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Harshi Peiris, Ph.D.

@Neuroscope_mp

Jun 7 • 10 tweets • 5 min read • Read on X

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BREAKING:
Scientists just ran the first-ever clinical trial of creatine in Alzheimer’s patients.
Brain creatine went up.
Memory and thinking improved.

But the same supplement FAILED a 5-year, 1,741-patient Parkinson’s trial in 2015.
What changed?
What does this mean for brain energy?
A thread on the most fascinating story in brain energy research right now. 🧵🧪

#Alzheimers #Parkinsons #Creatine

First: why does creatine even make sense for the brain?

Your brain is an energy hog. Your neurons are always energy-hungry.
They run on ATP.
Creatine = your brain’s emergency battery pack.
It rapidly regenerates ATP when demand spikes.

In both Parkinson’s and Alzheimer’s, this energy system breaks down.
Mitochondria fail. Neurons starve.

#BrainHealth #Mitochondria

In 2015, the NIH ran one of the largest nutritional supplement trials ever done.
1,741 Parkinson’s patients.
10g creatine/day. 5 years.

Result:
stopped early for futility.
No benefit on movement, thinking, or daily life.

This wasn’t a small study.
It was rigorous.
The failure is real and matters.

So why is creatine back in the headlines?

#Parkinsons

New 2025 imaging from Johns Hopkins helps explain why.

Using a technique called GuanCEST MRI, researchers mapped creatine levels across living Parkinson’s brains for the first time.

What they found:
Creatine depletion is HIGHLY localized — specific brain regions, not everywhere.
Oral creatine goes to muscles first. It may never reach the right places.

My opinion:
The dose in the earlier PD trial might not be sufficient.

#Parkinsons #Neuroimaging

Not all creatine+PD research failed.

One trial combined creatine + CoQ10 in Parkinson’s patients who also had early memory problems.
Over 18 months: cognitive decline was SLOWER than placebo.

Both groups still declined.
Motor symptoms: no difference.

My opinion:
Monotherapy is probably the wrong approach.
The doses need to be optimized.

Combinations targeting mitochondria from multiple angles — that’s where the field is moving.

Now here’s where it gets interesting ... Alzheimer’s.

Until May 2025, creatine had NEVER been tested in a clinical trial for Alzheimer’s disease.
Not once.
Parkinson’s had nearly 20 years of trials.
Alzheimer’s had zero.
That just changed.

The CABA trial:
20 Alzheimer’s patients,
20g creatine/day, 8 weeks. (double the dose in PD trial)

First question: Can creatine even reach the brain at this dose?
Answer: yes. 85% of patients showed increased brain creatine.
Average increase: +11%, confirmed by MRI.

(caveat - No control group. Small sample. But this is the first human evidence. It matters.)

So what actually happened to their thinking and memory?
8 weeks of creatine in 20 Alzheimer's patients:
✅ Overall cognition: improved (p=.02)
✅ Fluid cognition: improved (p=.004)
✅ Working memory: improved (p=.001)
✅ Reading recognition: improved (p<.001)
✅ Attention/inhibitory control: trending (p=.05)
No change in crystallized cognition or MMSE.

As I said ... Caveat ...No control group. Can't rule out practice effects.
But in a disease defined by decline, these numbers are worth watching.

Here’s what both stories are really pointing to:
Neurodegeneration may be, in large part, a disease of broken brain energy metabolism.
Not just plaques.
Not just alpha-synuclein.
The power supply is failing.

Creatine is one of the simplest tools scientists have to test that idea in real humans.
It’s a molecular probe as much as a potential therapy.

Important: this is not a green light to start taking creatine for brain disease.

The PD trial failed.
The AD trial had no control group and 20 people.

What we have: a compelling hypothesis, a cautionary tale, and genuinely exciting early data. What we need: larger, controlled trials.

Full article coming soon.

And there’s another piece of this puzzle — involving medications millions already take — coming soon. 🧵

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More from @Neuroscope_mp

Harshi Peiris, Ph.D.

@Neuroscope_mp

Jun 4

🚨 BREAKING Scientists may have just cracked the code on Alzheimer's and Parkinson's — WITH ONE PILL.

A drug called Buntanetap was just published in a peer-reviewed journal with Phase 3 data.
Phase 3 means that we are on the verge of FDA approval.

It targets the ROOT CAUSE of both diseases simultaneously.

Here's what you need to know 🧵👇
#Alzheimers #Parkinsons

Tweet 2
Most people think Alzheimer's and Parkinson's are totally separate diseases.
They're not.

At autopsy, ~1 in 3 Alzheimer's patients have Lewy body (Parkinson's-type) protein in their brain.

And ~50% of Lewy body dementia patients have full Alzheimer's pathology too.

Same brain. Multiple diseases. Quietly overlapping. 🧠
That's called co-pathology — and it's why targeting just one protein may never be enough. 👇
#Dementia #Neurodegeneration

There are FOUR driving neurodegeneration:
🔴 Amyloid-β
🟠 Tau
🟡 Alpha-Synuclein
🟢 TDP-43
Every approved drug targets just one of these.
Buntanetap targets all four — simultaneously.
That's not an upgrade. That's a completely different philosophy. 👇
#Alzheimers #Buntanetap

Read 15 tweets

Harshi Peiris, Ph.D.

@Neuroscope_mp

Jun 1

🚨 Scientists just identified a hidden 'molecular switch' that drives chronic brain inflammation in Alzheimer’s.

It’s a protein called STING that gets chemically stuck in the “on” position.

This could be a major new drug target. Thread 👇

From Scripps Research
published April 2026, highlighted again recently

In Alzheimer’s brains, STING undergoes a specific chemical modification (S-nitrosylation) → this keeps microglia (brain immune cells) in chronic overdrive, damaging neurons and synapses.

When researchers blocked this STING switch in mouse models:
Neuroinflammation dropped significantly
Brain cell connections were better protected

This is exciting because chronic inflammation is now considered a core driver of Alzheimer’s progression.

Read 6 tweets

Harshi Peiris, Ph.D.

@Neuroscope_mp

Jun 1

We've spent decades hunting for "the ALS cure."

I get it … when you're facing this disease, you want one answer. That's human.

But after 20 years in neurodegeneration, I can tell you: we've been asking the wrong question.

And new science proves it. Here's what's actually going on.

#ALSAwareness #PrecisionMedicine

Here's what I mean.

ALS … amyotrophic lateral sclerosis … is the name we give to a disease where motor neurons die.

But the biological reason they're dying? That differs from patient to patient.

Same diagnosis, but completely different machinery … breaking down underneath.

That's the part nobody told patients. And it matters more than almost anything else in ALS right now.

Think of it like this.

Imagine treating every type of cancer with the same chemotherapy, because they all cause tumors.

We'd never do that. We know cancer isn't one disease.

But that's essentially what ALS drug trials have been doing for decades.

Mixing patients with completely different underlying biology into one trial, then wondering why nothing works.

Read 12 tweets

Harshi Peiris, Ph.D.

@Neuroscope_mp

May 24

🚨 BREAKING:
Parkinson's disease may begin in your GUT — not your brain.

Peer-reviewed science now shows gut changes can precede motor symptoms by 10–20 YEARS.

And a deficiency in specific B vitamins may be driving the damage.
Thread 🧵👇

Before the tremors. Before the diagnosis.

Researchers consistently find these GI symptoms in people who later develop Parkinson's:
❌ Chronic constipation
❌ Delayed stomach emptying
❌ Bacterial overgrowth (SIBO)
❌ 'Leaky gut.'

This isn't a coincidence. It's the disease.

Here's the bombshell:
α-synuclein — the toxic protein that kills dopamine neurons in Parkinson's — is found in GUT neurons FIRST.

Scientists believe it travels from the gut → up the vagus nerve → to the brain.

Parkinson's may literally climb from your stomach to your brain.

Read 10 tweets

Harshi Peiris, Ph.D.

@Neuroscope_mp

May 19

🚨 BREAKING Scientists just gave 15 people a single IV drip.
No daily pills.
No monthly injections.
One time.
Done.

Their "bad" cholesterol dropped 50%.
Triglycerides dropped 55%.

And it may be PERMANENT.

This is CRISPR — and it just changed cardiology forever. 🧵

The drug is called CTX310.
It's made by CRISPR Therapeutics.

Here's how it works in plain English:
Your liver makes a protein called ANGPTL3.
That protein BLOCKS your body from clearing cholesterol.

CTX310 turns that gene OFF.
Permanently.

Like flipping a switch — and never having to flip it again. 🔬

Here's the wild part.

Some people are BORN with a broken ANGPTL3 gene.
What happens to them?
✅ Lifelong low cholesterol
✅ Lifelong low triglycerides
✅ Dramatically lower heart disease risk
❌ No harmful side effects

Scientists thought: what if we could give EVERYONE that mutation?

That's exactly what CTX310 does. 🧬

Read 12 tweets

Harshi Peiris, Ph.D.

@Neuroscope_mp

May 11

BREAKING: Scientists gave 20 patients a single cancer treatment.

All 20 had ZERO detectable cancer cells afterward.
None progressed.
None died.
This just published in Nature Medicine.

Here's what it actually means 🧵👇

The treatment is called CAR-T cell therapy.
Here's how it works:
→ Doctors take YOUR own immune cells
→ Re-engineer them in a lab to hunt cancer
→ Infuse them back in ONE single dose
Your own immune system becomes the weapon.
(2/10)

The trial is called CAR-PRISM.

Patients: 20 people with HIGH-RISK smoldering myeloma (a precancer stage — blood cancer before it fully develops)

Treatment: One infusion of cilta-cel (Carvykti)

Result: 100% had zero cancer detected.

Follow-up: 15 months. Still zero.
(3/10)