Former news anchor Jon Snow has revealed he is living with Alzheimer’s disease, the most common form of dementia
The reality of Snow’s life with the condition will feature in a powerful new documentary, ‘Jon Snow: A Last Big Story’, airing on Channel 4 on Saturday, 20 June.
Snow, 78, best known for presenting Channel 4 News between 1989-2021, was diagnosed with dementia, the UK’s biggest killer, in 2023.
Snow, who is supporting Alzheimer’s Society, has decided to open up about his diagnosis to raise awareness of the condition, which affects around a million people in the UK.
In an exclusive Daily Mail interview alongside his epidemiologist wife, Dr Precious Lunga, who has a PhD in neuroscience, Snow said ‘If I don’t speak out, who will?’
The article, part of Alzheimer’s Society’s Defeating Dementia campaign with the newspaper, reveals how following his retirement in 2021, Jon sank into a deep depression, became withdrawn and lost interest in things he once loved.
Precious said: ‘Friends kept asking me if Jon was alright and I would have to lie and say he’s fine, but I knew he wasn’t.’
Jon worried that friends were no longer contacting him: ‘Nobody ever rings,’ he said, ‘I’m forgotten.’ In reality, he had forgotten about the calls.
Jon Snow’s Alzheimer’s diagnosis
Despite being reluctant to see a doctor, insisting there was nothing wrong, a cognitive assessment and brain scan revealed that Jon had Alzheimer’s disease.
Snow still questions the diagnosis, saying: ‘I mean sometimes I doubt whether I’ve really got it. I don’t know if it’s widespread knowledge. I don’t feel disabled in any way,’ wondering if his behaviour is simply normal for his age.
Snow is not alone – it is a common misconception to question whether dementia is a normal part of ageing.
While people often forget things more as they get older, dementia is caused by diseases of the brain and its symptoms can include problems with planning and decision-making, language, and sometimes changes in mood or behaviour.
In the film, Snow says:
“At the beginning I wanted to hide it, there’s so much prejudice. Any sort of hint of mental decay, you’re sort of dead. There are moments when it pops up but it’s not an all day every day condition, and that’s what I cling onto.”
Snow’s diagnosis carried extra weight because his mother, Joan, had struggled with Alzheimer’s disease for a decade before dying in her eighties. He feared the same fate.
Reflecting on his mum’s diagnosis, Snow once said: ‘It is a horrible disease because she is still physically your mum. She sounds like her, but you can’t have a conversation with her.’
Staying involved while living with with dementia
Lunga believes people with dementia can still be valuable members of society.
‘Life doesn’t end with an Alzheimer’s diagnosis, but it changes dramatically,’ said Precious. ‘You can have Alzheimer’s and still be a valuable member of society but you need support to navigate it.’
In ‘Jon Snow: A Last Big Story’, viewers will see Snow coming out of retirement for one last investigation to uncover a mining disaster affecting local communities in Zambia, where he and Precious spend much of their time.
His news instinct remains strong, and he still wears a tie daily, but it’s clear his memory is fading.
Snow is seen at an appointment with his consultant, Professor Jonathan Rohrer, who explains that there is currently no cure for dementia, but there are treatments.
Snow was previously on a clinical trial and says he’s a ‘willing victim’ should there be others he could join.
Working with Alzheimer’s Society and Channel 4
Michelle Dyson CB, CEO of Alzheimer’s Society, said: “Jon’s decision to talk publicly about his dementia diagnosis is a real act of courage and his story will resonate with so many.
“His support for Alzheimer’s Society will help spark a national conversation about dementia that we so desperately need. Despite being the UK’s biggest killer, dementia is still not treated with the same urgency as other major health conditions like cancer.
“Alongside his wife Precious, Jon is shining a light on the need for faster, fairer access to diagnosis. An early diagnosis can unlock vital support, help families plan ahead and potentially open the door to participation in clinical trials.
“Yet too many people across the country are still waiting far too long for a diagnosis.
“‘”We look forward to working with Jon, whose long-standing commitment to speaking out against injustice will help ensure the harsh realities of dementia cannot be ignored by the UK Government and the NHS.
Illustration: Sarah Grillo/Axios. Stock: Getty Images
Planet Earth has roughly 180 currencies. But for a vast share of global transactions, people want to use just one: the United States dollar, Axios’ Neil Irwin writes.
Why it matters: This is a unique source of global power and responsibility. America’s role in the world over the next 250 years will be determined by its ability to maintain, and wisely steward, this role at the center of the global economy.
Yes, but: Other nations are increasingly chafing at the power the U.S. wields thanks to the dollar — and they’re seeking alternatives.
How it works: The dominance of the dollar in international trade and finance gives the U.S. the ability to exert its will far from our shores, without firing a gun.
This poweris evident when the U.S. fines European banks for doing business with Iran or cuts off Russian oil companies from the mainstream financial system.
It has also fueled global demand for Treasury debt that allows the U.S. to borrow vast sums, especially in crises.
This primacyis based on policy choices and structures built over decades — in some cases, centuries.
What we’re watching: Some of the underpinnings of U.S. dollar dominance are coming under question.
Sky-highU.S. fiscal deficits mean the world is being inundated with Treasury debt. The political independence of the Fed is in question. And many in the Trump administration see the costs of maintaining dollar dominance as a burden for Americans.
Perhapsmost importantly, the U.S. has used the threat of cutting off access to the dollar-based global financial system as an increasingly all-purpose weapon for economic warfare. That means major U.S. rivals (China, Russia) and frenemies (India, Brazil) are eager for dollar alternatives
. Reality check: So far, other leading powers seem to lack the willingness or ability to build alternatives.
More broadly, network effects are powerful things. Everybody uses dollars because everybody else uses dollars.
The bottom line: The role of the U.S. dollar in the world is secure for now, much as America’s rivals might not like the status quo. But global angst is simmering, and as the Dutch and British learned long ago, no dominant currency is forever.
“Radical Islam doesn’t want just a small caliphate in Iraq or Syria. They see the United States as the greatest evil on Earth and seek to dominate the entire West. Radical Islam is revolutionary, it wants endless expansion, terrorism, assassinations, and total control. They hate America, Europe, Israel, and every Muslim nation that partners with us. Orlando, Pensacola, and domestic attacks prove it.
Radical Islam is a clear and imminent threat to the world.”
Israeli Prime Minister Benjamin Netanyahu and President Trump. Photo illustration: Aïda Amer/Axios. Photos: Getty Images
On Thursday evening, President Trump called Israeli Prime Minister Benjamin Netanyahu with news he did not want to hear: He expected to sign a deal with Iran within days.
“This is the deal. It’s a great deal, and it’s time to end this war,” Trump told Netanyahu, according to a senior U.S. official.
Why it matters: When Netanyahu went to war alongside Trump, this is not how he envisioned it ending, Axios’ Barak Ravid writes.
Flashback: Netanyahu made clear from the beginning that he believed the war could spur regime change in Tehran.
Now, four months out from an election, Netanyahu’s rivals are accusing him of making Israel a “vassal state” by simply accepting Trump’s terms for peace.
Anthropic CEO Dario Amodei is interviewed on “The Circuit with Emily Chang” at Anthropic headquarters in San Francisco in April. Photo: Jason Henry/Bloomberg via Getty Images
When you use Claude this morning, it tells you: “Claude Fable 5 is currently unavailable.”
Here’s the backstory, as scooped last night by Axios’ Alex Isenstadt and Maria Curi:
The Trump administration is blocking foreign governments, companies and individuals from accessing Anthropic’s most advanced AI models.
The company promptly took the model down for everyone, just two days after releasing it with great fanfare.
Why it matters: The move marks an escalation in Washington’s effort to treat cutting-edge AI systems as national security assets. Anthropic is on a Pentagon blacklist deeming it too dangerous for the government’s own use, and in a Commerce Department licensing regime calling it too dangerous for foreign use.
Commerce Secretary Howard Lutnick sent a letter to Anthropic CEO Dario Amodei yesterday saying that the Mythos 5 and Fable 5 models would be subject to export controls to any location outside of the U.S. and to all foreign persons within the country.
An administration official told Axios the Commerce Department decided to take the action after another company claimed it was able to jailbreak Mythos, alarming the administration about possible national security risks.
The administration tried to get Anthropic to pause releasing the latest models but was unsuccessful, the official said, prompting the export control letter.
The model needs to remain locked down until the U.S. government’s national security apparatus is hardened, the official said, adding that could happen in the next few weeks.
Summary: Researchers deciphered the molecular chain reaction that converts the brain’s internal immune defenses into a destructive force following a concussion.
Utilizing both rat and mouse models of mild-to-moderate traumatic brain injury (TBI), the research team isolated a novel, highly specific pathobiological cascade: the TLR4-MMP-9 axis. Following impact, toll-like receptor 4 (TLR4) inside neurons triggers an immediate, upstream activation of the enzyme MMP-9.This structural enzyme rapidly breaks down the brain’s supportive extracellular matrix scaffolding, dropping network inhibition and causing excessive, un-coordinated neural noise.
Crucially, the trial unmasked a fascinating biological paradox. While this pathway drives long-term network hyperexcitability, memory loss, and seizures post-injury, TLR4 acts as an indispensable homeostatic stabilizer in healthy brains, meaning clinical therapies must strictly target this pathway during a narrow, post-concussive window.
Key Facts
The TLR4-MMP-9 Trajectory: Head trauma quickly up-regulates the innate immune receptor TLR4 inside neurons. This activation triggers an immediate, downstream explosion of the enzyme MMP-9, establishing the crucial molecular link between early immune signaling and progressive brain damage.
Shattering the Extracellular Scaffold: In normal physiological states, baseline MMP-9 activity performs controlled remodeling of neuronal connections and the surrounding extracellular matrix. Post-TBI, hyperactive MMP-9 destabilizes the structural scaffold, eroding the delicate balance between excitatory and inhibitory signals.
The Noise Interference Loop: When structural matrix inhibition drops, brain networks lose communication precision. Instead of conveying meaningful signals required for cognitive function, the circuits generate massive, chaotic electrical noise that directly prevents learning, memory formation, and accurate recall.
Pharmacological and Genetic Validation: To prove absolute upstream causality, investigators blocked TLR4 using targeted pharmacology in rats and genetic knockouts in mice. In both scenarios, suppressing TLR4 completely halted the post-injury spike in MMP-9, proving that the immune receptor dictates the downstream enzymatic surge.
The Post-Injury Intervention Window: Animals subjected to TBI displayed highly restricted synaptic plasticity and severe spatial memory failures during behavioral tracking conducted one month later. Strikingly, administering TLR4 or MMP-9 inhibitors within an early 48-hour post-injury window completely rescued long-term learning performance.
The Homeostatic Dual-Role Paradox: In an extraordinary twist, researchers discovered that TLR4 operates within a narrow Goldilocks zone. In uninjured brains, blocking TLR4 actually causes memory failure and hyperexcitability, proving the receptor shifts from a vital homeostatic stabilizer into an abnormal, disruptive force exclusively following an impact.
The Micro-Mobility Mandate: Dr. Subramanian emphasizes that these findings carry immediate societal relevance given the global surge in young people riding electric scooters or bicycles without helmets. The data proves that even mild, sub-clinical concussions internally trigger a progressive structural cascade capable of causing lifelong neurological deficits if left un-intercepted. https://8ee9ec7af0c3b027214d86e45b32f807.safeframe.googlesyndication.com/safeframe/1-0-45/html/container.html
Source: UCR
Traumatic brain injuries (TBI) — even mild concussions — may trigger a chain reaction in the brain that disrupts neuronal communication, long-term memory, and cognition, according to University of California, Riverside research investigating how the brain’s immune system responds after injury.
The study, published in the Journal of Neuroinflammation, identifies a novel interaction between an innate immune receptor in the brain called toll-like receptor 4, or TLR4, and an enzyme called MMP-9 after brain injury. In normal conditions, MMP-9 activity plays an important role in remodeling neuronal connections and the brain’s extracellular matrix, the structural scaffold surrounding neurons.
Concussive brain injuries trigger a progressive neuro-immune cascade via the TLR4-MMP-9 axis, where the activation of neuronal immune receptors drives an enzymatic breakdown of the extracellular matrix to cause chronic circuit noise and spatial memory deficits. Credit: Neuroscience News
Deepak Subramanian, an assistant professional researcher in the Department of Molecular, Cell and Systems Biology and the study’s corresponding author said the findings show that TLR4 activation after a concussive brain injury enhances MMP-9 activity downstream.
“Brain injury activates TLR4 in neurons,” he said. “TLR4 signaling causes MMP-9 levels to increase. Increased MMP-9 alters how neurons talk to each other, resulting in heightened network excitability associated with seizures and impaired cognition. This direct connection between neuronal TLR4 and MMP-9 in the injured brain is the crucial link.”
The research used both rat and mouse models of mild-to-moderate concussive brain injury. The scientists observed that levels of both TLR4 and MMP-9 were upregulated rapidly after injury. But when researchers blocked TLR4 signaling — either pharmacologically in rats or genetically in mice — MMP-9 levels remained unchanged.
“That told us TLR4 is upstream of MMP-9,” Subramanian said. “By recruiting an enzyme that destabilizes neuronal communication, the immune receptor is driving the changes in neuronal activity patterns. This is important because it has been a puzzle to understand how the immune signaling can alter neuronal function; our finding directly addresses this question.”
The team also found that blocking either TLR4 signaling or MMP-9 activity limited changes in brain circuits disrupted after injury. Normally, healthy brain function depends on a precise balance between excitatory and inhibitory signaling. After trauma, that balance can break down, creating unstable and overly excitable networks.
“When inhibition drops or excitation becomes excessive, the network activity patterns lose precision,” Subramanian said. “Instead of meaningful communication, you get excessive noise across the network, which interferes with learning, memory formation, and recall.”
The researchers found the animals with TBI showed reduced synaptic plasticity — the brain’s ability to strengthen or reorganize neural connections during learning. Consequently, injured animals showed deficits in spatial memory in behavioral tests conducted one month later. To the researchers’ surprise, animals treated with TLR4 or MMP-9 inhibitors early after brain injury performed significantly better.
The findings suggest that early intervention targeting this pathway after brain injury could influence long-term neurological outcomes. In the study, treatments were administered to the animals within 48 hours after injury, but benefits were still measurable one month later.
“The timing is critical,” Subramanian said. “There’s a narrow window after brain injury where intervention may shape long-term outcomes.”
Current TBI treatments primarily focus on immediate symptom management rather than halting the progressive, underlying brain damage. This study isolates a highly specific, therapeutic target (the TLR4–MMP-9 axis) that can be intercepted in the critical window immediately following a concussion or head trauma to prevent lifelong neurological consequences.
“In a fascinating twist, we find that TLR4 isn’t just a ‘bad guy.’ In healthy, uninjured brains, TLR4 acts as a homeostatic regulator — a stabilizer keeping brain activity balanced,” said co-corresponding author Viji Santhakumar, a professor of molecular, cell and systems biology in whose lab the research was conducted.
Paradoxically, when the researchers blocked TLR4 signaling in healthy subjects, it caused memory issues and brain hyperexcitability.
“By identifying that the TLR4-MMP-9 pathway is activated exclusively after injury, we hope to move closer to pathway-specific preventive treatments without impacting normal brain function,” Santhakumar said.
Subramanian said the study also highlights the importance of taking all head injuries seriously, including mild concussions often associated with sports or falls, especially with the increase in the number of young people riding scooters without a helmet.
“Even mild concussions can internally trigger long-term changes in the brain,” he said.
The researchers caution that therapeutic targeting of immune signaling remains complex because both TLR4 and MMP-9 appear to play important roles in normal brain function as well.
“These systems operate within a very narrow Goldilocks zone,” Subramanian said. “Too much activation is harmful, but too little is also harmful because TLR4 and MMP-9 are necessary for normal brain plasticity and stability.”
The next phase of the research will focus on identifying the downstream molecular targets of MMP-9.
“We would like to understand the molecular underpinnings of the biological ‘switch’ that converts the stabilizing influence of TLR4 to an abnormal disruptive force after brain injury, and how these processes impact learning and memory,” Santhakumar said.
Funding: The study was funded primarily by the U.S. Department of Defense, with additional support from the National Institutes of Health and American Epilepsy Society.
Santhakumar and Subramanian were joined in the study by Erick Contreras, Laura Dovek, Razieh Jaberi, and Iryna M. Ethell. Two UCR undergraduate researchers, Emmanuel Greene and Ysabelle K. Lao, also contributed to the study.
Key Questions Answered:
Q: Why does a mild concussion cause long-term memory problems weeks after the initial physical impact?
A: Because the physical impact triggers a progressive, long-term molecular chain reaction. The concussion activates an immune receptor inside neurons called TLR4, which forces an enzyme named MMP-9 to flood the brain. This enzyme aggressively eats away at the extracellular matrix, the structural scaffold that holds neurons together. Without this scaffold, the brain loses its ability to balance electrical signals, replacing clear thoughts with chaotic network noise that permanently blocks memory formation.
Q: If blocking the TLR4-MMP-9 pathway cures brain injury damage, why can’t we take a daily preventative pill for it?
A: Because this pathway follows a strict Goldilocks zone and is required for everyday brain health. In a healthy, uninjured brain, TLR4 and MMP-9 act as essential stabilizers that maintain memory formation and baseline stability. Paradoxically, if you block this pathway in a healthy brain, it triggers the exact same hyperexcitability and memory problems seen in a concussion. Therefore, treatments must be strictly pathway-specific and deployed exclusively within a narrow window following a confirmed head injury.
Q: What is the most critical takeaway from this study regarding young people and modern sports or scooter injuries?
A: That mild concussions must be taken seriously because the internal damage is progressive. Many young people dismiss minor head bumps from falls or riding scooters without helmets because they feel fine a few hours later. This UC Riverside study proves that even mild concussions instantly set off an invisible neuro-immune cascade that slowly degrades brain circuits over the course of 30 days. Intervening within the first 48 hours is essential to halt this underlying damage before it translates into lifelong cognitive deficits.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this concussion and neurology research news
Author: Iqbal Pittalwala Source: UCR Contact: Iqbal Pittalwala – UCR Image: The image is credited to Neuroscience News
Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury
Neuroinflammatory pathways activated by traumatic brain injury (TBI) are critical mediators of long-term neurological dysfunction and represent promising therapeutic targets. Toll-like receptor 4 (TLR4), an innate immune receptor, was previously shown to contribute to increased seizure susceptibility and cognitive deficits in rats after lateral fluid percussion injury (FPI).
However, the cellular and molecular mechanisms underlying TLR4-mediated circuit dysfunction early after brain injury are not fully understood.
In this study, we define a cell- and circuit- specific neuroimmune-enzyme effector signaling axis that mediates early post-TBI circuit dysfunction in the hippocampal Dentate Gyrus (DG). Using ex vivo electrophysiology in rat and mouse models one week after brain injury, we demonstrate that neuronal TLR4 signaling regulates both excitatory and inhibitory synaptic inputs to dentate granule cells (DGC).
Collectively, pharmacological inhibition of TLR4 in rats and cell-type-specific deletion of TLR4 in mice show that neuronal TLR4 mediates injury-driven increase in DGC excitatory input frequency and relies on downstream activation of Matrix Metalloproteinase-9 (MMP-9). In contrast, TLR4 signaling contributed to a decrease in inhibitory current frequency after injury, but independent of MMP-9, revealing a mechanistic divergence.
Systemic inhibition of either TLR4 signaling or MMP-9 activity in rats within 24 h after injury reduced network hyperexcitability and improved long-term potentiation (LTP) in the DG measured in vivo one week after injury. Either TLR4 or MMP-9 inhibition early after injury effectively attenuated spatial memory deficits in a Barnes maze task one month post-injury.
Paradoxically, in sham controls, inhibition of TLR4 increased the frequency of both excitatory and inhibitory inputs to DGCs and augmented network excitability, without altering MMP-9 levels, identifying context-dependent roles for TLR4 signaling.
Together, these results identify a novel TLR4 -MMP-9 axis as a key driver of early post-TBI dentate gyrus circuit dysfunction and behavioral deficits.
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Why it matters: This is a unique source of global power and responsibility. America’s role in the world over the next 250 years will be determined by its ability to maintain, and wisely steward, this role at the center of the global economy.
Yes, but: Other nations are increasingly chafing at the power the U.S. wields thanks to the dollar — and they’re seeking alternatives.
How it works: The dominance of the dollar in international trade and finance gives the U.S. the ability to exert its will far from our shores, without firing a gun.
This primacy is based on policy choices and structures built over decades — in some cases, centuries.
What we’re watching: Some of the underpinnings of U.S. dollar dominance are coming under question.
Reality check: So far, other leading powers seem to lack the willingness or ability to build alternatives.
The bottom line: The role of the U.S. dollar in the world is secure for now, much as America’s rivals might not like the status quo. But global angst is simmering, and as the Dutch and British learned long ago, no dominant currency is forever.
Flashback: Netanyahu made clear from the beginning that he believed the war could spur regime change in Tehran.
Anthropic CEO Dario Amodei is interviewed on “The Circuit with Emily Chang” at Anthropic headquarters in San Francisco in April. Photo: Jason Henry/Bloomberg via Getty Images
The administration tried to get Anthropic to pause releasing the latest models but was unsuccessful, the official said, prompting the export control letter.
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