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.
Itâ€™s a wonderful question to ask, how early in life a-beta [amyloid beta] can build up. The only situation that I am aware of, two situations in which it builds up very early are the condition called Down syndrome, or trisomy 21, and very rare cases of familial Alzheimerâ€™s disease due to a mutation in a gene called presenilin, one of the genes that makes a-beta. But those look like an Alzheimerâ€™s [disease] picture from the beginning. If a patient with Down syndrome dies at age 12 of a car accident or of some other complication of Down syndrome, one will already see telltale plaques of a-beta in the brain, so itâ€™s an Alzheimerâ€™s-like picture that begins very early. If a child has an abnormality of the entorhinal cortex and its connectivity, from one part of the entorhinal cortex to another part of the hippocampus, that in itself wonâ€™t predict Alzheimerâ€™s disease. Itâ€™s only these two conditions we know of that could already predispose people to Alzheimerâ€™s [disease] as early as childhood: Down syndrome and a rare familial form of Alzheimerâ€™s [disease] in which the problem is too much a-beta production. Many other conditions in the brain in childhood or during development that can lead to impaired cognition or can even predispose a person to another kind of dementia, not Alzheimerâ€™s [disease] â€“ those do not relate to amyloid beta protein. Just these two conditions: Down [syndrome] and rare forms of early-onset familial Alzheimerâ€™s [disease] relate to a-beta early in life.
alzheimer, amyloid, plaque, a-beta, beta, trisomy 21, down syndrome, dennis, selkoe
Professor Dennis Selkoe discusses an experiment by his group, which found that a-beta oligomers temporarily injected into rats' brains caused temporary forgetfulness.
An overview of Alzheimer's disease-related content on Genes to Cognition Online.
Professor Dennis Selkoe concludes that neurons are not the only type of cell affected in Alzheimer's disease.
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Professor Donna Wilcock describes amyloid plaques as clumps of protein in the brain that are one of the three hallmarks of Alzheimer's disease.
Professor Dennis Selkoe discusses the finding that amyloid beta seems to decrease the uptake of glutamate by synapses.
Professor Kenneth Kosik describes senile plaques, an extracellular collection of a-beta protein. It is one of the hallmarks of Alzheimer's disease.
Professor Dennis Selkoe notes amyloid beta oligomers are very potent inhibitors of long-term potentiation (LTP) and can 'short circuit' synapses in the hippocampus.
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 discusses the largely linear relationship between a-beta and cell death in the brain.