Professor Kenneth Kosik describes senile plaques, an extracellular collection of a-beta protein. It is one of the hallmarks of Alzheimer's disease.
Transcript:
As many people now are aware, the classical stigmata of Alzheimer’s disease, the classical hallmarks, are plaques and tangles. The senile plaque is an extracellular collection of protein. It’s a protein that is referred to as the a-beta. It’s a fragment of a normal protein we all have called the amyloid precursor protein. It gets chopped into a smaller piece called a-beta that then collects, assembles outside of cells, and forms this aggregate mass that forms a ball between the neurons, between the interstices of the brain, and pushes aside all of the fine ramifications and connections of brain cells to form what we call a plaque.
Professor Kenneth Kosik describes the relationship between the amyloid precursor protein (APP) and Alzheimer’s disease. APP mutations are linked to early-onset Alzheimer’s disease.
Professor Kenneth Kosik discusses neurofibrillary tangles, which form inside a cell and are made up of a protein called tau. There is a strong relationship with plaques and amyloid deposition.
Professor Kenneth Kosik defines Alzheimer's disease as a slowly progressing illness that deteriorates the brain and impairs many major cognitive functions.
Professor Dennis Selkoe compares the amyloid precursor (or parent) protein to a Bic pen. The clasp part seems to be the bad guy, and is part of a network involving presenilin and ApoE4.
Professor Dennis Selkoe explains that amyloid beta oligomers - small assemblies of amyloid beta protein associated with Alzheimer's disease - do not cause plaques but prevent them.
Professor Dennis Selkoe discusses the age at which plaque-forming a-beta can begin to build up. Children with Down syndrome may have these plaques, otherwise childhood instances are rare.