The Daily Express claimed that scientists have discovered a possible “cake ‘cure’ for dementia”, which “could be the ‘holy grail’ in slowing or even eradicating dementia in patients”.
This news story is based on a laboratory and animal study that examined the effect of an extract from cinnamon bark on the build-up of a protein called amyloid beta. Groups, or aggregates, of amyloid beta proteins develop in the brains of people with Alzheimer’s disease. These form “amyloid plaques”, which are thought to contribute to the nerve cell death that causes Alzheimer’s symptoms. The study found that the extract reduced the formation of these aggregates in the lab, and improved brain function in mice with a form of Alzheimer’s.
It is important to note that this was an animal study and its findings may not apply to humans. Also, these experiments used a cinnamon extract rather than cinnamon itself, and it is not clear whether eating cinnamon would have the same effect. It is also unclear how much cinnamon it would be necessary to eat to have an effect, and there are chemicals in cinnamon bark that may have harmful effects if eaten in large quantities.
This is preliminary research and more investigation is needed to determine whether this extract is safe and works in humans. It is much too early to claim that this extract could be the “holy grail” for slowing or eradicating Alzheimer’s disease.
Where did the story come from?
The study was carried out by researchers from Tel Aviv University in Israel and Northwestern University in the US. The authors did not report any funding sources or competing interests. The research was published in the peer-reviewed scientific journal PLoS ONE .
The Daily Express overstated the findings of this study. Stating that a “Cake cure for dementia” has been discovered is premature as this study examined the impact of a specific extract derived from cinnamon, not cake, in animal models of dementia rather than in humans.
What kind of research was this?
This laboratory and animal study looked at the effect of an extract of cinnamon bark on the aggregation of the amyloid beta protein in the brain. In Alzheimer’s disease, solid deposits (or plaques) of amyloid beta build up in the brain. These aggregates are thought to play a role in the nerve cell death that causes the disease.
The researchers point out that Alzheimer’s disease is a progressive, irreversible neurological disorder with no cure. They say previous research has established that amyloid beta aggregates can have toxic effects on nerve cells, while un-aggregated amyloid beta does not have this effect. It is also currently unknown whether the damage to nerve cells in Alzheimer’s is caused by smaller, soluble aggregates of amyloid beta or larger, insoluble fibrils (strands) of the protein.
The researchers examined the effect of the cinnamon extract on both types of aggregate. Their theory was that if the cinnamon extract could reduce the aggregation of amyloid beta, it might prevent or reduce the toxic effects of these aggregates in animal models of Alzheimer’s disease. They said that if this were the case, this extract might have potential for the treatment of human Alzheimer’s disease.
What did the research involve?
The study involved experiments on a cinnamon extract called CEppt in the laboratory, in cell culture and animal models of Alzheimer’s.
In the first laboratory-based part of the study, the researchers tested whether CEppt could prevent amyloid beta proteins from grouping together, as well as its ability to prevent the formation of amyloid beta fibrils, which can tangle together to form plaques. They also tested the ability of CEppt to inhibit the toxic effects of amyloid beta in rat brain cells in the laboratory.
In their animal experiments, the researchers tested the impact of CEppt on the lifespan and climbing ability of flies with a form of Alzheimer’s disease. These flies were genetically engineered to produce human amyloid beta proteins in their nervous systems. They have a shorter lifespan and reduced climbing ability compared to normal flies. Lifespan and climbing ability were compared between flies that produced amyloid beta but were not fed CEppt, flies that produced amyloid beta and were fed CEppt, and control flies that did not produce the protein. The flies that were fed CEppt received it from their larval stage until adulthood.
In the final set of animal experiments, researchers tested the impact of CEppt in a mouse model of Alzheimer’s disease. The mice used in these experiments carried five genetic mutations which, in humans, can cause a rare early-onset form of Alzheimer’s. The mice displayed amyloid beta plaque formation in their brains from the age of two months, as well as impaired cognitive function from four months and nerve cell death in the brain from nine months. The researchers tested CEppt’s effect on the mice’s memory, motor functions and amyloid beta plaque formation in the brain. These outcomes were compared between untreated mouse models of Alzheimer’s, Alzheimer’s model mice fed CEppt, and normal (control) mice. Mice receiving CEppt were given it from the age of two months in drinking water for 120 days. At 180 days, their memory was tested by analysing their reaction to new objects. The mice were then humanely killed and the size and number of amyloid beta plaques were measured and compared between the groups.
What were the basic results?
In the laboratory and cell culture experiments, the researchers found that CEppt:
- inhibited the grouping of amyloid beta proteins in a dose-dependent manner, which means that higher concentrations of CEppt were associated with less grouping of proteins
- inhibited the formation of amyloid beta fibrils, which can tangle together to form plaques
- inhibited the toxic effect of amyloid beta on rat neurones in the laboratory in a dose-dependent manner, so that higher concentrations of CEppt were associated with less toxicity
In their fly experiments, the researchers found that CEppt:
- improved the lifespan of the Alzheimer’s model flies that produced human amyloid beta, to the extent that there was no difference in lifespan between the treated flies and the control flies
- had no impact on the lifespan of control flies
- improved the climbing ability of flies that produced amyloid beta, so that there was little difference in climbing ability between treated flies and the controls
- had no impact on the climbing ability of control flies
In their mouse experiments, the researchers found that Alzheimer’s model mice treated with CEppt had:
- improved memory compared to untreated Alzheimer’s model mice in an object-recognition test
- nearly identical cognitive performance compared to control mice
- no difference in motor functions compared to untreated Alzheimer’s model mice
- a 60% reduction in toxic amyloid beta levels in their brains compared to untreated Alzheimer’s model mice
- fewer (35-63% depending on the measurement method) and smaller amyloid beta plaques compared to untreated Alzheimer’s model mice
How did the researchers interpret the results?
The researchers say their findings suggest that treatment with CEppt, an extract from cinnamon bark, inhibits the aggregation of amyloid beta, reduces the deposits of the protein in the brains of a mouse model of Alzheimer’s disease and improves cognitive function in these animals.
However, they also point out that it is not known how this compound affects amyloid beta aggregation, and further research is necessary to determine both how it works and which specific chemical in the extract is responsible for its action.
This early-stage study in flies and mice investigated whether an extract from cinnamon bark had an effect on the aggregation of amyloid beta proteins, which are thought to play a key role in the development of Alzheimer’s disease. The results are likely to spur further research into the therapeutic potential of this substance.
As the main findings of this study are from animals, their implication for human Alzheimer’s disease is as yet unclear. This is because there are inherent differences between flies, mice and humans. The substance used in this study was an extract from cinnamon bark, and the animals in the study were not fed cinnamon bark directly. Therefore, it is not clear whether cinnamon as a spice would contain enough of the active ingredients to have the same effects. The authors also note that chemicals in cinnamon bark could possibly have harmful effects if eaten in large quantities. They produced their extract in a way that avoided including these chemicals.
This was preliminary research and more investigation is needed to determine whether the extract is safe and works in humans. It is much too early to claim that this extract could be the “holy grail” for slowing or eradicating Alzheimer’s disease.