Traumatic brain injuries generate toxic tau oligomers that cause nerve cells to clump together and spread to other parts of the brain. These damaging protein assemblages can contribute to memory deficits, seizures, and disruptions in the sleep-wake cycle.
SourceUniversity of Texas Medical Branch at Galveston·JournalJournal of Biological Chemistry·DateMay 29, 2013
Scientists at Cambridge's Department of Chemistry have mapped the pathway that generates 'aberrant' forms of proteins, which are at the root of neurodegenerative conditions like Alzheimer's. The breakthrough opens up possibilities for a new generation of targeted drugs and earlier diagnosis of neurological disorders.
SourceUniversity of Cambridge·JournalProceedings of the National Academy of Sciences·DateMay 20, 2013
A study has found a key difference between brains of people with Alzheimer's disease and those who are cognitively normal but have brain plaques. Researchers detected smaller molecules of amyloid beta called oligomers, which were more closely correlated with dementia symptoms.
SourceWashU Medicine·JournalAnnals of Neurology·DateOct 22, 2012
Researchers found that curcumin prolongs the lives of fruit flies with Alzheimer's symptoms by up to 75% and maintains their mobility. However, it did not dissolve or decrease the amyloid plaque, but instead accelerated its formation by reducing precursor forms.
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New research reveals that tau oligomers, smaller structures formed before neurofibrillary tangles, are the most toxic entities in Alzheimer's. High levels of tau oligomers have been found in some Alzheimer's brains, and their presence has been linked to various biochemical behaviors and structures.
SourceUniversity of Texas Medical Branch at Galveston·JournalThe FASEB Journal·DateFeb 2, 2012
Scientists at the Stowers Institute for Medical Research found that oligomers of a synapse protein are essential for forming long-term memory. The discovery supports a new theory about memory and may have implications for understanding diseases such as Alzheimer's and prion diseases.
SourceStowers Institute for Medical Research·JournalCell·DateJan 27, 2012
Researchers at Mount Sinai School of Medicine found that Alzheimer's pathology begins with Amyloid-Beta oligomers in the brain, rather than previously thought amyloid plaques. The study suggests that these clumps, not plaques, are toxic to brain cells and may be a major target for new treatments.
SourceThe Mount Sinai Hospital / Mount Sinai School of Medicine·JournalAnnals of Neurology·DateApr 27, 2010
A new enzyme-linked immunosorbent assay can detect Alzheimer's disease by measuring high molecular weight A-Beta oligomers in spinal fluid. The test showed direct correlation between A-Beta oligomer levels and memory impairment, enabling early diagnosis of the disease.
SourceFederation of American Societies for Experimental Biology·JournalThe FASEB Journal·DateMar 25, 2010
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Researchers identified naturally occurring antibodies in human blood that selectively target toxic beta amyloid oligomers, potentially offering a natural defense mechanism against Alzheimer's. The antibodies recognize misfolded shapes of proteins, which could have implications for immune therapy of other neurodegenerative diseases.
SourceNew York- Presbyterian Hospital/Columbia University Medical Center·DateJun 11, 2007
Researchers found that amyloid growth can occur independently of oligomers in yeast prion protein Sup35. The study suggests that creating conditions favoring fiber growth while inhibiting oligomer formation might limit the toxic effects of amyloid plaques.
Researchers found that small toxic molecules triggering cell damage in degenerative diseases have a similar structure. This discovery implies that these molecules are suitable targets for new drugs or vaccines that could halt progression of many degenerative diseases.
SourceUniversity of California - Irvine·JournalScience·DateApr 17, 2003