The Immune System in the Brain: Microglia and Neuroinflammation

Microglia are the brain’s innate immune cells. They monitor brain tissue for signs of infection, injury, or dysfunction. In a healthy brain, microglia clean up debris and support neurons.

But in Alzheimer's, these cells become chronically activated, releasing pro-inflammatory cytokines and reactive oxygen species that damage neurons.

In short, chronic microglial activation can result in a vicious cycle of inflammation → neuronal damage → more microglial activation. Here’s the catch.

Amyloid as a Defender, Not the Villain

New research suggests amyloid-beta might act as an antimicrobial peptide — like an immune response to infection. Scientists, Rudolph Tanzi and Robert Moir (Harvard) showed that amyloid-beta can trap microbes, such as herpes simplex virus and bacteria, by forming sticky plaques.

The idea is that plaques are like scabs that protect the brain from pathogens or trauma. The real problem arises when this protective mechanism goes haywire or fails to shut down — like an autoimmune response spiraling out of control.

Alzheimer's as a Self-Destructive Immune Response

The autoimmune model kicks when the brain misidentifies its own structures as threats (e.g., damaged synapses, tau proteins, etc.). So the immune cells launch an attack and so neurons suffer collateral damage.

This misdirected immune activity causes sustained neuroinflammation, accelerating the progression of dementia.

Therefore, amyloid and tau may be secondary effects, markers of an immune system under siege — not root causes.

Clues from Genetics & Autoimmune Links

1. TREM2 Mutations

TREM2 is a gene involved in regulating microglial response. Mutations here are strongly linked to Alzheimer’s risk. These mutations make microglia more reactive, leading to chronic inflammation and impaired debris clearance.

2. APOE4 and Immunity

APOE4, the strongest genetic risk factor for AD, also affects lipid metabolism and immune regulation. Some researchers believe APOE4 carriers may have an exaggerated immune response to stressors or infections.

Why This Matters for Caregivers and Families

Understanding Alzheimer’s as a neuroimmune disorder can help caregivers and families feel more empowered. It opens up new strategies for care — and hope.

If the immune system plays a central role, then early intervention, lifestyle support, and anti-inflammatory approaches could become powerful tools in the fight against dementia.

That's why we at MCI and Beyond, are committed to sharing the latest insights that support informed caregiving, proactive prevention, and holistic brain health. This blog, by the way, will only give you reader hopeful news!

Conclusion

Thankfully, we may be looking at a paradigm shift where Alzheimer’s and other dementia diseases are no longer seen as a “plaque problem” but as a complex disorder involving the immune system, metabolism, and possibly infections. That doesn’t mean amyloid is irrelevant — but perhaps it's part of the body's response, not the enemy itself.

So dementia, a group of cognitive impairments including Alzheimer’s disease, may not be as mysterious as it once seemed. By shifting the focus from plaques to the immune system, we can better understand the true roots of cognitive decline, and create smarter, more compassionate solutions for those affected.

MCI and Beyond continue to explore the science, stories, and strategies that support brain health at every stage of life. This is a noble mission!

Join us by signing up for our biweekly newsletter. Stay tuned. Share this post. Thanks for reading.

References:

• Moir RD, Tanzi RE. "Amyloid-beta as a defense protein." Neuron (2016)
• Heneka MT et al. "Neuroinflammation in Alzheimer's disease." Lancet Neurology (2015)
• Keren-Shaul H et al. "A unique microglia type associated with restricting development of Alzheimer's disease." Cell (2017)
• Itzhaki RF. "Herpes simplex virus type 1 and Alzheimer's disease: possible mechanisms and signposts." FASEB Journal (2017)
• Dodiya HB et al. "Gut microbiota-driven brain inflammation in Alzheimer’s disease." Neuron (2022)

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