Website Search

Flash Player may be required. Please install and enable Flash.

ID 2139

Cell death and a-beta levels

Description:
Professor Dennis Selkoe discusses the largely linear relationship between a-beta and cell death in the brain.
Transcript:
There is a linear relationship between a-beta build-up and neuronal dysfunction, and ultimately neuronal death. Nowadays in Alzheimer’s disease we are more interested in the subtle dysfunction of a neuron, long before it gives up the ghost. So we don’t even talk or focus as much on neuronal death, although unequivocally that happens in the fullness of time with Alzheimer’s [disease] patients. By and large there is a linear relationship. It’s not a perfect line; it’s scattered along an axis that goes up diagonally between a-beta amount and age, but within that scatter you can draw a statistically significant relationship. So that happens, for example, and we’ve published some of this work some years ago. It happens with a-beta levels and ApoE4. There is a correlation between ApoE4 genotype and a linear rise in a-beta buildup. The more a-beta you get, you eventually exceed a threshold, and then you’re very likely to have enough a-beta in your brain that these doublets and triplets and quadruplets and perhaps somewhat higher oligomers are going to short circuit nerve cells in the hippocampus and cause synaptic function to decline. So, by and large, it’s a quantitative issue, not a qualitative issue in Alzheimer’s [disease], at least that’s what we believe right now.
Keywords:
a-beta, abeta, alzheimers, cell, death, neuron, brain, dennis, selkoe
Downloads:
Creative Commons License This work by Cold Spring Harbor Laboratory is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 United States License.

Related content:

2142. Cells affected in Alzheimer's disease
Professor Dennis Selkoe concludes that neurons are not the only type of cell affected in Alzheimer's disease.
2227. Alzheimer's disease
An overview of Alzheimer's disease-related content on Genes to Cognition Online.
2140. Cells - a-beta inhibits long-term potentiation
Professor Dennis Selkoe notes amyloid beta oligomers are very potent inhibitors of long-term potentiation (LTP) and can 'short circuit' synapses in the hippocampus.
2138. ApoE4, a-beta, and Alzheimer's disease susceptibility
Professor Dennis Selkoe discusses the degree to which the ApoE4 gene is associated with early onset Alzheimer's disease.
2137. Amyloid plaques - rarely found in childhood
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.
2136. Amyloid beta causing forgetfulness
Professor Dennis Selkoe discusses an experiment by his group, which found that a-beta oligomers temporarily injected into rats' brains caused temporary forgetfulness.
2135. APP - amyloid clearance and production
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.
2028. Senile plaques and Alzheimer's disease
Professor Kenneth Kosik describes senile plaques, an extracellular collection of a-beta protein. It is one of the hallmarks of Alzheimer's disease.
2141. Glutamate uptake decreased in Alzheimer's disease
Professor Dennis Selkoe discusses the finding that amyloid beta seems to decrease the uptake of glutamate by synapses.
2134. Amyloid hypothesis - beta oligomers and plaques
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.
Cold Spring Harbor Laboratory
CSHL HomeAbout CSHLResearchEducationPublic EventsNewsstandPartner With UsGiving