the blood-testis barrier to decoding hormonal cues, these cells embody a fascinating blend of structure, function, and adaptability.

🔗 Read the full feature on Medium:

👉 Sertoli Cells — Masters of Male Reproductive Order

🖋️ Credits:
Art by Renske Hoste | Animation by Dr. Emanuele Petretto | Words by Dr. Christy Kestner
Project Coordinator: Dr. Masia Maksymowicz-Trivedi | Series Director: Dr. Radhika Patnala
Published by Sci-Illustrate & Endosymbiont

About the series:

The League of Extraordinary Cell types

The team at Sci-Illustrate and Endosymbiont bring to you an exciting series where we dive deep into the wondrous cell types in our body, that make our hearts tick ❤.

Sci-Illustrate, Endosymbiont

I’m so honored to share that my neuroscience article, “From Ice Picks to Neuromodulation: How an Innovative Device Rewrote the History of Neurosurgery,” was recently featured in the 1st anniversary celebration of Science Spectrum, one of Medium’s leading science publications.

Founded by Cole Frederick and Harlan Brothers, Science Spectrum has grown to over 12,000 followers and 400+ articles in its first year, covering everything from AI and chemistry to ecology and neuroscience. Their mission, making complex science and math accessible to everyone, is exactly what drives Brain & Beyond.

It’s humbling to see my work highlighted alongside such talented scientists and communicators who are helping bridge the gap between research and public understanding. I’m so grateful to be part of this growing community that celebrates curiosity, learning, and storytelling in science.

🧬 Read the full article here:
👉 From Ice Picks to Neuromodulation

Here’s to more collaborations, shared discoveries, and stories that make science human.

Two patients arrive in the ER within the same hour.

One is a young driver, dazed after a high-speed collision. The other, a retired teacher, suddenly can’t lift her right arm or form words; a clot has cut off circulation in her brain.

On the surface, these are two different conditions: traumatic brain injury (TBI) and stroke. But inside the brain, a surprisingly similar story unfolds. An ancient part of our immune system, called the complement system, rushes to help. Sometimes it clears debris and restores order. However, sometimes it goes too far, exacerbating inflammation, pruning healthy synapses, and complicating the recovery process.

This paradox, that our natural defenders can also become saboteurs, was the heart of my PhD research. In this article, I’ll share what complement is, how it shapes outcomes after brain injury, and why targeting it could open new doors for therapies.

The Complement System: Our Overeager First Responder

Think of the complement as the body’s rapid response team. It’s a cascade of more than 30 proteins circulating in the blood, waiting for a signal. Once activated, it’s like toppling dominoes: one protein activates the next, amplifying the response.

Complement has three main jobs:

• Tagging threats: Marking bacteria or debris so immune cells can clear them.

• Sounding the alarm: Releasing fragments (C3a, C5a) that summon immune reinforcements.

• Finishing the job: Forming the membrane attack complex (MAC), a pore that punches holes in pathogens.

In infections, this speed and force can be lifesaving. But the brain is delicate. Once complement leaks past the blood–brain barrier after trauma or stroke, it can’t always distinguish between a bacterium and a stressed neuron. That’s when problems start.

Complement in Traumatic Brain Injury

When the head sustains trauma, whether from a fall, crash, or blast, the first wave of damage is mechanical. Neurons stretch and tear, blood vessels rupture, and the blood–brain barrier weakens. Complement proteins flood in.

At first, this seems helpful: they tag dead or dying cells, and microglia (the brain’s immune cells) clear the debris. But in TBI, complement overshoots. It starts labeling stressed but salvageable synapses as disposable. Microglia then “prune” them away, eroding healthy connections alongside damaged ones.

This contributes to secondary injury, the wave of inflammation, edema, and cell death that unfolds hours to days after the initial hit. It’s part of why TBI patients can look “stable” at first, then deteriorate.

And the story doesn’t always end in the acute phase. Complement activity can linger for months, keeping microglia on high alert. This chronic smoldering inflammation may help explain why TBI survivors face higher risks of cognitive decline, depression, and even neurodegenerative diseases like Alzheimer’s or Parkinson’s later in life.

Complement in Stroke

Stroke is another situation where timing is everything. In an ischemic stroke, a clot blocks blood flow, starving neurons of oxygen and nutrients. In a hemorrhagic stroke, bleeding directly injures brain tissue. In both cases, the blood–brain barrier is disrupted, and complement activation is triggered.

In the penumbra, the area of brain tissue that is at risk but not yet dead, complement can decide the fate of neurons.

• Too little response, and dead cells pile up.

• Too much response, and complement-tagged neurons that could have survived are engulfed.

Doctors can sometimes reopen blocked vessels with clot-busting drugs or surgery, but fewer than 10% of patients get these treatments in time. And even when they do, reperfusion doesn’t always equal recovery: complement-driven inflammation can continue to kill neurons in the penumbra hours or days later.

The Double-Edged Sword

So, is complement friend or foe? The answer is, frustratingly, both.

• It helps clear debris and set the stage for repair.

• It hurts when it keeps firing, damaging tissue that could otherwise recover.

This makes it a tantalizing therapeutic target, but a tricky one. We can’t just shut complement off entirely; patients would be left vulnerable to infections. Instead, the future lies in targeted, time-limited inhibition; nudging complement to step back when it’s overreacting, then letting it resume its protective roles.

A New Generation of Therapies

Some drugs that block complement already exist for rare immune disorders. Researchers are testing whether these can be repurposed for brain injury. Others are developing new approaches explicitly designed for TBI and stroke.

One strategy, which I studied during my PhD, involves injury-site targeting. Imagine an inhibitor that only binds where complement is overactive, right at the site of brain injury, leaving the rest of the immune system intact. In preclinical models, this approach preserved brain tissue, reduced swelling, and even enhanced cognitive recovery.

It’s still early days. But the fact that we can design complement inhibitors with a therapeutic window of 24 hours or more, and without increasing infection risk, is an exciting step forward.

Why Comorbidities Matter

Real patients aren’t just brains in a vacuum. They bring risk factors: aging, smoking, and cardiovascular disease that shape how their brains respond to injury.

Take smoking. It nearly doubles stroke risk and worsens recovery. In experimental models, cigarette smoke exposure increased complement activation, swelling, and hemorrhage after stroke. Aging brains also exhibit higher baseline levels of inflammation and complement proteins, rendering them more susceptible to overactivation.

This is one reason why many therapies look promising in young, healthy rodents but fail in human clinical trials. Future studies need to account for these comorbidities if we want therapies that truly translate.

Rehabilitation and Recovery

The story doesn’t end with the immune response. Rehabilitation, physical, speech, and occupational therapy, is critical in shaping long-term outcomes. But even here, inflammation plays a role.

Early, intensive rehab is linked with better recovery, but some clinicians worry it could “overstress” the brain. Emerging evidence suggests the opposite: activity may actually help dial down inflammation.

This is where biomarkers could help. If we can track inflammatory signals, including complement fragments, in real-time, we could tailor rehabilitation, pushing patients when their brains are ready and easing off when inflammation is still high. It’s a precision-medicine approach to neurorehabilitation.

Traumatic Brain Injury and the Long Shadow

Unlike stroke, which has a clear event, TBI often unfolds in shades of gray. Concussions may resolve quickly, or they may spark symptoms that linger for months. Repeated injuries, especially in athletes or veterans, can lead to chronic traumatic encephalopathy (CTE), a condition marked by memory loss, mood changes, and progressive decline.

Complement may also be part of that story. Studies, including my own, show that complement activity can persist long after the initial injury, quietly fueling microglial overactivity and synapse loss.

If that’s true, therapies that target complement might not only help acutely but also protect patients from the long tail of TBI. These cognitive and emotional aftershocks surface years later.

What My PhD Taught Me

My dissertation focused on three main areas:

1. Biomarkers in stroke recovery: Certain inflammatory markers can predict outcomes; however, larger, standardized studies are needed.

2. Comorbidities in stroke models: Smoking and aging make strokes worse, partly through complement. Modeling these factors in the lab improves translation.

3. Microglia–complement interactions in TBI: Complement tags neurons and synapses, and microglia clear them, sometimes too aggressively.

Together, these studies reinforced one lesson: complement is a major player in brain injury, but it’s not all bad. Our challenge is learning how to control it, when to let it work, and when to rein it in.

Looking Forward

Here’s what excites me most about the future of this field:

• Targeted inhibitors that home in on the injury site.

• Biomarker-guided rehab that uses inflammation profiles to customize therapy.

• Comorbidity-aware models that better reflect real patients.

• Chronic-phase interventions for TBI survivors at risk of long-term decline.

None of these is science fiction. They’re on the horizon, and they could mean the difference between a life of dependence and one of independence for millions of patients worldwide.

Final Reflection

When I started my PhD, I thought I was “just studying proteins.” Years later, I understand those proteins as part of a much bigger story: how the brain tries to heal, and how sometimes its defenders go too far.

The complement system reminds me of that tension. It’s a reminder that biology is rarely black and white. The same molecules that save us from infection can, in the wrong context, deepen brain injury.

However, that also means the story isn’t set in stone. With the right interventions, we can shift the balance and preserve speech, movement, and memory after trauma or stroke.

That’s why I’m still fascinated by complement. Because at the smallest molecular scale, it holds the power to change the most significant human recoveries.

We’ve all heard it:
“It’s just mom brain.”
“She’s probably forgetful, it’s menopause, you know.”

But here’s the truth: these aren’t punchlines or excuses. Neuroscience shows that pregnancy and menopause bring real, measurable changes to the brain. From structural shifts in grey matter to hormonal surges that reshape memory and attention, these transitions highlight the brain’s remarkable adaptability.

I just published a new article on Medium, diving into this fascinating science, and why dismissing these changes does women a huge disservice.

👉 [Medium.com]

I’d love to hear your thoughts: Have you experienced (or seen) these changes that are often misunderstood?

#Neuroscience #WomensHealth #BrainAndBeyond

New Article: From Ice Picks to Neuromodulation
I’m excited to share my latest piece, now published on Science Spectrum!

This article traces the remarkable evolution of neurosurgery, from the controversial lobotomy procedures that once defined the field to the development of neuromodulation, a precision-based therapy that is reshaping modern brain health.

It’s a story of how science learns from its past, moves beyond invasive mistakes, and opens doors to innovative, patient-centered approaches.

Read the full article here: [Science Spectrum]

#Neuroscience #Neurosurgery #BrainHealth #MedicalInnovation #ScienceCommunication

New Article: HeLa Cells and the Ethics of Scientific Progress
I’m excited to share my latest piece, now published on Science Spectrum! HeLa cells have been instrumental in countless medical breakthroughs, but their legacy also raises important questions about ethical practices in research.

Read the full article here: [Science Spectrum]

#HeLaCells #MedicalEthics #ScienceCommunication #Research

If your immune system is so powerful, then why does it so often fail to detect cancer?

Most of us think of the immune system as a protective force, like a SWAT team, constantly working to protect us from harmful invaders like bacteria, viruses, and other threats. It’s incredibly good at recognizing and attacking things that could cause harm and don’t belong in the body. But cancer cells are different and sneaky; they actually originate from our own bodies and evolve tactics to evade immune detection, essentially cloaking themselves from attack.

In this article, we’ll break down how cancer hides, why it matters for treatment, and how scientists are learning to expose it. The answer to why the immune system doesn’t always fight cancer lies in the origin of cancer and the way that our immune cells have evolved to tolerate (not respond to) the cells and tissues in our own bodies. Let’s jump in!

Immune Cells Undergo Rigorous Testing to ‘Tolerate’ Self

Our immune cells are tested during development—before they are released into the bloodstream and the body—to ensure only those cells that do not identify cells and tissues in our own bodies as a target survive. Those that do recognize—and have the ability to attack—cells within our own body are destroyed. This destruction is meant to eliminate immune cells that could, in theory, spark an autoimmune attack.

More specifically, it is the B cells and T cells of the immune system that are tested because these cells have individual specificity. Like a snowflake, each B cell and each T cell are slightly different and recognize a different target. The target of one T cell could be a tiny piece of the spike protein on the surface of SARS-CoV-2 (the virus that causes COVID-19) while the target of a different T cell could be a tiny piece of hemagglutinin (the ‘H’) on the surface of the influenza virus. No matter the target, only B cells and T cells that have specificity for something that is not part of the body or ‘self’ should be released into the body.

The Immune System’s Dilemma: Cancer is ‘Self’

Cancer presents a unique challenge to the immune system. Unlike pathogens, which are clearly foreign, cancer cells originate from the body's own “self” cells, undergoing changes that allow them to grow uncontrollably. Although cancer cells are abnormal and dangerous, they look very similar to normal, healthy cells, making it hard for the immune system to tell the difference. In this article, we’ll explore how cancer hides in plain sight and the innovative strategies that scientists are exploring to help the immune system recognize and destroy it.

How Cancer Pulls It Off - Core Strategies

Turning Off the Alarms

Cancer cells are essentially normal cells that—for a variety of reasons—are growing out of control. You can think of cancer cells as cars that have stopped using the brakes, are pushing hard on the gas pedal and are completely out of control. As a result of this uncontrolled growth, some cancer cells stop producing molecules (called major histocompatibility proteins) that act like tiny flags on their surface that would normally alert T cells that there is a problem. This mechanism is similar to turning off a home security system. By reducing or eliminating the display of these molecules, cancer cells avoid triggering an immune response. In a healthy immune system, T cells would usually recognize these flags as signals of danger and attack the abnormal cells. Without these markers, cancer cells can hide in plain sight, making it much more difficult for the immune system to detect and destroy them.

Creating a ‘Bad Vibe’ Immune-Suppressive Environment

Cancer cells secrete substances that create an environment around themselves that suppresses immune responses and makes it harder for immune cells to do their job. It's like a huge crowd of people arriving at an airport security checkpoint at the same time that luggage scanning machines break; the movement of people through the checkpoint slows to a crawl. A similar phenomena can happen with cancer. Cancer often recruits T regulatory cells (Tregs) and myeloid-derived suppressor cells (MDSCs) that create an immune-suppressive microenvironment. These cells secrete anti-inflammatory cytokines that play a role in preventing the immune system from effectively targeting and destroying cancer cells. In essence, the cancer cells confuse the immune system by inviting the wrong cells into the tumor microenvironment, which further hampers the body’s natural defenses.

Blocking Access or Infiltration: The Tumor Fortress Defense

The tumor microenvironment (TME) is a complex ecosystem that surrounds and supports a tumor. It can be in the form of a "fortress," employing a combination of physical and biochemical barriers that defend it from immune surveillance. These barriers not only exclude immune cells from the tumor but can also suppress the effectiveness of therapies that are immune-activation based. When outside forces penetrate the fortress, the inside defenses, such as the immune evasion mechanisms, step in and protect the tumor.

Cancer consists of tumors that grow uncontrollably, using the microenvironment to enhance their growth and spread, leading to the formation of secondary tumors. Tumors often express extracellular matrix (ECM) proteins or stromal cells that physically block immune cell traffic, while also secreting immunosuppressive cytokines like TGF-β to change immune cell behavior. Additionally, the abnormal structure of tumor blood vessels reduces perfusion, preventing the delivery of immune cells and therapeutic agents. We'll dive deeper into the complexities of the TME and its impact on immune evasion in an upcoming article.

Disabling the Immune Brakes

Many cells in our body have molecules on their surface—called checkpoint molecules—that exist as brakes to stop T cells from mistakenly attacking self cells. It’s a built-in safety mechanism to prevent autoimmunity.

But in cancer, these brakes work against us by telling T cells to back off and leave the cancer cells alone. Through years of research, scientists have discovered this cancer trick, and have developed a type of immunotherapy called immune checkpoint inhibitors to block the brakes. Immune checkpoint inhibitors are proteins (antibodies to be precise) that bind to the checkpoint molecules and hide the brake so that any T cells that recognize and target cancer cells are allowed to stay ‘on’ and attack the cancer.

One example where immune checkpoint inhibitors have been completely game changing is melanoma. By blocking checkpoint molecules like PD-1 and CTLA-4, which normally act as brakes on immune responses, these immunotherapies allow T cells to stay active and fight cancer more effectively. This approach has significantly improved survival rates in patients with advanced melanoma, offering long-term remission for patients who previously had very limited options and often succumbed to disease.

Why This Matters

Understanding how cancer cells avoid immune detection is key to explaining uncontrolled tumor growth and immunotherapy failure. Cancer cells destabilize the body's own protective immune mechanisms to escape immune surveillance and avoid elimination, thereby leading to uncontrolled tumor growth. This process is especially undesirable in cancer treatment, since the immune system, which is usually adept at detecting and recognizing foreign intruders, is caught off-guard by these evasive strategies.

In our daily life, immune evasion explains why certain patients, despite having access to therapies like checkpoint inhibitors, don't experience substantial benefits. However, if the tumor microenvironment has already established effective immune evasion mechanisms, these treatments may not be enough.

However, by understanding the mechanisms behind immune evasion, scientists and clinicians are developing more effective cancer therapies. Combination therapy that strikes several immune targets, along with the use of checkpoint inhibitors with other drugs, is showing promise in bypassing these roadblocks. Furthermore, ongoing research is advancing personalized medicine, where new treatments are tailored to the specific tumor type of each patient to enhance their chances of success.

The Science Strikes Back

Researchers are fighting back against immune evasion with innovative strategies designed to outsmart the tumor’s defenses. Checkpoint inhibitors, which block the pathways tumors use to suppress immune activity, have already shown promise, but scientists are taking it a step further.

Chimeric antigen receptor (CAR) T cell therapy engineers a patient’s own immune T cells to recognize specific markers found only on cancer cells. Adding this engineered receptor to the patient’s own T cells redirects their specificity and gives the body a powerful new system to target and destroy the cancer. Cancer vaccines are another innovative approach designed to train the immune system to identify and respond to cancer cells, much like traditional vaccines prepare the body to fight viruses. Together, these tools are helping the immune system see cancer for what it really is—a dangerous invader that needs to be stopped.

Additionally, researchers are focusing on targeting regulatory T cells (Tregs) and other suppressive elements within the tumor microenvironment. By eliminating these immune-suppressing factors, therapies can reinvigorate the body’s immune system to better fight the cancer.

This shift from blunt-force treatments to precision immunotherapy marks a transformative moment in cancer research. Rather than attacking cancer indiscriminately, researchers are now fine-tuning their approaches to selectively disrupt immune evasion, making treatments more effective and less harmful to healthy tissue.

Cracking Cancer’s Code: What Comes Next

Cancer's sneaky success lies in its ability to stay under the radar by disguising itself. Not only does it do this, but it also requires that the immune system not interfere. It is as if a master of disguise slipped past the guards and took refuge in a well-fortified camp. But science is starting to catch up. Tools like checkpoint inhibitors, CAR T cells, and cancer vaccines are beginning to reveal this intruder and reinforce our immune defenses. The next step? Destroy cancer's hideout itself: the tumor microenvironment. In our next piece, we will dive into the stronghold that cancer builds around itself and explore how scientists are breaching its defenses to bring the immune system back into the fight.

Full story below:

Originally published on Medium

Hi Brain & Beyond readers,
I’m thrilled to share my first published article for The League of Extraordinary Celltypes, a collaborative science storytelling project by Endosymbiont.

This piece is all about myoepithelial cells, the muscle-like, architecture-shaping, tumor-suppressing powerhouses that protect our glands and shape our tissues.

Credit:

Written by me, Dr. Christy Kestner
Art by Dr. Bruna Di Giacomo
Set in motion by Dr. Emanuele Petretto
Project Coordination: Dr. Masia Maksymowicz-Trivedi
Series Director: Dr. Radhika Patnala
Published via Sci-Illustrate Stories

Read the full article here:
https://medium.com/sci-illustrate-stories/myoepithelial-cells-13223ee43a11

This is the first of several pieces I’ve written for this series, and I’m excited to keep sharing the extraordinary work happening at the cellular level.

Let me know your favorite part! Had you ever heard of these cells before?

In addition to leading Brain & Beyond, I work as a science writer at Endosymbiont, a company that provides life science companies, research institutes, and organizations with a reliable, scientifically informed platform for their design, science communication, and marketing needs. I contribute to Sci-Illustrate Stories: The League of Extraordinary Celltypes, developing blog posts, social media content, and multimedia assets that highlight cellular biology through compelling, evidence-based storytelling. I also review and edit content to ensure scientific accuracy, clarity, and consistency, all while working with a creative team to enhance the visual storytelling of cellular processes.

I have an ongoing collaboration with MedEvidence and other news sites, contributing healthcare and medical content alongside my science communication work. I look forward to sharing more as the partnerships progress.

I’m committed to making science more engaging and understandable for everyone. Whether I’m creating content for my platform, collaborating with scientists, or reviewing cutting-edge research, I strive to make science a little less intimidating and a lot more exciting.

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