Which disease are associated with amyloid plaques?
Amyloid plaques and neurofibrillary tangles are hallmark pathologies that characterize Alzheimer’s disease (AD). Amyloid plaques consist primarily of a 40–42 amino acid peptide called amyloid-β (Aβ) that is aggregated in fibrils that contain a high β-sheet structure.
What removes amyloid plaque from the brain?
Now, researchers at Washington University School of Medicine in St. Louis have identified an antibody that, in mice, removes amyloid plaques from brain tissue and blood vessels without increasing risk of brain bleeds. The antibody targets a minor component of amyloid plaques known as apolipoprotein E (APOE).
How do you treat amyloid plaque?
In June 2021, the Food and Drug Administration (FDA) approved aducanumab for the treatment of some cases of Alzheimer’s disease. This is the first drug approved in the United States to treat the underlying cause of Alzheimer’s by targeting and removing amyloid plaques in the brain.
What are the different types of KCNQ2 related diseases?
The groups is made up of various different diseases whose signs and symptoms vary. The conditions range from the less severe form KCNQ2-related benign familial neonatal epilepsy (KCNQ2-BFNE) to the more severe form KCNQ2-related epileptic encephalopathy (KCNQ2-NEE).
Where are amyloid plaques found in the body?
Amyloid plaques are aggregates of misfolded proteins that form in the spaces between nerve cells. These abnormally configured proteins are thought to play a central role in Alzheimer’s disease.
What happens if you have a KCNQ2 genotype?
Overview. Carrying a KCNQ2 variant can have very broad range of consequences, from self-limiting neonatal epilepsy to a severe developmental disorder. Although it is not always possible to predict the phenotype from the genotype, some general genotype-phenotype correlations have become apparent.
Is the KCNQ2 gene a voltage gated potassium channel?
KCNQ2. This is the Epilepsiome page on KCNQ2, an ion channel gene that encodes a subunit of a voltage-gated potassium channel. Known for years as a gene for a familial and self-limiting neonatal epilepsy syndrome, mutations are now also shown to be a frequent cause of neonatal epileptic encephalopathy.