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Mysterious treasures in cerebral blood vessels: What is cerebral amyloid angiopathy and why does it cause cerebral hemorrhage?
In the medical community, cerebral amyloid angiopathy (CAA) is regarded as an important but often overlooked area of cerebrovascular disease. This disease is characterized by the deposition of amyloid beta peptide on the walls of blood vessels in the central nervous system and meninges, leading to fragility of the vessels and an increased risk of bleeding. As the elderly population grows, concern about this pathology increases.
However, why do these amyloids only form inside the brain and are not associated with other types of amyloidosis?
Types and causes of cerebral amyloid angiopathy
Cerebral amyloid angiopathy can be divided into many types, some of which are familial variants. Most often, it is associated with amyloid beta peptide, but other types involve different amyloid peptides, for example the "Icelandic type" is related to cystatin C amyloid (ACys), while the "British type" and "Danish type" ” are related to British amyloid (ABri) and Danish amyloid (ADan) respectively. Each of these different types of variation is related to a specific genetic mutation.
The causes of CAA can be divided into sporadic (usually occurring in older people in the population) and familial cases. Pathologically, CAA is characterized by the deposition of amyloid beta (Aβ) in the meninges and cerebrovascular walls. The cause of increased Aβ deposition in sporadic CAA remains unclear, but there are currently many hypotheses, such as increased production and impaired clearance of this peptide. Under normal circumstances, Aβ is cleared from the brain through four pathways: endocytosis, enzymatic hydrolysis, and clearance of the blood-brain barrier by brain astrocytes and microglia. Abnormalities in any pathway may lead to CAA. occurrence.
Signs and symptoms of cerebral hemorrhage
One of the most common complications of cerebral amyloid angiopathy is cerebral hemorrhage, especially microbleeds. This is because amyloid deposits can damage blood vessels and impede normal blood flow, making them more susceptible to rupture. According to research, although CAA is closely linked to Alzheimer's disease, it is not limited to people with cognitive impairment. It may also affect patients without any history of dementia.
In particular, bleeding is usually limited to specific brain lobes, unlike cerebral hemorrhage caused by hypertension, which more often occurs in deep brain regions such as the basal ganglia and pons.
Diagnosis and imaging technology of cerebral amyloid angiopathy
Currently, the only way to diagnose cerebral amyloid angiopathy is through a follow-up autopsy. Biopsies are also helpful in some suspicious cases, and when tissue samples are unavailable, doctors often use the Boston criteria to identify possible cases of CAA from MRI or CT scan data. These criteria require evidence of multiple lobar or cortical hemorrhages to flag a patient for possible CAA.
On imaging studies, CAA may appear as lobar subcerebral hemorrhages or intracerebral microbleeds. Imaging tests, such as CT and MRI, can help identify these abnormalities. CT scan will show the high-density bleeding area and low-density edema around the bleeding site, while the gradient echo sequence and sensitivity weighted imaging (SWI) of MRI are particularly effective in detecting microbleeds and iron deposition in the cerebral cortex.
Management and Treatment
There is currently no cure for cerebral amyloid angiopathy, and treatment usually focuses on symptom management. Therefore, physical therapy, occupational therapy, and speech therapy may be helpful for affected patients.
Future Outlook
From Gustav Oppenheim's first report of amyloid beta deposition in cerebral blood vessels in 1909 to the increasing attention to cerebral amyloid angiopathy today, research in this field has continued to progress. Although we already understand some of the mechanisms of this pathology, many mysteries remain to be solved. Let us wait and see how cerebral amyloid angiopathy can be identified and treated more effectively in the future?
