MDMA THERAPY

Interest in psychedelics in medical science is growing, including around neurodegenerative disorders such as Alzheimer's. The blog title “New connections: psilocybin and Alzheimer’s in recent research” touches upon an intriguing question: can psilocybin play a role in Alzheimer’s, for example through neuroplasticity and improved brain connectivity, or in other words, new connections? The honest answer is that we are still a long way from clear conclusions. However, publications do appear occasionally that make the conversation substantively more interesting, such as a recent case report that was discussed online.

In this article, we outline what such a case report can and cannot say, which hypotheses researchers often mention (such as BDNF and connectivity), and which safety and context points remain important. In doing so, we make a clear distinction between theory, early observations, and solid clinical evidence. We make no medical claims and do not provide individual advice.

What is meant by “psilocybin and Alzheimer’s”?

Psilocybin is a substance found in certain mushrooms. In the body, it is converted into psilocin, which acts on serotonin receptors (particularly 5-HT2A), among others. In a research context, psilocybin is primarily studied in relation to psychological complaints such as depression and anxiety. The step to Alzheimer's is not straightforward, because Alzheimer's is primarily a neurodegenerative disorder with underlying processes such as amyloid and tau accumulation, inflammation, and loss of neurons.

Nevertheless, there is scientific interest in a possible indirect effect: not so much a “cure” of Alzheimer’s, but a potential influence on factors such as mood, engagement, behavioral problems, quality of life, and theoretically also on aspects of brain plasticity. It is important to keep that distinction clear. For example, a drug can temporarily influence behavior or perception without changing the disease progression itself.

The recent case report: what is described?

The forum discussion upon which this article builds refers to a case report published in June 2026. In it, a woman with advanced Alzheimer's reportedly showed remarkable changes after using psilocybin-containing mushrooms, such as improvements in communication, memory, emotional engagement, and daily self-reliance.

If these kinds of observations are correct, that is undoubtedly interesting. It aligns with a hypothesis often seen in the psychedelics field: that psilocybin can temporarily “loosen” patterns in the brain and promote new connections or communication between brain regions. However, there are a few essential caveats right from the start.

First: a case report describes one person. That can be a valuable signal, but it is not proof that psilocybin can cure or reverse Alzheimer's. Nor does it show whether the effect is reproducible, how long it lasts, or which dose and context were relevant.

Secondly, with a single patient, it is difficult to rule out alternative explanations. Consider differences in day-to-day functioning, environment, diet, sleep, medication, stress levels, social interaction, expectations of loved ones, or the natural progression with temporary “good days.” Fluctuations can occur in advanced Alzheimer’s, and precisely because of this, it is difficult to establish a clear cause-and-effect relationship.

Thirdly: without standardized before- and after measurements, and without a control group, the interpretation remains vulnerable. A case report can primarily serve as a starting point for better research: randomized studies, or at least small open-label studies with clear measurement instruments and follow-up.

For those wishing to view the forum source: the discussion is described here in its continuous form: https://trip-forum.nl/qa/kan-psilocybine-helpen-bij-alzheimer/. It is good to read such a source as context, but remain critical of what has and has not been proven.

The hypothesis: neuroplasticity, BDNF, and “connection” in the brain

The core of the frequently cited hypothesis revolves around neuroplasticity. This is the brain's ability to adapt, form new connections, and strengthen or weaken existing ones. Some research areas are looking at factors such as BDNF (brain-derived neurotrophic factor), a protein involved in the growth and maintenance of neurons and synaptic plasticity.

It is important to note: “BDNF increase” and “improved connectivity” are sometimes simplified in popular explanations. In science, these involve complex, context-dependent processes. A temporary change in brain connectivity (for example, measured with fMRI) does not automatically mean that someone functions better permanently, let alone that degenerative changes are reversed.

However, the concept of “connection” can have two meanings here:

1) Neurobiological connection: possible temporary changes in communication between brain networks, which can affect flexibility in thinking, emotions, or behavior.

2) Psychological and social connection: increased emotional openness, contact, and responsiveness, which can be experienced as very meaningful by people with cognitive decline and their environment.

The case report mentioned seems to fit primarily with the idea that functions are sometimes still present that are intermittently accessible. The hypothesis is then not necessarily that psilocybin “creates new brain cells,” but that it provides temporary access to existing capacity or alters communication pathways. That is interesting, but it remains speculative until it has been tested under controlled conditions.

Why one positive observation is not enough

In medicine and psychology, it is tempting to view an impressive story as a breakthrough. Especially with conditions that have a major impact and limited treatment options, hope can grow quickly. That is precisely why nuance is essential.

A single case can, for example, be influenced by:

Placebo and expectation effects: not only with the person themselves, but also during observations by relatives or caregivers.

Setting and attentionExtra guidance, calm, closeness, and focus can temporarily improve behavior and mood, independent of the subject matter.

Measurement problems“Memory improved” can be subjective if it has not been measured with valid tests.

Risk of selective reporting: striking improvements are written down and shared more quickly than neutral or negative outcomes.

That does not mean the case report is worthless. It does mean, however, that its primary role is to refine a hypothesis and formulate substantiated questions for follow-up research. For example: in which subgroup of Alzheimer's would an effect be plausible at all, how do you reliably measure change, and how do you ensure safety?

Safety and harm reduction: extra complex in Alzheimer's

Regardless of whether psilocybin works, safety is a key issue. With Alzheimer's, additional risks and vulnerabilities often play a role, such as disorientation, anxiety, the risk of falls, medication interactions, physical comorbidities, and a limited ability to understand the experience or integrate it retrospectively.

In addition, consent and capacity to make decisions are essential themes. In advanced Alzheimer's, it is often complicated to obtain informed consent in a careful manner. This makes research protocols strict, and rightly so.

In a harm reduction approach, the emphasis is on limiting risks: no irresponsible combinations, attention to set and setting, screening for vulnerabilities, and avoiding situations in which someone could endanger themselves or others. For people with cognitive decline, this is generally more difficult, making caution especially important.

Where do we stand scientifically speaking?

At present, the field appears to be in an early phase: theory and preclinical indications, occasional human observations, and the need for well-designed clinical research. The case report from the forum discussion can increase relevance, precisely because it concerns a real-world observation in a human rather than just animal studies or models. However, it remains a first step.

What you would ideally like to see in the coming years:

• Small feasibility studies with strict safety criteria
• Clear, predetermined outcome measures (cognition, behavior, quality of life)
• Follow-up at multiple time points to assess duration and stability
• Transparent reporting of both positive and negative outcomes

Only then comes the phase in which broader conclusions are possible at all.

How does this relate to MDMA sessions and the therapy context?

This blog is primarily about psilocybin and Alzheimer's. However, it is useful to mention one broader context: sessions involving psychoactive substances are often discussed in the Netherlands in terms of research, therapy, and harm reduction. Regarding MDMA, it is explicitly stated that MDMA sessions can currently only be discussed within scientific research or in clinical practice via harm reduction. This distinction is important to prevent misunderstandings about what is and is not permissible, and what has and has not been researched.

Anyone considering guided sessions in general would do well to pay close attention to the setting, screening, experience of the facilitators, aftercare, and realistic expectations. If you would like to discuss this or register for a guided MDMA session in a harm-reduction context, you can do so via https://mdmatherapie.nl/aanmelden-mdma-sessie/. This is separate from claims regarding Alzheimer's and is not intended as advice for people with dementia.

Conclusion

The idea that psilocybin can support new connections via neuroplasticity and altered brain connectivity is an interesting hypothesis. A recent case report in advanced Alzheimer's, as discussed on the forum, may provide a first human lead for this hypothesis. At the same time, one case is not proof and says nothing definitive regarding efficacy, duration, safety, or applicability in Alzheimer's. The most important value now lies in stimulating careful follow-up research, with clear measurements and strict safety frameworks.