Health
Earliest Alzheimer's disease biomarker found in mouse model may point to new targets
A surge of neuron-specific proteins in the brain is one of the earliest biomarkers of Alzheimer's disease, reported researchers at the University of Illinois at Urbana-Champaign studying mouse models of the disease. Additionally, increased protein activity triggered seizures associated with early stages of neurodegeneration, and inhibiting the protein in mice slowed the onset and progression of seizure activity.
PSD-95, a neuron-specific protein, could represent a new target for research, early diagnosis and treatment of Alzheimer's disease, said study leader Nien Pei Tsai, a professor of molecular and integrative physiology at Illinois State. Ta.
Tsai's group is studying mice that produce more of the protein that forms amyloid beta, which in Alzheimer's disease gradually clumps together to form plaques in the brain that impede neural activity. However, in the new study, the research group focused on a much earlier period in the mice's lives than other studies, when no other markers or abnormalities were reported, Tsai said.
“We thought that if we could catch what was happening early enough, we might be able to find a way to diagnose the disease earlier or slow its progression,” Tsai said. “We know that Alzheimer's disease is irreversible. However, if we can slow the progression or even delay the onset of Alzheimer's disease, we can improve the quality of life for patients.”
The researchers observed elevated levels of PSD-95 while observing early neural development, first in neuron cultures and then in live mice. The PSD-95 protein's job is to attract and attract other receptors to the synaptic surface, the space where two neurons pass signals to each other.
“Our data suggest that elevated PSD-95 contributes to brain hyperexcitability, a phenotype commonly seen in patients in the early stages of Alzheimer's disease. They “They tend to exhibit brain hyperexcitability or increased seizure susceptibility, which precedes and worsens brain agitation, followed by neurodegeneration,” said Tsai, who is also affiliated with the Beckman Institute for Advanced Science and Technology in Illinois.
To confirm that increased PSD-95 was the driving force behind seizure activity, the researchers inhibited PSD-95 in a cohort of mice. They observed decreased receptor activity at synapses, fewer seizures in the mice, and decreased mortality from seizures.
“Our findings show that PSD-95 critically contributes to hyperexcitability in the early stages of Alzheimer's disease. PSD-95 therefore increases the likelihood that a patient has Alzheimer's disease and “We believe this could be an early biomarker of increased susceptibility. With further clinical research, antibody inhibitors against PSD-95 may be useful in the early onset of Alzheimer's disease.”
The group published their findings in the journal EMBO report.
The researchers hope to partner with clinical research teams to determine whether the findings in mice correlate with human patient samples. They also plan to study other receptors that PSD-95 interacts with on the synaptic surface to see if PSD-95 plays a role in other symptoms or stages of the disease's progression.
“For example, NMDA receptors have been shown to contribute to neuronal cell death in Alzheimer's disease. So by inhibiting PSD-95, we are also inhibiting this specific NMDA receptor to slow cell death.” I'm trying to see if I can do it.”
The National Institutes of Health and the Alzheimer's Association supported this research.
The National Institutes of Health supported this research through grants R01NS105615, R01MH124827, and R21AG071278.
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Sources 2/ https://www.sciencedaily.com/releases/2024/03/240306203058.htm The mention sources can contact us to remove/changing this article |
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