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From the past to the present: How amazing is the discovery of amyloid plaques?
Amyloid plaques, also known as neuritic plaques or senile plaques, are exogenous deposits that are primarily found in the gray matter of the brain and are primarily composed of amyloid β (Aβ) protein. The story of how these plaques were discovered and studied over time is full of amazing stories involving the hard work and discoveries of many scientists.
Plaques in the gray matter were first described by Paul Block and George Marinescu in 1892, calling them "nodules of glial sclerosis."
Since then, amyloid plaques have been an important focus of Alzheimer's disease research. In 1898, Emil Redlich observed plaques in three patients, two of whom had clinically confirmed dementia, and first used the term "rice-grained sclerosis" to describe these plaques. As other scientists delved deeper into Alzheimer's disease, they came to understand the causes of plaques and their role in the development of the disease. Alois Alzheimer first linked these plaques to dementia in a 1906 report, but his report focused on tangles of nerve fibers and gave a relatively brief description of amyloid plaques.
The amyloid nature of plaque deposits was first proposed by Max Bierschowski in 1911 and later confirmed by Paul DeVry.
As the scientific community continues to study amyloid plaques, a number of technological advances have enabled researchers to better identify and analyze these plaques. These amyloid plaques are composed of aggregates of Aβ proteins, which usually have at least 40 to 42 amino acids. The production process of these proteins involves the enzymatic cleavage of Aβ precursor protein (APP), during which Aβ protein is released outside the cell and may trigger a series of pathological changes.
The maturation of Aβ involves two enzymes, first β-secretase and then γ-secretase, both of which are located on the cell membrane.
The presence of amyloid plaques is closely associated with many areas of the brain. For example, initial plaques appear in the neocortex, and as the disease progresses, they gradually expand to other important brain regions, such as the hippocampus and basal ganglia. This pathological progression not only links amyloid plaques to the onset of Alzheimer's disease, but also clarifies their important role in the disease process.
Amyloid plaques vary in composition, from small, fuzzy deposits to large, dense or diffuse masses. The so-called "classical plaque" contains a dense Aβ-amyloid core surrounded by relatively loose Aβ, accompanied by abnormal neuronal processes and activated astrocytes and microglia. . The activation of these cells suggests that chronic inflammation may be involved in the formation of plaques.
Studies have shown that amyloid plaques are one of the two indispensable lesions in the pathological diagnosis of Alzheimer's disease.
The probability of developing amyloid plaques in the brain increases with age, with the proportion increasing from 60 years old (10%) to 80 years old (60%). The study found that women are slightly more likely than men to develop amyloid plaques, and Alzheimer's disease in people with Down syndrome is often accompanied by the formation of amyloid plaques. This is mainly because the APP gene is located on chromosome 21, and in Down syndrome there are three copies of this chromosome, resulting in excessive production of Aβ.
The research on amyloid plaques has never stopped, and many studies from human samples and experimental models have clearly shown that the biochemical characteristics of amyloid plaques are receiving continuous attention and analysis. Researchers are not only focusing on how amyloid plaques form and spread, but also working to explore how they can be detected and prevented in life. Some recent evidence suggests that the formation of amyloid plaques is directly linked to microvascular damage in the brain, and these are at the forefront of scientific research.
As our understanding of amyloid plaques deepens, whether we can find effective treatments to stop or reverse this process in the future will become an important task for scientists. Will humans be able to effectively fight this deadly neurodegenerative disease in the future?
