Field Report: The Immune System Was in the Room All Along

Last night, while researching something else entirely, I came across a 2026 review in Immunity that reframes Alzheimer’s as a stage-specific neuroimmune disease.

If that sounds technical, it is.

But what it means is something very human.

For decades, the public story about Alzheimer’s has focused on plaques and tangles. Amyloid and tau. The working idea was simple. Remove the buildup and perhaps the problem recedes.

That model is not wrong.

But it may be incomplete.

The review synthesizes years of genetic, cellular, and translational research. It does not claim a cure. It does not discard amyloid. What it suggests is this.

The brain’s immune system may play a central and stage-dependent role in how Alzheimer’s develops and progresses.

 
What That Means
Certain genetic risk factors, including variants of APOE, influence how microglia behave.

Microglia are the brain’s resident immune cells. They monitor the environment, respond to perceived threats, and help clear debris.

Early in disease, microglia may help contain damage.

Later, under genetic and inflammatory pressure, they can shift into states that amplify injury.

Even antibody therapies such as lecanemab and donanemab rely on microglial immune mechanisms to clear amyloid. The immune system is not a side character in these treatments.

It is part of the mechanism.

The review also discusses T cells, immune cells that can enter the brain and influence disease progression. Some appear protective. Others may worsen damage. Timing matters.

This review does not eliminate amyloid from the conversation. It reframes how immune responses may shape when and how pathology progresses.

 
Stage Specificity
The key idea is stage specificity.

Not “inflammation is bad.”

Not “boost the immune system.”

Not “clear the plaque and you are done.”

Instead, immune responses in Alzheimer’s appear to change across disease stages. Protective at one point. Harmful at another.

That is not a simple story.

But it may be a more accurate one.

 
Why This Matters to Families
I am not an immunologist.

I am not a clinician.

I do have a resident scientist in my life who patiently fields my questions and corrects my enthusiastic overreach, and I am grateful for his invaluable input.

But I am also a wife.

I live in a house where this diagnosis is not theoretical.

For years, the dominant public narrative sounded like corrosion. Accumulation. Inevitable decline.

Something builds up. Something spreads. Something cannot be stopped.

If Alzheimer’s is, at least in part, a mis-timed immune response inside the brain, a defense system that becomes dysregulated, that changes the emotional architecture.

Decay feels final.

Dysregulation feels complex.

And complex systems, while harder to understand, are not the same as hopeless.

They are dynamic.

Dynamic systems can sometimes be influenced.

Not cured overnight. Not simplified. But studied. Adjusted. Modulated.

That difference matters at two in the morning.

 
Why Isn’t This Front Page News
Because it does not promise rescue.

Because it demands timing, precision, and humility.

Because nuance rarely trends.

Paradigm shifts often look quiet while they are happening.

Ten years later, we call them obvious.

 
Where MiM Fits
MiM exists in the space between diagnosis and daily life.

If Alzheimer’s involves stage-dependent immune changes, timing becomes even more important.

Timing of intervention.
Timing of structure.
Timing of routine.
Timing of support.

We cannot control every biological variable.

But we can influence daily systems.

We can reduce avoidable stress.
We can reinforce routine.
We can support cognitive engagement.
We can move families from crisis mode to operating system.

The immune system was in the room all along.

If that framing holds, it does not erase suffering.

But it may refine the questions we ask next.

Better questions are where real progress begins.

I will let you know what my resident scientist says.

 
Vanessa.