Tag: cognitive decline

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Nose-Picking Linked to Alzheimer’s?

Could Nose-Picking Raise Alzheimer’s Risk?

Introduction: Surprising Links

Given the research we do for this channel, I am no stranger to surprising, sometimes controversial—and occasionally disgusting—claims regarding Alzheimer’s disease.

In a previous video, we explored how something as mundane as earwax buildup—or, more technically, cerumen impaction—could lead to hearing loss and, by extension, cognitive decline.

Today, we’re looking at a physical habit.

It’s often dismissed as a minor social faux pas—and was even the subject of jokes in an old Seinfeld episode. But recent research suggests this common behavior might create a pathway for certain pathogens to reach the brain.

We’re talking about nose-picking—and its potential link to late-onset dementia.

For the companion video, see here:

The Griffith University Study

A team of researchers at Griffith University in Australia published a 2022 study in the journal Scientific Reports. They focused on a bacterium called Chlamydia pneumoniae.

This common airborne bacterium—sometimes called the Taiwan Acute Respiratory Agent—is primarily known for causing bronchitis and pneumonia. However, it has also been detected in a significant number of human brains affected by late-onset dementia.

Using mouse models, the researchers tracked how this bacterium travels. What they found was striking: it can move along the olfactory nerve—from the nasal cavity directly into the brain.

In these models, infection reached the central nervous system within 24 to 72 hours. Once inside, it triggered amyloid-beta deposition—the same protein associated with Alzheimer’s plaques.

One interpretation is that amyloid-beta may function as part of the brain’s immune response to infection. However, if that infection becomes chronic or repeatedly facilitated—potentially through damage to the nasal lining—this process could contribute to neurodegeneration.

In short: this research suggests that certain behaviors might make it easier for pathogens to access the brain.

Connection: The Earwax Analogy

You may remember from our earwax discussion that conductive hearing loss involves a physical obstruction—something like earwax blocking sound transmission.

In a similar way, the nasal epithelium acts as both a physical and immunological barrier.

The Griffith University study found that when this barrier was damaged, infections in the mice became significantly more severe.

Think of the nasal lining as a security checkpoint: if it’s intact, most threats are stopped. If it’s compromised, things can slip through.

Just as we cautioned against inserting objects into the ear canal, scientists now warn that picking—or plucking nose hairs—can damage this delicate lining. That damage may give pathogens a clearer route to the brain.

Why This Matters

As geriatrician Maria Carney noted in our earwax discussion, “most people don’t even realize that they have an issue.”

That lack of awareness is a recurring theme in both Alzheimer’s prevention and detection.

While nose-picking is often associated with children, it remains common in adults. In fact, one study found that about 91% of people admit to it.

I’m curious how that compares with this audience—so I’ve put up an anonymous poll if you’d like to weigh in.

As many viewers know, age alone—especially over 65—significantly increases Alzheimer’s risk.

If we add environmental exposures, such as introducing pathogens through repeated nasal damage, this could represent an additional, potentially modifiable risk factor.

Caveats and Disclaimers

To be clear: this is early-stage research conducted in mice. We do not yet have direct evidence that this pathway operates the same way in humans.

Human trials would be needed to confirm whether a similar mechanism is at work.

And of course, Alzheimer’s disease likely involves multiple contributing factors—including acetylcholine loss, plaque formation through other mechanisms, neurofibrillary tangles, and nutritional or metabolic influences.

So yes—this hypothesis may sound farfetched.

But it is being seriously explored, and it may be worth paying attention to.

Practical Advice and Conclusion

One of the core goals of the Alzheimer’s Proof project is prevention. And unfortunately, there is no single solution—no magic bullet.

What we can do is try to stack the odds in our favor.

Protect the Barrier

Avoid plucking nose hairs and minimize behaviors that could damage the nasal lining. Chronic irritation may increase vulnerability.

Use Safer Alternatives

If needed, consider electric trimmers for grooming. For congestion, saline sprays or nasal irrigation may help. If using a neti pot, always use distilled or properly purified water.

Keep It Clean

If you must manually clear your nose, ensure your hands are clean—before and after. Also keep fingernails trimmed and smooth to reduce the risk of micro-injury.

Stay Aware

Consult a healthcare provider if you experience persistent irritation, bleeding, or signs of infection.

The key takeaway here isn’t panic—it’s awareness.

Small habits, repeated over time, can shape long-term brain health.

And if reducing Alzheimer’s risk comes down—even in part—to eliminating preventable factors, then even small changes may be worth considering.

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References:

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CBD, Brain Inflammation, and a New Alzheimer’s Model

CBD and Dementia Inflammation

For decades, Alzheimer’s research has chased the same target — plaques and tangles.

And despite billions of dollars… results have been limited and often disappointing.

But… what if we’ve been aiming at the wrong problem entirely?

A new study suggests the real driver may be something more fundamental: inflammation.

And a compound called CBD might be able to dial it down.

Context: ‘Autoinflammatory’ Theory

To understand this breakthrough, we have to look at the “autoinflammatory” view of Alzheimer’s.

Traditionally, inflammation has been looked at as if it were a symptom of Alzheimer’s. But… researchers at Augusta University are arguing that chronic neuroinflammation is actually a core driver of the disease (along with other factors).

Translating that into dicey but everyday language, they’re starting to come around to the idea that inflammation is more of a contributing cause, not an effect.

Recall that, in general, “inflammation” is one of the body’s responses to illness or injury. In parts of our bodies we can see – an elbow, for instance (or…almost see!) – inflammation is what causes the hurt area to feel hot and painful, look red, swell in size, and so on.

Inflammation is often associated with loss of function. If your elbow is injured or inflamed, you can’t expect to be playing racquetball anytime soon.

Well… In Alzheimer’s disease, inflammation has to do with the brain’s immune system becoming chronically overactive. The brain gets stuck in a state of chronic immune activation. Yes, your brain can get inflamed, too.

This can also start a chemical chain reaction where usually functional neuronal “signals” begin to cause damage to nerve cells, instead of protecting them.

As a technical point, though, we don’t want to confuse inflammation (in the sense of haywire immune signaling and cellular activation) with what doctors call edema (i.e., large-scale fluid accumulation that increases pressure within the skull).

Think of it like this.

Your brain has a specialized immune system.

When it senses trouble, it sends out “first responders” like microglia and astrocytes.

In a healthy brain, these get to the scene of the accident, bandage the wounded, clean up, and go home.

But in Alzheimer’s, these cells get stuck in the “on” position. The emergency situation just goes on and on.

They stay “agitated,” and end up releasing toxic chemicals that (accidentally) kill the very neurons they were summoned to protect.

And this is where CBD enters the picture.

Science: IDO and cGAS

The study in question was led by Dr. Babak Baban. He and his team set out to see if cannabidiol, abbreviated “CBD,” could (so to speak) step into this mess as a peacekeeper.

CBD is already well known for its anti-inflammatory properties.

The researchers used a mouse model specially designed to mimic Alzheimer’s in humans.

They had these mice inhale CBD daily for four weeks. What they found wasn’t just “general” improvement. They identified two specific molecular “switches” that CBD was able to flip.

Two Molecular Switches

The first is an enzyme called IDO. It’s involved in how the brain processes tryptophan. You know, the essential amino acid that’s found in poultry – like your Thanksgiving turkey – which, by the way, has a largely undeserved “bad rep” for supposedly causing the “turkey coma” after you indulge. But that’s another story.

When overactive, IDO can shift tryptophan metabolism toward compounds that promote inflammation and neurotoxicity.

The second switch is a sensor called cGAS. This is basically a DNA-sensing pathway that can trigger powerful innate immune responses when activated.

In the Alzheimer’s-affected brains, both of these pathways were screaming at full volume.

But after the CBD treatment, the expression of IDO and cGAS dropped significantly.

Specifically, it quiets down the brain inflammation including in regions like the entorhinal cortex — a region critical for memory formation, and one of the first areas affected in Alzheimer’s.

By calming these two pathways, the CBD essentially told the brain’s immune system to “stand down.”

Results: Memory and Behavior

So, the biology changed, but did the behavior change? The symptoms?

Those are the “big” questions.

And the answer was… yes.

Remember, this is so far only demonstrated in animal studies. But…

The mice treated with CBD performed significantly better on recognition memory tests. And they showed more “exploratory behavior” than the untreated group. They weren’t just neurologically “calmer”; which researchers interpreted as improved cognitive function.

But here’s why this study is particularly exciting for the future of human medicine.

CBD appears to be a “multi-target” intervention.

While this specific study focused on inflammation, Dr. Baban’s team noted that their earlier work showed CBD may also influence plaque and tangle pathology through different mechanisms.

This is to say that, instead of a drug that only does one thing, we’re looking at a compound that might clear the trash, quiet the alarms, and protect the neurons all at the same time.

And notably, it’s derived from a plant.

Conclusion: The Road Ahead

Now. We have to be realistic.

This was only one study.

On mice.

While mouse models are essential for understanding these brain “switches” in a generic sense, humans — and our brains — are much more complex.

We still need rigorous human clinical trials to see if these results translate, what the right dosage is, and if long-term use is safe for seniors.

But…

If this line of research holds up, it changes the entire strategy.

Not just clearing damage — but preventing it at the source.

Not a single target — but an entire system reset.

And that raises a bigger question: Have we been looking for a silver bullet… when Alzheimer’s is really a systems-level failure?

If so, the future of treatment may not look like a drug that does one thing — but a therapy that brings the brain back into balance.

The question is: are we ready to rethink everything?

Including that an answer to one of our most complex diseases might be found in the chemistry of one of our most misunderstood plants.

What are your thoughts? Do you think the future of Alzheimer’s treatment lies in CBD, or are you still skeptical of cannabis-based medicine? Or are you more skeptical of pharmaceutical treatments? I’d love to read your comments.

By the way, if you’re interested in this idea of multi-target therapies, we’ve explored it before. In one video, we break down how CBD and THC interact with the brain.

And in another, we look at the controversial research into Lysergic acid diethylamide (or “LSD” and dementia — where, interestingly, a similar “systems-level” approach has been proposed. So if this direction intrigues you, those are worth watching next.

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Alzheimer’s Isn’t Just Plaques — Brain ‘Cleanup’ May Be FAILING

Introduction: The Mechanism of Amyloid Clearance

AT A GLANCE: Amyloid‑β plaques = a hallmark of Alzheimer’s disease; Most drugs target plaques directly

Alzheimer’s may involve a failure of brain “cleanup,” not just toxic buildup.

What if Alzheimer’s isn’t just caused by toxic buildup in the brain — but by the brain’s own cleanup crews being quietly dismantled from the inside?

If you’ve been around the block, when it comes to Alzheimer’s, you probably realize that a primary “pathological hallmark” is the accumulation of – what are called – “amyloid-beta plaques” within the brain.

  • AT A GLANCE: What if the problem is impaired clearance—not just plaque formation?

For over a century — since Alzheimer’s was first described in 1906 — drug development has largely focused on stopping plaque formation or clearing plaques after they appear.

And a critical area of this investigation involves taking a close look at the brain’s innate ability to clear these toxic proteins.

Recent research from the Indiana University School of Medicine has identified a specific enzyme that, when it is present, appears to be a factor when someone’s brain-clearing mechanisms go haywire.

And, in this video, we’ll look at a CliffsNotes’ version of the results.

https://www.youtube.com/embed/t0G-diPs2yU?si=lXQ5cl1JulI-IZmt

  • AT A GLANCE: IDOL = Inducible Degrader of the LDL receptor controls how many LDL receptors remain on brain cells

The enzyme is abbreviated I‑D‑O‑L, or “IDOL,” short for “Inducible Degrader of the LDL receptor.” That expression (a mouthful, for sure) designates a protein that controls how many LDL receptors survive on the surface of brain cells.

But… what the heck is it? And, more importantly, how would its inhibition (quote, unquote) represent a promising shift in doctors might approach Alzheimer’s treatments?

The Molecular Rôle of “IDOL”

  • AT A GLANCE: Receptors = cellular “locks” that trigger actions

To even begin to understand this discovery — and to be perfectly honest, that’s about the most ambitious goal I can realistically aim for — we need to talk about something called a low‑density lipoprotein, or “LDL,” receptor.

First, in the relevant context, a “receptor” is a protein on a cell — or in a cell — that acts like a lock. When the right chemical “key” comes along, that lock opens and tells the cell to do… something.

  • AT A GLANCE: LDL receptors pull material into cells for use or disposal

An LDL receptor is one of these locks. Its job is to grab so‑called “bad” cholesterol — LDL — and pull it into cells so it can be used or gotten-rid-of.

Think of it like a trash‑pickup claw that grabs garbage from the streets of the body and pulls it inside for disposal.

  • AT A GLANCE: In the brain, LDL receptors help manage APOE and amyloid‑β

In the central nervous system, LDL receptors also play a crucial role in regulating APOE, a protein involved in the transport and clearance of amyloid‑beta.

So far, so good?

  • AT A GLANCE: IDOL tags LDL receptors for destruction

Now for this IDOL business.

IDOL is not a receptor itself. It’s a protein that comes along and “tags” LDL receptors for destruction — that’s the “inducible degrader” part of its full name.

  • AT A GLANCE: Overactive IDOL à fewer LDL receptors; (-) Amyloid clearance à (+) plaque buildup

It’s like removing the trash‑pickup claws and throwing them away instead of the “bad” cholesterol. Reducing the number of LDL receptors on cell surfaces is a bit like getting rid of trash trucks in the heart of a crowded city. It’s not good.

When IDOL becomes overactive, too many LDL receptors are destroyed, weakening the brain’s ability to clear APOE and toxic amyloid‑beta proteins. This allows plaques to accumulate and neurodegeneration to accelerate.

In effect, an overactive cellular “shutdown switch” disables the brain’s cleanup crews at precisely the moment they’re needed most.

Receptor Inhibitors — and Why IDOL Is Different

  • AT A GLANCE: IDOL inhibitors protect receptors; They stop destruction — not signaling

At this point, it helps to understand what scientists mean by a “receptor inhibitor.” Usually, a receptor inhibitor blocks a lock so that even when the correct key shows up, the cell can’t respond. But that’s not quite what’s happening here.

An IDOL inhibitor doesn’t block the lock — it stops the demolition crew from tearing the lock off the door. In other words, inhibiting IDOL prevents LDL receptors from being destroyed, allowing the brain’s cleanup machinery to stay in place and keep doing its job.

IDOL Proteins Aren’t the Problem in and of Themselves

Let’s register a couple caveats.

Number one, it’s important to understand that IDOL proteins aren’t “bad” in and of themselves. They’re normal control mechanisms within the complex anatomy-biology of the body.

And they don’t come from “outside.” Your own cells make IDOL proteins automatically.

  • AT A GLANCE: IDOL is a normal control mechanism; Problems arise when it shuts things down too aggressively

Think of their part in in the trash-removal process as akin to that of a “thermostat” that off the air conditioner or furnace when the desired temperature is reached.  When a cell thinks it’s cleaned up enough LDL cholesterol, these IDOL proteins shut down the whole process.

In the context of Alzheimer’s Disease, overactive IDOL proteins lead to a depletion of these trash-removal receptors. In turn, this loss diminishes the brain’s capacity to clear amyloid-beta. And that, researchers, suspect, leads to – or makes worse – the formation of the plaques that lead to neurodegeneration.

Whew!

  • AT A GLANCE: Evidence so far: animal + cellular studies

It’s also important to note that this entire IDOL–LDL receptor mechanism has been demonstrated primarily in animal and cellular studies. While the evidence strongly implicates IDOL in Alzheimer’s pathology, human treatments are still in-process.

Research Findings

Neuronal vs. Microglial IDOL

AT A GLANCE: Microglial IDOL removal à little effect; Neuronal IDOL removal à major plaque reduction]

The study in question was led by Dr. Hande Karahan and Dr. Jungsu Kim, who sought to determine which cell types were most responsible for IDOL-mediated damage. Historically, the scientific community focused on microglia — the brain’s immune cells — as the primary drivers of plaque-clearance.

However, using a series of “knockout models,” the Indiana University team found that removing IDOL from microglia had a negligible effect on plaque levels.

  • AT A GLANCE: “Knockout” = a gene deliberately switched off to study its function

A “knockout model” is a genetically engineered animal — usually a mouse — in which a gene like IDOL is “switched off” so scientists can see how the brain behaves without it.

They take out a gene to see what breaks — or improves — when it’s gone.

When IDOL was “deleted” specifically from neurons, the results were deemed significant. The researchers observed a substantial reduction in amyloid-beta deposition.

  • AT A GLANCE: Lower APOE4 levels observed; APOE4 = strongest genetic risk factor for late‑onset Alzheimer’s

Additionally, the deletion of neuronal IDOL led to a decrease in APOE4 levels. As APOE4 is the most significant genetic risk factor for late-onset Alzheimer’s, this suggests that targeting IDOL could directly mitigate the risks associated with this specific genotype.

Clinical Implications and Synaptic Health

  • AT A GLANCE: IDOL inhibition linked to improved ‘synaptic plasticity’; Healthier connections = better learning & memory support

What distinguishes this research from current treatments — such as antibodies that target existing plaques — is its focus on enhancing the brain’s internal environment.

The researchers also observed a second effect – beyond reducing toxic amyloid-beta. This is to say that inhibiting IDOL was also associated with improvements in synaptic plasticity — the brain’s ability to adjust and strengthen connections involved in learning and memory.

It refers to how the brain “rewires” itself.

Conclusion: The Path to Small-Molecule Therapeutics

  • AT A GLANCE: Targeting IDOL may improve the brain’s internal environment

From a pharmaceutical perspective, the IDOL enzyme is a highly viable (read: commercially promising) target.

So, the upshot is that drug-researchers believe they may be able to engineer an oral medication capable of inhibiting the trash-removal inhibition!

  • AT A GLANCE: Goal: oral drugs that cross the blood‑brain barrier; Less invasive than antibody infusions

From a cost-per-treatment standpoint, this would an advancement over the current method, which requires expensive – and invasive – intravenous infusions required to deliver antibody treatments to try to dissolve plaques.

The Indiana University School of Medicine team is still a “preclinical” phase. Its focus is on screening for “small molecules” that can effectively cross the blood-brain barrier to inhibit IDOL. While further trials are obviously necessary, this research provides a roadmap for a new generation of Alzheimer’s therapies.

For those you still here, thank you for sticking with it! I know it was heavy-going.

If you’d like to dig deeper, here’s a link to the original study — because this is one of those cases where the data itself really is the story.

https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.70949
https://medicine.iu.edu/news/2026/02/alzheimers-drug-discovery-pathway-2026