Cancer and Alzheimer’s disease are two of the most feared diagnoses in medicine, but they rarely strike the same person. For years, epidemiologists have noticed that people with cancer seem less likely to develop Alzheimer’s, and those with Alzheimer’s are less likely to get cancer, but nobody could explain why.

A new study in mice suggests a surprising possibility: certain cancers may actually send a protective signal to the brain that helps clear away the toxic protein clumps linked to Alzheimer’s disease.

Alzheimer’s is characterised by sticky deposits of a protein called amyloid beta that build up between nerve cells in the brain. These clumps, or plaques, interfere with communication between nerve cells and trigger inflammation and damage that slowly erodes memory and thinking.

In the new study, scientists implanted human lung, prostate and colon tumours under the skin of mice bred to develop Alzheimer‑like amyloid plaques. Left alone, these animals reliably develop dense clumps of amyloid beta in their brains as they age, mirroring a key feature of the human disease.

But when the mice carried tumours, their brains stopped accumulating the usual plaques. In some experiments, the animals’ memory also improved compared with Alzheimer‑model mice without tumours, suggesting that the change was not just visible under the microscope.

The team traced this effect to a protein called cystatin‑C that was being pumped out by the tumours into the bloodstream. The new study suggests that, at least in mice, cystatin‑C released by tumours can cross the blood–brain barrier – the usually tight border that shields the brain from many substances in the circulation.

Once inside the brain, cystatin‑C appears to latch on to small clusters of amyloid beta and mark them for destruction by the brain’s resident immune cells, called microglia. These cells act as the brain’s clean‑up crew, constantly patrolling for debris and misfolded proteins.

In Alzheimer’s, microglia seem to fall behind, allowing amyloid beta to accumulate and harden into plaques. In the tumour‑bearing mice, cystatin‑C activated a sensor on microglia known as Trem2, effectively switching them into a more aggressive, plaque‑clearing state.

Surprising trade-offs

At first glance, the idea that a cancer could “help” protect the brain from dementia sounds almost perverse. Yet biology often works through trade-offs, where a process that is harmful in one context can be beneficial in another.

In this case, the tumour’s secretion of cystatin‑C may be a side‑effect of its own biology that happens to have a useful consequence for the brain’s ability to handle misfolded proteins. It does not mean that having cancer is good, but it does reveal a pathway that scientists might be able to harness more safely.

The study slots into a growing body of research suggesting that the relationship between cancer and neurodegenerative diseases is more than a statistical quirk. Large population studies have reported that people with Alzheimer’s are significantly less likely to be diagnosed with cancer, and vice versa, even after accounting for age and other health factors.

This has led to the idea of a biological seesaw, where mechanisms that drive cells towards survival and growth, as in cancer, may push them away from the pathways that lead to brain degeneration. The cystatin‑C story adds a physical mechanism to that picture.

However, the research is in mice, not humans, and that distinction matters. Mouse models of Alzheimer’s capture some features of the disease, particularly amyloid plaques, but they do not fully reproduce the complexity of human dementia.

We also do not yet know whether human cancers in real patients produce enough cystatin‑C, or send it to the brain in the same way, to have meaningful effects on Alzheimer’s disease risk. Still, the discovery opens intriguing possibilities for future treatment strategies.

One idea is to develop drugs or therapies that mimic the beneficial actions of cystatin‑C without involving a tumour at all. That could mean engineered versions of the protein designed to bind amyloid beta more effectively, or molecules that activate the same pathway in microglia to boost their clean‑up capacity.

The research also highlights how interconnected diseases can be, even when they affect very different organs. A tumour growing in the lung or colon might seem far removed from the slow build up of protein deposits in the brain, yet molecules released by that tumour can travel through the bloodstream, cross protective barriers and change the behaviour of brain cells.

For people living with cancer or caring for someone with Alzheimer’s today, this work will not change treatment immediately. But the study does offer a more hopeful message: by studying even grim diseases like cancer in depth, scientists can stumble on unexpected insights that point towards new ways to keep the brain healthy in later life.

Perhaps the most striking lesson is that the body’s defences and failures are rarely simple. A protein that contributes to disease in one organ may be used as a clean‑up tool in another, and by understanding these tricks, researchers may be able to use them safely to help protect the ageing human brain.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

A compound found in cannabis may help protect the brain from early memory and social problems linked to Alzheimer’s disease. A new animal study published in Neuropsychopharmacology found that cannabidiol prevented cognitive decline in rats by reducing brain inflammation and activating key brain receptors.

Alzheimer’s disease is a progressive brain disorder best known for causing memory loss, but it also affects thinking, decision-making, and social engagement. Scientists increasingly recognize that inflammation in the brain plays a major role in driving these symptoms, especially in the early stages of the disease.

Cannabidiol is a chemical compound extracted from the cannabis plant that does not cause a “high.” In recent years, it has gained attention for its potential anti-inflammatory and neuroprotective properties. While cannabidiol is already used in some medical treatments, its possible role in preventing or slowing Alzheimer’s disease remains under investigation.

Roni Shira Toledano and Irit Akirav from the University of Haifa, Israel, wanted to explore whether cannabidiol could stop Alzheimer-like symptoms from developing in the first place, rather than trying to reverse damage after it occurs. They were particularly interested in the role of type 1 cannabinoid receptors, which are found throughout the brain and are involved in memory, learning, and inflammation control.

To test this, the scientists conducted experiments using male rats. The rats were injected with a substance known as streptozotocin, which triggers brain changes similar to those seen in Alzheimer’s disease, including amyloid β-protein accumulation and tau phosphorylation. Some of the rats then received regular doses of cannabidiol, while others did not.

The researchers monitored the animals’ behavior using standard tests of memory, learning, and social interaction. They also examined brain tissue to measure levels of inflammation and to determine whether type 1 cannabinoid receptors were involved in cannabidiol’s effects.

The results revealed that the rats that did not receive cannabidiol showed clear memory problems and reduced interest in social interaction—behaviors commonly seen in Alzheimer’s disease. In contrast, rats treated with cannabidiol performed normally on memory tasks and continued to interact socially with other rats.

Brain analysis revealed that cannabidiol-treated rats had lower levels of inflammation compared to untreated rats. When researchers blocked type 1 cannabinoid receptors using a different substance, many of cannabidiol’s protective effects disappeared, suggesting that these receptors play an important role in how cannabidiol protects the brain.

The findings suggest that cannabidiol may help prevent cognitive and social decline by calming inflammation in the brain and supporting normal brain signaling. The researchers emphasize that cannabidiol did not simply mask symptoms, but appeared to prevent damage from developing in the first place.

“As current Alzheimer’s disease treatments are limited, our study highlights cannabidiol as a promising candidate, demonstrating for the first time that a low dose can prevent behavioral and molecular deficits in a rodent model of [the disease],” the authors concluded.

However, the study has important limitations. It was conducted only in male rats, and animal models do not perfectly replicate human Alzheimer’s disease. Additionally, the study focused on early-stage changes rather than long-term disease progression.

The study, “Cannabidiol prevents cognitive and social deficits in a male rat model of Alzheimer’s disease through CB1 activation and inflammation modulation,” was authored by Roni Shira Toledano and Irit Akirav.

New research suggests that the electrical complexity of the brain diminishes in early Alzheimer’s disease, potentially signaling a breakdown in the neural networks that support conscious awareness. By stimulating the brain with magnetic pulses and recording the response, scientists found distinct differences between healthy aging adults and those with mild dementia. These findings appear online in the journal Neuroscience of Consciousness.

The human brain operates on multiple levels of awareness. Alzheimer’s disease is widely recognized for eroding memory, but the specific type of memory loss offers clues about the nature of the condition. Patients typically lose the ability to consciously recall events, facts, and conversations. This is known as explicit memory.

Yet, these same individuals often retain unconscious capabilities, such as the ability to walk, eat, or play a musical instrument. This preservation of procedural or implicit memory suggests that the disease targets the specific neural architecture required for conscious processing while leaving other automatic systems relatively intact.

Andrew E. Budson, a professor of neurology at Boston University Chobanian & Avedisian School of Medicine, has proposed that these “cortical dementias” should be viewed as disorders of consciousness. According to this theory, consciousness developed as part of the explicit memory system. As the disease damages the cerebral cortex, the physical machinery capable of sustaining complex conscious thought deteriorates. This deterioration eventually leads to a state where the individual is awake but possesses a diminishing capacity for complex awareness.

To investigate this theory, a research team led by Brenna Hagan, a doctoral candidate in behavioral neuroscience at the same institution, sought a biological marker that could quantify this decline. They turned to a metric originally developed to assess patients with severe brain injuries, such as those in comas or vegetative states. This metric is called the perturbation complexity index, specifically an analysis of state transitions.

The measurement acts somewhat like a sonar system for the brain. In a healthy, conscious brain, a stimulus should trigger a complex, long-lasting chain reaction of electrical activity that ripples across various neural networks. In a brain where consciousness is compromised, the response is expected to be simpler, local, and short-lived. The researchers hypothesized that even in the early stages of Alzheimer’s, this capacity for complex electrical integration would be reduced compared to healthy aging.

The study included 55 participants in total. The breakdown consisted of 28 individuals diagnosed with early-stage Alzheimer’s disease or mild cognitive impairment and 27 healthy older adults who served as controls. The research team employed a technique known as transcranial magnetic stimulation, or TMS, paired with electroencephalography, or EEG.

During the experiment, participants sat comfortably while wearing a cap fitted with 64 electrodes designed to detect electrical signals on the scalp. The researchers placed a magnetic coil against the participant’s head. This coil delivered a brief, focused pulse of magnetic energy through the skull and into the brain tissue. This pulse is the “perturbation” in the index’s name. It effectively rings the brain like a bell.

The researchers targeted two specific areas of the brain. The first was the left motor cortex, which controls voluntary movement on the right side of the body. The second was the left inferior parietal lobule, a region involved in integrating sensory information and language. By stimulating these distinct sites, the team hoped to determine if the loss of complexity was specific to certain areas or if it represented a global failure of the brain’s networks.

As the magnetic pulse struck the cortex, the EEG electrodes recorded the brain’s immediate reaction. This recording captured the “echo” of the stimulation as it propagated through the neural circuits. The researchers then used a complex mathematical algorithm to analyze these echoes. They looked for the number of “state transitions,” which are shifts in the spatial pattern of the electrical activity. A higher number of state transitions indicates a more complex, integrated response, implying a healthier and more connected brain.

The analysis revealed a clear distinction between the two groups. The participants with Alzheimer’s disease displayed a reduced level of brain complexity compared to the healthy controls. The average complexity score for the Alzheimer’s group was 20.1. In contrast, the healthy group averaged 28.2. This downward shift suggests that the neural infrastructure required for high-level conscious thought is compromised in the disease.

The reduction in complexity was consistent regardless of which brain area was stimulated. The scores obtained from the motor cortex were nearly identical to those from the parietal lobe. This suggests that the loss of neural complexity in Alzheimer’s is a widespread, global phenomenon rather than a problem isolated to specific regions. The disease appears to affect the brain’s overall ability to sustain complex patterns of communication.

The researchers also examined whether these complexity scores correlated with standard clinical measures. They compared the EEG data to scores from the Montreal Cognitive Assessment, a paper-and-pencil test commonly used to screen for dementia.

Within the groups, there was no strong statistical relationship between a person’s cognitive test score and their brain complexity score. This lack of correlation implies that the magnetic stimulation technique measures a fundamental physiological state of the brain that is distinct from behavioral performance on a test.

“Despite their impaired conscious memory, individuals with Alzheimer’s disease may be able to use intact implicit, unconscious forms of memory, such as procedural memory (often termed ‘muscle memory’) to continue their daily routines at home,” Budson explains. He adds that when patients leave familiar settings, “their home routines are not helpful and their dysfunctional conscious memory can lead to disorientation and distress.”

There are caveats to these findings that warrant attention. While the difference between the groups was clear, the absolute scores raised questions. A surprising number of participants in both groups scored below the threshold typically used to define consciousness in coma studies. Specifically, 70 percent of the Alzheimer’s patients and 29 percent of the healthy volunteers fell into a range usually associated with unconsciousness or minimally conscious states.

This does not mean these individuals are unconscious. Instead, it indicates that the mathematical cutoffs established for traumatic brain injury may not directly apply to neurodegenerative diseases or aging populations. The metric likely exists on a spectrum. The physiological changes in an aging brain might lower the baseline for complexity without extinguishing consciousness entirely.

The study opens new paths for future research. Scientists can now explore how this loss of complexity relates to the progression of the disease. It may be possible to use this metric to track the transition from mild impairment to severe dementia. The lack of correlation with behavioral tests suggests that this method could provide an objective, biological way to assess brain function that does not rely on a patient’s ability to speak or follow instructions.

This perspective also informs potential therapeutic strategies. If the disease is viewed as a progressive loss of conscious processing, treatments could focus on maximizing the use of preserved unconscious systems. Therapies might emphasize habit formation and procedural learning to help patients maintain independence.

“This research opens the avenue for future studies in individuals with cortical dementia to examine the relationship between conscious processes, global measures of consciousness, and their underlying neuroanatomical correlates,” Budson says. The team hopes that future work will clarify the biological mechanisms driving this loss of complexity and lead to better diagnostic tools.

The study, “Evaluating Alzheimer’s disease with the TMS-EEG perturbation complexity index,” was authored by Brenna Hagan, Stephanie S. Buss, Peter J. Fried, Mouhsin M. Shafi, Katherine W. Turk, Kathy Y. Xie, Brandon Frank, Brice Passera, Recep Ali Ozdemir, and Andrew E. Budson.