Alzheimer’s disease is a condition that affects many older people around the world, and it can cause problems with memory and thinking.
There are two types of Alzheimer’s disease: early-onset familial Alzheimer’s disease (fAD) and late-onset sporadic Alzheimer’s disease (sAD).
Both types of disease involve the formation of amyloid plaques in the brain, but they have different genetic causes.
Scientists have been trying to figure out the best way to treat Alzheimer’s disease, especially the common sAD.
One idea is to target the amyloid plaques directly. However, researchers have been wondering whether this is the right strategy for treating sAD.
A group of scientists from the Interdisciplinary Research Center on Biology and Chemistry at the Shanghai Institute of Organic Chemistry of the Chinese Academy of Sciences conducted a study to answer this question.
They found a link between the most common risk factor for sAD, called ApoE4, and the genetic factors that cause fAD.
The scientists discovered that mutations in certain genes that are involved in processing a protein called amyloid precursor protein (APP) cause fAD by promoting the formation of amyloid plaques.
However, most people with sAD don’t have these mutations. Instead, people who carry two copies of ApoE4 are at a higher risk of developing sAD than those with normal ApoE3.
Another variant called ApoE2 can actually reduce the risk of sAD.
The scientists discovered that the different ApoE variants have a direct and differential effect on the processing of APP.
ApoE2 was found to be the most effective at inhibiting the formation of amyloid plaques, while ApoE4 lost this activity. This suggests that abnormal processing of APP is a common cause of both fAD and sAD.
The researchers suggest that the C-terminal region of ApoE could be used as a potential treatment for Alzheimer’s disease.
Their study provides new insights into the genetic causes of Alzheimer’s disease and suggests new avenues for developing treatments.
How to prevent Alzheimer’s disease
There is no known cure for Alzheimer’s disease, but there are steps that you can take to help reduce your risk of developing the condition:
Exercise regularly: Regular physical exercise has been linked to a lower risk of Alzheimer’s disease.
Eat a healthy diet: Eating a diet that is rich in fruits, vegetables, whole grains, lean protein, and healthy fats can help reduce your risk of Alzheimer’s disease.
Stay mentally active: Engaging in mentally stimulating activities, such as reading, playing games, and learning new skills, can help keep your brain healthy and reduce your risk of Alzheimer’s disease.
Get enough sleep: Poor sleep has been linked to an increased risk of Alzheimer’s disease. Make sure you are getting enough sleep every night.
Manage chronic conditions: Chronic conditions, such as high blood pressure, high cholesterol, and diabetes, can increase your risk of Alzheimer’s disease.
Manage these conditions through medication, lifestyle changes, and regular check-ups with your doctor.
Stay socially active: Social isolation and loneliness have been linked to an increased risk of Alzheimer’s disease.
Stay socially active by spending time with family and friends, joining social clubs, and volunteering in your community.
Protect your head: Head injuries have been linked to an increased risk of Alzheimer’s disease. Protect your head by wearing a helmet when cycling or participating in contact sports.
Remember, while these steps can help reduce your risk of developing Alzheimer’s disease, there is no guaranteed way to prevent it. If you are concerned about your risk of Alzheimer’s disease, talk to your doctor.
If you care about Alzheimer’s, please read studies about new evidence how Alzheimer’s attacks the brain, and scientists find one important cause of Alzheimer’s disease.
For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and epilepsy drug may help treat Alzheimer’s disease.
The study was conducted by Xianglong Hou et al and published in Neuron.
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