A breakthrough in Alzheimer's research reveals that an abnormal build-up of fat droplets in the brain may cause or speed up the disease. The finding promises to open new avenues in the search for a cure or new treatments.
The research, led by the Research Center of the University of Montreal Hospital (CRCHUM) in Canada, is published in the journal Cell Stem Cell.
The researchers note how, for the first time since 1906, when Dr. Alois Alzheimer first described the disease that takes his name, they found accumulations of fat droplets in the brains of patients who died of the disease. They have also identified the type of fat.
They were astonished to find fat droplets near the stem cells in the brains of mice bred to develop a form of Alzheimer's disease.
First author and doctoral student Laura Hamilton says she and her colleagues realized that Alzheimer himself had noted the presence of fat build up in patients' brains after they died. This was dismissed and largely forgotten, however; at the time, the biochemistry of the fat was too complex to study.
According to the World Health Organization, there are 48 million people worldwide living with dementia - a general term for loss of memory and other mental abilities serious enough to interfere with daily life. Alzheimer's disease accounts for two-thirds of dementia cases.
Significant fat build up in brains of people who died of Alzheimer's disease
The team went on to compare the brains of nine patients who died from Alzheimer's disease with the brains of five people who did not die of the disease. They found significantly more fat droplets in the brains of the patients with Alzheimer's disease.
- While its greatest known risk factor is age, Alzheimer's disease is not a normal part of aging
- The most common early symptom is difficulty remembering newly learned information
- Although current treatments cannot stop the disease progressing, they can slow symptoms for a while.
Then, using advanced mass spectrometry, the researchers identified the fat deposits to be triglycerides enriched with specific fatty acids, which can also be found in animal fats and vegetable oils.
The team believes the finding could prove to be a missing link in the field of Alzheimer's research.
Senior author Karl Fernandes, a CRCHUM researcher and professor at the University of Montreal, explains:
"We discovered that these fatty acids are produced by the brain, that they build up slowly with normal aging, but that the process is accelerated significantly in the presence of genes that predispose to Alzheimer's disease."
The researchers found that the brains of mice predisposed to the disease build up these fatty acid deposits at 2 months, which in human terms would be the early twenties.
"Therefore, we think that the build-up of fatty acids is not a consequence but rather a cause or accelerator of the disease," Prof. Fernandes says.
The team says inhibitor drugs that are already being tested for metabolic diseases such as obesity, can block the enzyme that produces these fatty acids and stop them accumulating. Tests on mice predisposed to the disease confirmed this. Prof. Fernandes concludes:
"The impact of this treatment on all the aspects of the disease is not yet known, but it significantly increased stem cell activity. This is very promising because stem cells play an important role in learning, memory and regeneration."
The risk of developing Alzheimer's disease doubles every 5 years after the age of 65. In line with this, a study that Medical News Today covered recently shows that the brain's ability to clear away a toxic protein fragment associated with the disease is much reduced in older people.