Alzheimer's-delaying gene variant works by suppressing brain inflammation, study finds
Alzheimer's disease
works by suppressing inflammation in the brain's immune cells, a new study states.
The findings, published in the journal Immunity, support the notion that inflammation in the brain is a major driver of neurodegenerative, or ageing-related disorders, researchers, including those from Weill Cornell Medicine, US, said.
In Alzheimer's disease, one's memory, thought processes, and decision-making steadily decline, eventually affecting daily routine activities.
A permanent change in the DNA of a gene, which can occur over time and be passed down generations, results in a 'gene variant' -- not all of them produce a harmful effect.
The team found that the gene variant 'APOE3-R136S' rendered protection against Alzheimer's disease by blocking an inflammation process 'cGAS-STING', known to be part of one's innate immune system, and abnormally triggered in neurodegenerative diseases.
One is born with an innate immune system, which is the body's first line of defense against diseases. It does not rely on exposure to disease-causing bacteria or fungi to learn how to fight infections.
Blocking the brain's inflammation process through drugs was found to produce protective effects due to the gene variant -- also called the '
Christchurch mutation
' -- in a preclinical model (used before proceeding to clinical trials).
"This is an exciting study because it suggests that inhibiting this cGAS-STING pathway could make the brain more resistant to the Alzheimer's process, even in the face of significant
tau accumulation
," senior author Li Gan, a professor in neurodegenerative diseases at Weill Cornell Medicine, said.
A hallmark feature of a brain affected by Alzheimer's is the clumping up of tau proteins -- essential for maintaining a brain cell's structure and function, but abnormal changes can cause an accumulation.
The development of drugs targeting clumps of tau is a common target for developing drugs against the disorder.
The Christchurch mutation gene is important in protecting against this mechanism of tau proteins from clumping up, potentially preventing cognitive decline, the researchers said.
For the study, the team engineered the Christchurch mutation into the APOE gene in mice with tau accumulation and found that the gene variant protected the animals from hallmark features of Alzheimer's -- including tau accumulation, damage to connections of brain cells, and disrupted activity.
The protective effects were traced to suppression of the cGAS-STING pathway, which is triggered normally against a viral infection, but chronically in Alzheimer's disease, the researchers said.
"We are particularly encouraged that this mutation ameliorates disease at the level of brain function, which has not been shown before," the first author on the study, Sarah Naguib, Weill Cornell Medicine said.
Studies have also suggested that manipulating the Christchurch mutation gene itself -- through
gene therapy
-- can offer protection against Alzheimer's disease.
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