- HDL cholesterol is often thought of as the “good cholesterol” that helps prevent cardiovascular disease.
- However, new research indicates it may also play a role in brain health.
- More HDL in the brain was linked to better cognitive performance and higher levels of a peptide called amyloid-beta 42.
- Scientists say that drugs that target HDL activity may help prevent Alzheimer’s disease.
- Several medications are under investigation at this time.
Most of the time people hear about cholesterol within the context of preventing cardiovascular disease.
There is the so-called “bad cholesterol,” LDL (low-density lipoproteins), which can increase your risk for clogged arteries, heart attack, and stroke when you have too much of it.
There is also the “good cholesterol,” HDL (high-density lipoproteins), which protects you by carrying cholesterol to your liver for disposal.
However, a group of researchers say HDL may also play an important role in brain health by lowing the risk of Alzheimer’s disease.
Dr. Hussein Yassine, an associate professor of medicine and neurology at the Keck School of Medicine of USC, and his team recruited 180 healthy adults aged 60 and over, with an average age just under 77, for their study.
In order to count and measure the size of HDL participles in the study participants’ blood plasma and cerebrospinal fluid, they used a technique called ion mobility.
In addition, out of the larger group, 141 people also took part in a battery of cognitive tests.
The team then analyzed the results.
“Individuals with greater levels of small HDL particles in the brain did better on cognitive tests and had less amyloid plaques,” said Yassine.
This effect existed regardless of their age, educational level, sex, or whether they were carriers of the APOE4 gene, which has been previously linked to a higher risk for Alzheimer’s disease.
The link was even stronger in those people with no cognitive impairment, although the effect was less once people had developed cognitive impairment, Yassine told Healthline.
A higher number of small HDL particles was also associated with higher levels of a peptide called amyloid-beta 42.
Amyloid-beta 42 can contribute to Alzheimer’s disease when it folds improperly, allowing it to adhere to brain cells and create plaques.
According to Dr. Paul E. Schulz, a neurologist with UTHealth Houston and Memorial Hermann-Texas Medical Center, these plaques increase in number over time and another protein, called tau protein, also begins to be deposited.
Eventually, inflammation occurs, probably as a reaction to the amyloid plaques and tau protein deposition.
Over time, the brain cells slowly die, Schulz explained.
This leads to the symptoms of Alzheimer’s disease, including memory loss, poor judgment, and mood and personality changes, finally culminating in the person being unable to recognize or interact with other people.
However, when amyloid-beta 42 is circulating within the brain and spinal fluid it can reduce the risk for the disease, according to the study authors.
Yassine said their study was significant because it was the first time the measurement of small HDL particles in the brain had been linked to improved cognitive function.
He believes these particles may be involved in clearing out the peptides that form amyloid plaques.
Yassine said that the implication of their findings is that the mechanisms that promote small HDL formation in the brain could play a role in Alzheimer’s disease prevention.
“Now that we have a good target to monitor, we can find what interventions (diet, exercise and drugs) increase brain small HDL with the hope that this will translate into protecting our brains,” said Yassine.
Schulz cautions, however, that this study is an early effort that needs to be investigated further.
“This [study] tells us to stay tuned to the brain fat metabolism story,” said Schulz. “As we discover more compounds that have a positive effect on this system, we may be able to reduce the risk of Alzheimer’s disease significantly.”
Schulz said there were a number of medications already under study using mouse models that appear to result in fewer amyloid deposits and improved cognitive function.
“If we could raise the activity of ‘good fat carriers,’ like HDL, and decrease the activity of the ‘bad ones,’…it could produce better brain health and protection from Alzheimer’s disease,” he explained.
Describing Alzheimer’s disease as “maybe the worst disease there is,” Schulz said, “This motivates all of us studying Alzheimer’s disease to work intensely on it to develop better treatments for this nasty disease.”