According to data from the Alzheimer's Association , over 7 million Americans are living with Alzheimer's, a number which is projected to reach 13 million by 2050. The disease is more common in people 65 or older and even more common in women.
Numerous steps including a review of the medical history, neurological tests, blood and urine tests, brain imaging and more are conducted to diagnose Alzheimer's. But now, a team of researchers from Florida International University (FIU) examined a brain protein previously associated with brain inflammation in Alzheimer's patients to get a deeper understanding of the relationship between the protein and the disease. The results could be an early signal of neurodegeneration that could eventually cause dementia.
The shocking experiment
In the research published in Acta Neuropathologica , mouse models of Alzheimer's had elevated levels of 18 kDa or TSPO , a translocator protein, which was found in animals as young as six weeks, corresponding to 18-20 years of age in humans. This was found in the subiculum, a part of the brain vital for memory.
A similar pattern was found in human brain tissue taken postmortem from nine people in Colombia with a genetic mutation that causes them to develop Alzheimer's relatively early in their 30s and 40s.
" Neuroinflammation is a very early event in Alzheimer's that influences its onset," says neuroscientist Tomás Guilarte, from FIU.
"If we can use TSPO to detect it early, right at the beginning stages of the disease, it could mean slowing progression or delaying symptoms by five or six years. That's five or six years where someone has a better quality of life."
Additionally, researchers found higher levels of the protein in female mice, mirroring data that shows women are more prone to developing Alzheimer's. They also observed that the increase in the protein coincided with the increase in amyloid-beta plaques, which are protein clumps associated with the disease.
A point to note is that the boost in the protein was in the form of immune cells called microglia which were in contact with the plaques and had an increase in number and protein due to them.
Why does this mean?
These observations provide an enlightening insight into the chemical reactions involved with the early onset of the disease and can be used to slow or even stop its progress.
"We didn't see any TSPO increase in the other glial cells, like the astrocytes, which reveals the microglia are driving the majority of the inflammatory response," says Guilarte. "What we believe is happening is something goes wrong with the microglia."
"They stop doing their job in removing the plaques and just keep sending out TSPO signals. This constant signal of neuroinflammation is like adding wood to a fire."
Numerous steps including a review of the medical history, neurological tests, blood and urine tests, brain imaging and more are conducted to diagnose Alzheimer's. But now, a team of researchers from Florida International University (FIU) examined a brain protein previously associated with brain inflammation in Alzheimer's patients to get a deeper understanding of the relationship between the protein and the disease. The results could be an early signal of neurodegeneration that could eventually cause dementia.
The shocking experiment
In the research published in Acta Neuropathologica , mouse models of Alzheimer's had elevated levels of 18 kDa or TSPO , a translocator protein, which was found in animals as young as six weeks, corresponding to 18-20 years of age in humans. This was found in the subiculum, a part of the brain vital for memory.
A similar pattern was found in human brain tissue taken postmortem from nine people in Colombia with a genetic mutation that causes them to develop Alzheimer's relatively early in their 30s and 40s.
" Neuroinflammation is a very early event in Alzheimer's that influences its onset," says neuroscientist Tomás Guilarte, from FIU.
"If we can use TSPO to detect it early, right at the beginning stages of the disease, it could mean slowing progression or delaying symptoms by five or six years. That's five or six years where someone has a better quality of life."
Additionally, researchers found higher levels of the protein in female mice, mirroring data that shows women are more prone to developing Alzheimer's. They also observed that the increase in the protein coincided with the increase in amyloid-beta plaques, which are protein clumps associated with the disease.
A point to note is that the boost in the protein was in the form of immune cells called microglia which were in contact with the plaques and had an increase in number and protein due to them.
Why does this mean?
These observations provide an enlightening insight into the chemical reactions involved with the early onset of the disease and can be used to slow or even stop its progress.
"We didn't see any TSPO increase in the other glial cells, like the astrocytes, which reveals the microglia are driving the majority of the inflammatory response," says Guilarte. "What we believe is happening is something goes wrong with the microglia."
"They stop doing their job in removing the plaques and just keep sending out TSPO signals. This constant signal of neuroinflammation is like adding wood to a fire."
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