Magic mushrooms are better known for producing hallucinations and altering people’s sense of reality than for treating brain diseases. Most people associate them with tripping, rather than Alzheimer’s disease.
But a report on an individual patient has prompted scientists to ask whether psilocybin , the psychedelic compound in magic mushrooms, could have unexpected effects on the ageing brain.
The report describes changes observed in a Japanese-American woman in her 80s with advanced Alzheimer’s disease after she received psilocybin-containing mushrooms. Dementia is a broad term for symptoms that affect memory, thinking and everyday independence. Alzheimer’s disease is its most common cause.
The woman had experienced progressive decline for a decade. For the previous five years, she had largely communicated using single words and relied heavily on others for everyday care. She also had difficulty walking and dressing herself and experienced chronic urinary incontinence.
She received 5g of psilocybin-containing mushrooms. The exact amount of psilocybin is unclear because mushroom potency varies. During the experience, she sweated heavily and entered a prolonged sleep-like state. Around 19 hours later, she began speaking spontaneously and recalling memories from her own life.
Over the following days and weeks, caregivers reported that she seemed more alert, recognised family members, walked more independently, began dressing herself and regained urinary continence. One month later, she received a second supervised session involving 3g of mushrooms and again appeared more expressive and agile.
The case has drawn comparisons with neurologist Oliver Sacks’s 1973 book Awakenings , which described patients who unexpectedly regained lost abilities after treatment with the Parkinson’s drug L-dopa , also known as levodopa. The diseases and drugs are entirely different. Both raise questions about how much function may remain hidden within a damaged brain.
However, the report does not show that psychedelics reverse Alzheimer’s disease.
It involved one person, rather than a controlled clinical trial. Her diagnosis was based on her clinical history, rather than confirmed using biomarkers: biological signs of Alzheimer’s disease that can be detected using tests such as brain scans or analysis of spinal fluid. There was no comparison group and no standardised testing of memory and thinking before and after treatment. Observations were largely based on reports from caregivers and family members.
Alzheimer’s disease involves abnormal proteins, inflammation, damage to connections between brain cells and, ultimately, the death of neurons , or nerve cells. There is no evidence that psilocybin reversed these underlying disease processes.
The authors suggest that psilocybin may temporarily have altered communication between surviving brain networks: groups of brain regions that work together. This could have made some abilities more accessible for a limited period. Because the report did not include brain scans, this remains an untested hypothesis.
Scientists are interested in this possibility partly because of the brain’s ability to adapt.
For much of the 20th century , scientists believed that the adult brain was relatively fixed. It is now known that the brain can reorganise itself throughout life. New connections can form and networks can change in response to experience.
This process, known as neuroplasticity , supports learning, memory and recovery from injury. It generally becomes less efficient with ageing and dementia.
Psilocybin acts mainly through a serotonin receptor called 5-HT2A. Serotonin is a chemical messenger involved in mood, perception and other functions. Receptors are proteins that allow cells to respond to chemical signals.
Studies in animals suggest that psilocybin can encourage the formation of dendritic spines: tiny protrusions on nerve cells that help them communicate. Psychedelics may also affect signalling pathways involving brain-derived neurotrophic factor , or BDNF, a protein involved in maintaining nerve-cell connections.
Brain-imaging studies suggest that psilocybin temporarily changes communication between large-scale brain networks. Some networks become less rigidly separated, while familiar patterns of activity are disrupted.
Over the past decade, clinical trials have produced promising results in depression. Smaller studies have also examined psilocybin-assisted therapy for anxiety and some forms of addiction.
Other research has explored possible anti-inflammatory effects. This is relevant because chronic inflammation is thought to contribute to Alzheimer’s disease and other neurodegenerative disorders: conditions in which nerve cells gradually become damaged or die.
Laboratory and animal research therefore suggests that psychedelics may influence nerve-cell growth, inflammation and brain-network activity. Whether these effects occur in people with Alzheimer’s disease remains unknown.
Separate research at the University of California, Berkeley , is examining how psilocybin affects cognitively healthy adults aged 60 to 85. The study is not testing a dementia treatment. Participants will receive synthetic psilocybin and undergo brain scans and tests of memory and thinking.
There are important reasons for caution.
Psilocybin is not risk-free . Psychedelic experiences can be frightening and disorienting, particularly for vulnerable people. Older adults may face increased risks of falls, heart and circulation problems and interactions with medications.
The woman experienced heavy sweating, suspected high body temperature and a prolonged sleep-like state. The absence of lasting complications does not establish that the approach is safe.
It would be dangerous to interpret the report as a reason to experiment with psychedelic mushrooms outside a closely supervised research or clinical setting.
The case raises a possibility: even after years of severe cognitive decline, some abilities may remain temporarily accessible. Whether psilocybin played a direct role, how it might have done so and whether similar effects could be reproduced in other people remain unknown. Answering those questions will require controlled research.
