Brain Aging Has a Cleanup Problem. A New Study Puts NAD+ in the Middle of It.

A 2026 study mapped more than 100 NAD+ and mitophagy-related genes across 12 areas of the human brain. What researchers found gives us a better picture of mitochondrial cleanup, brain aging, and where NMN actually fits.

We usually talk about mitochondria when we talk about energy.

Fair enough. They help make ATP, the energy cells use to keep running.

But making energy is only part of the job.

Mitochondria get damaged.

And your cells have to notice.

Then separate the damaged parts, break them down and recycle what they can.

That cleanup process has a name: mitophagy.

When that system starts falling behind, old and damaged mitochondria can accumulate.

A new 2026 study suggests that this mitochondrial housekeeping problem may be closely connected with what happens in the aging brain. And NAD+ sits right inside that system.

What did the new NAD+ and brain-aging study find?

Researchers from Norway and an international team analyzed the NAD+–mitophagy axis, the network connecting NAD+ metabolism with the systems cells use to maintain and remove mitochondria.

This was a large computational study.

The researchers looked at 102 NAD+ and mitophagy-related genes across 12 human brain regions, using 77 public datasets spanning healthy aging and several neurodegenerative diseases.

The main finding was clear:

The NAD+–mitophagy network changed during normal brain aging and was more severely disrupted in neurodegenerative disease.

That matters because neurons have expensive energy bills.

They need functioning mitochondria to keep electrical signals moving, maintain connections and do the basic work of being brain cells.

A damaged mitochondrion hanging around isn't particularly useful company.

What is mitophagy?

Mitophagy is the process cells use to identify and remove damaged mitochondria.

Think maintenance, rather than demolition.

Mitochondria constantly change shape. Parts split apart. Healthy sections can fuse back together. Damaged sections can be isolated and sent to lysosomes, the cellular structures that break unwanted material down.

That turnover helps cells maintain a healthier pool of mitochondria.

And aging appears to interfere with it.

Previous research has found that damaged mitochondria accumulate in aging neurons, while impaired mitophagy has been linked with several age-related neurological conditions. The new study looked at the genes behind that process in much greater detail.

Five genes kept showing up

The researchers then used the PandaOmics AI platform to rank genes that looked especially relevant.

Five made the cut:

ULK1, LAMP2, MFN1, OPA1 and ATP6V0E1.

The names are ugly.

Their jobs are easier.

ULK1 helps start autophagy, the wider cellular recycling process that includes mitophagy.

LAMP2 helps lysosomes break down material the cell has marked for removal.

MFN1 and OPA1 help manage mitochondrial fusion and structure.

ATP6V0E1 contributes to the acidic environment lysosomes need to break cellular material down.

Different jobs. Same problem.

A brain cell has to know what is damaged, separate it, dispose of it and keep the healthier mitochondrial network running.

Miss enough steps and the rubbish starts staying in the building.

What happened when researchers disrupted those genes?

This is where the paper moved beyond data analysis.

The researchers tested several of the targets in C. elegans worms, a human Tau cell model and human iPSC-derived cortical neurons.

When some of the mitochondrial fusion and lysosomal genes were reduced in worms, neuronal function suffered.

In the human Tau cell model, reducing MFN1 or LAMP2 increased Tau aggregation.

Researchers also tested a compound that promotes mitochondrial fusion in human cortical neurons carrying the APOE4/4 genotype. After treatment, levels of phosphorylated Tau 217 were lower in that experimental model.

Interesting?

Absolutely.

A human treatment result?

No.

Those are two very different sentences.

Where does NAD+ fit into mitochondrial cleanup?

NAD+ is nicotinamide adenine dinucleotide, a molecule cells use in energy metabolism and many other cellular processes.

Mitochondria depend on NAD+ metabolism.

Mitophagy is also connected with NAD+-dependent pathways.

Researchers call this relationship the NAD+–mitophagy axis.

The 2026 study found that genes across this system change with age in the human brain, and that disruption becomes greater in the neurodegenerative disease datasets they studied.

That adds another layer to the usual NAD+ conversation.

Energy gets most of the attention.

Maintenance may be just as interesting.

Your cells don't simply need mitochondria producing energy today. They need a working system for dealing with the mitochondria that stop doing their job properly.

So where does NMN fit?

This is the part worth being precise about.

NMN, or nicotinamide mononucleotide, is a precursor the body can use to make NAD+.

That link has human evidence.

In a randomized, double-blind, placebo-controlled study in healthy older men, 250 mg of NMN per day increased whole-blood NAD+ and related metabolites compared with placebo. Other human trials have also reported increases in blood NAD+ after oral NMN supplementation.

That gives NMN a clear place in the conversation:

NMN can support NAD+ availability.

Then we hit the line the internet tends to sprint straight past.

Did this study show that NMN cleans damaged mitochondria from the human brain?

No.

The 2026 brain-aging study did not give people NMN.

It did not measure what happened to mitophagy in the brains of people taking NMN.

It did not show that NMN prevents Alzheimer's disease, Parkinson's disease or other neurodegenerative conditions.

And it did not prove that increasing blood NAD+ will automatically produce the mitochondrial effects seen in worms or cell models.

The researchers themselves say more studies in higher organisms and longer-term research are needed.

That limitation makes the study more useful, not less.

We now have a better map of the system.

We don't yet have every road tested in humans.

What does this mean for NMN and brain aging?

The strongest takeaway is narrower than the headline you'll probably see floating around social media.

The study gives more evidence that NAD+ metabolism and mitochondrial quality control are connected with brain aging.

It also identifies specific genes inside that system that researchers can now study more closely.

NMN enters the story one step earlier.

It is an NAD+ precursor.

Human studies show oral NMN can raise blood NAD+.

Whether NMN can meaningfully improve mitophagy in the human brain, slow brain aging or change neurological disease risk is still an open research question.

That's the honest state of the science.

And frankly, it's already interesting enough.

Why mitochondrial cleanup deserves more attention

Most longevity conversations focus on what we can add.

More NAD+.

More supplements.

More exercise.

More protein.

Cells have another problem to solve every day: what to do with the parts that no longer work properly.

Mitochondria don't stay pristine because you bought a longevity supplement.

They get used.

Some get damaged.

The system has to keep sorting them.

That makes mitophagy one of the more interesting areas in longevity research because it deals with maintenance at the point where cellular energy and cellular damage meet.

The new study gives researchers five specific targets to follow and a much clearer map of how NAD+ and mitochondrial cleanup change across the aging brain.

The next question is harder.

Can we safely change that system in humans in a way that matters?

That study hasn't been done yet.

Where Genevity+ NMN fits

We sell NMN for the part we can stand behind.

NMN is a precursor to NAD+, and controlled human studies have shown that oral NMN can increase blood NAD+ levels.

The 2026 brain study gives us another reason to keep watching NAD+ research closely.

It doesn't give us permission to turn a promising mechanism into a medical promise.

If you're interested in supporting NAD+ as part of your daily longevity routine, you can explore Genevity+ NMN and read more of our breakdowns of the latest human NMN research.

Study details

The main study discussed in this article is:

Sofie Lautrup, Shu-qin Cao, Xi Long, et al. A combined artificial intelligence–wet lab approach identifies a pivotal role of the NAD+–mitophagy axis on aging and neurodegeneration. Alzheimer's & Dementia. 2026;22(8):e71680. DOI: 10.1002/alz.71680. First published August 21, 2026.

Human NMN evidence referenced:

Masaki Igarashi et al. Chronic nicotinamide mononucleotide supplementation elevates blood nicotinamide adenine dinucleotide levels and alters muscle function in healthy older men. npj Aging. 2022;8:5. DOI: 10.1038/s41514-022-00084-z.

This article is for educational purposes only. Genevity+ products are not intended to diagnose, treat, cure or prevent any disease.