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The mood at the recent 2026 AD/PD International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders in Copenhagen was notably different from the mood that has hung over much of neurodegeneration research for the past decade.

There was still plenty of caution, and plenty of unanswered questions, and certainly no shortage of technical nuance. But there was also something more concrete than hope: a growing sense that the field now has enough tools, biological insight, and clinical momentum to start probing more deeply and stratifying pathologies of neurodegenerative diseases in patients, at varying stages of progression.

That shift was visible across the meeting. It was there in conversations about co-pathologies, the increasingly central role of inflammation and the rapid maturation of blood-based biomarkers. It also featured in the way industry and academia alike talked about therapy: not as a search for a single silver bullet, but as a move toward combination treatment strategies more familiar from the fields of oncology, cardiology, and other complex chronic diseases.

Henrik Zetterberg, PhD, Gothenburg University, University College London, and a guest professor at University of Wisconsin-Madison, one of the field’s most influential biomarker researchers, put the central theme plainly: “I think disease heterogeneity will be the mantra in the coming years, to dissect the molecular underpinnings of this heterogeneity.”

Heterogeneity moves from caveat to core concept

Zetterberg described how biomarker-enabled phenotyping is exposing just how different patient trajectories can be once amyloid begins to accumulate. Some people decline quickly. Others remain resilient for a decade or longer. Some cases that appear clinically similar may in fact be driven by very different molecular constellations.

Geoff Kerchner, MD, PhD, vice president, global head of neurodegeneration at Roche, made a similar point from the therapeutic side. In Alzheimer’s disease, he said, some features remain strikingly consistent across patients.

But once one moves beyond core pathology, “the rate at which that happens varies from person to person,” and that variance is shaped in part by co-pathologies, including alpha-synuclein, TDP-43, and vascular disease.

Steve Williams, MD, PhD, chief scientific officer at Alamar Biosciences, pushed the same logic further, arguing that mixed biology is not the exception but the rule. “Everyone with neurodegeneration is carrying around some combination of other pathologies,” he said. “It’s almost inevitable because it’s a feature of aging.”

That view has major consequences. It means the field is increasingly moving away from asking whether a patient is amyloid-positive or tau-positive in a binary sense and toward asking what additional pathological burden may be present, what that burden means for progression, and how it should influence treatment choice.

Betty M. Tijms, PhD, head of science Alzheimer Center Amsterdam at Amsterdam UMC, offered a useful example from discovery research. In her work integrating CSF proteomics and lipidomics, she described signals that shift depending on tau status and amyloid background. At one point, she noted that these patterns “will inform which type of patients may require their own, personalized therapies.” It captures the direction of travel: from broad molecular mapping to biologically meaningful subtyping.

Inflammation is no longer a side story

Andréa Lessa Benedet, PhD, University of Gothenburg, discussed findings showing that people with faster progression in tau-related pathology had “higher expression of many inflammatory markers in plasma and in CSF.” That observation alone is not enough to settle the longstanding question of whether inflammation is driving disease, responding to it, or doing both. But it adds to a growing body of work suggesting that immune biology is closely tied to the pace of progression.

What made Benedet’s description especially interesting was that the signal was not identical across biofluids. The proteins elevated in CSF were not the same as those elevated in plasma. Yet when her group mapped those proteins to cell types and pathways, the two compartments converged on similar biology. In other words, the field may not always be looking for one-to-one molecular matches between brain-adjacent and peripheral compartments. It may instead be learning to recognize pathway-level concordance.

Benedet pointed to evidence suggesting that amyloid pathology together with inflammation may influence how tau spreads through the brain. That “bit of both” view—driver and response, cause and consequence—may be unsatisfying if one wants a simple mechanism. It may also be closer to biological reality.

The therapeutic implication is obvious. If inflammatory processes help define faster-progressing biology, then they are not merely descriptive. They become candidates for stratification and, eventually, intervention.

Blood-based biomarkers as research infrastructure

Few topics drew more sustained attention in Copenhagen than blood-based biomarkers. Kerchner called blood-based biomarkers one of the biggest themes of the meeting saying they could “really democratize the diagnosis of Alzheimer’s disease.”

Democratization here is about health equity—geography, trial access, earlier identification, and the possibility of shifting neurodegeneration research beyond the relatively narrow populations that have historically been easiest to recruit and deeply phenotype. That broader perspective surfaced in a session on sex differences in neurodegeneration, where Jacob Vogel, PhD, assistant professor at Lund University and SciLifeLab, presented findings suggesting that brain cells responding to Alzheimer’s pathology have different expression patterns in men and women. Seen that way, the field needs tools that are sophisticated enough to capture the true biological complexity of disease across different patients.

However, one excellent blood-based biomarker, such as brain-derived p-tau217, does not solve the co-pathology problem. As Niranjan Bose, PhD, managing director at Gates Ventures put it, there is a growing “need to do better when it comes to co-pathologies so we can stratify participants better.” A strong single analyte may be enough to identify one core process very well; it is not enough to capture the layered biology of aging brains. That is why the discussion is shifting from singleplex to multiplex, from favorite markers to models.

Zetterberg spoke about the new NULISA Neuro 220 panel from Alamar Biosciences, as a research tool that can help the field probe lysosomal and synaptic biology, alpha-synuclein-related processes, and other pathways relevant to co-pathology. He also highlighted the importance of brain-derived tau readouts, arguing that they may reduce confounding from peripheral tau expression and make blood results easier to interpret in diseases where peripheral neuropathy or other non-CNS biology could muddy the picture.

Zetterberg said, “Those broader panels will be the engines for discovery.” In other words, the value of broad biomarker panels is not that every protein measured will someday be run routinely in a clinical lab. It is that broad panels can reveal reproducible patterns, identify hub biology, and narrow the search toward robust clinical assays.

Combination treatment is becoming the default future

The conference’s other major shift was therapeutically focused. Even where amyloid remained central, the discussion increasingly assumed that amyloid-directed therapy alone will not be the endpoint.

Michael Irizarry, MD, senior vice president and deputy chief clinical officer at Eisai US, put it bluntly: “Alzheimer’s is being used as the example of precision medicine.” That is a striking statement, because for years Alzheimer’s was more often framed as the place where precision medicine had failed to arrive. What changed is that biomarkers, imaging, and fluid measures have advanced enough to stage disease more accurately and begin matching interventions to biology and timing.

Irizarry also described an emerging combination logic already being tested clinically. “The hope is that by targeting multiple processes we can get a greater treatment effect,” he said, referring to efforts to combine anti-amyloid therapy with a tau-directed antibody strategy. The reasoning is straightforward: if amyloid clearance slows disease but does not stop it, then other mechanisms—including tau propagation—remain actionable targets.

Kerchner made the same point in even broader terms. “The combination of therapies attacking different aspects of Alzheimer’s disease and Parkinson’s disease is almost surely going to be needed,” he said. He compared the situation to hypertension, diabetes, and cardiovascular disease—complex chronic illnesses that are almost never controlled with one intervention alone.

If the field is moving toward a wider therapeutic lens, with multiple mechanisms and intervention points in play, then there is value in creating space for a broader range of emerging approaches. That was visible in the Startup Hub, now in its second year, where early-stage companies gave short five-minute pitches that often echoed the meeting’s main scientific themes. ScandBio was one example: its Phase III clinical trial of a combined metabolic drug targeting mitochondrial dysfunction in Alzheimer’s disease connected to the conference session on mitochondrial pathways in neurodegeneration and therapy.

Taken together, these developments pointed to the same conclusion: as the biology becomes more layered, the response from the field is becoming more layered too. Combination therapy only becomes rational if disease heterogeneity is measurable. It only becomes practical if blood-based biomarkers can help define stage, likely response, and co-pathology burden without requiring every patient to undergo repeated PET imaging. And it only becomes truly precise if inflammation, synaptic injury, lysosomal dysfunction, vascular change, can be integrated into the treatment model rather than treated as background noise.

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