Amyloid plaques are considered to be a pathological feature closely linked to Alzheimer's disease. These plaques are mainly composed of amyloid beta (Aβ) proteins and form in the gray matter of the brain, and their number increases significantly with age. This article takes an in-depth look at the formation, structure, and impact of amyloid plaques on brain health.
The discovery of amyloid plaques dates back to the 19th century, and was first described in 1892 by Paul Block and Giorgio Marinescu. Subsequently, the definition of these plaques has been revised and supplemented by many scientists. In 1911, Alois Alzheimer first linked amyloid plaques to dementia, marking a new phase in plaque research:
"By 1911, Max Bierschowski had proposed the nature of amyloid plaques, and Paul Dufry confirmed that they had specific optical properties."
Amyloid beta (Aβ) is a small protein, typically composed of 40 to 42 amino acids, derived from a long protein called Aβ precursor protein (APP). This protein is particularly abundant in neurons and generates Aβ through the sequential cleavage process of β-secretase and γ-secretase:
"Any abnormality in the formation of Aβ may lead to the accumulation of amyloid plaques."
Amyloid plaques vary in appearance and size, ranging from tiny, loose cloud-like forms under the microscope to larger, dense masses. These so-called "classic plaques" often contain surrounding irregular neurons. Processes and activated astrocytes and microglia. These cells all indicate the presence of abnormal conditions in the brain.
Amyloid plaques and neurofibrillary tangles are the main pathological signs in the diagnosis of Alzheimer's disease. Although the number of neurofibrillary tangles is more closely related to the degree of dementia, Aβ plays a central role in the risk, onset and progression of the disease:
“By detecting the presence of Aβ plaques with radioactive labeling agents, it is now possible to assess pathological changes in the brain in vivo.”
The probability of amyloid plaques increases with age, from 10% at age 60 to 60% at age 80. This phenomenon is particularly evident in women and individuals with Down syndrome. All this information points to the prevalence and importance of amyloid plaques in the aging brain.
Multiple studies on amyloid plaques are ongoing, including examining the association between amyloid plaques and psychovascular trauma. Despite these findings, we still need to learn more about the mechanisms of amyloid plaque formation and their interactions with other factors:
"Many aspects of the biology of amyloid plaques remain to be fully understood, particularly how to prevent or remove these plaques."
With the advancement of scientific research, the formation mechanism of amyloid plaques has become increasingly clear. In response to the growing demand, the scientific community has invested considerable resources in the hope of finding effective ways to curb this progressive pathological process. And are you also thinking, can current technology reveal all the secrets of amyloid plaques and their impact on the future?