A UCLA School of Nursing study concluded that a protein buildup in the brain’s synapses impairs memory recall and development, and may contribute to Alzheimer’s disease.
Karen Gylys, who is a nursing professor, and her research team compared cognitively normal brains against brains with dementia. Alzheimer’s patients’ brains had higher concentrations of the protein amyloid beta in their synapses, which inhibits the formation and recall of memories.
According to the press release, p-tau protein only builds up in brains with late-stage Alzheimer’s. Amyloid beta buildups are found in healthy brains and brains with Alzheimer’s, but the study indicated that once that protein passes a certain threshold, the brain begins to develop Alzheimer’s. The study was published in the American Journal of Pathology in January.
Researchers used flow cytometry on more than 5,000 synapses at a time to analyze the two proteins that indicate dementia. The laser technology allowed researchers to suspend cells in fluid and use an electronic detector to measure levels of these proteins. A conventional microscope can only examine two synapses at a time, but flow cytometry allowed researchers to electronically measure protein levels in fluid. Researchers also cooled tissue samples to a very low temperature using cryogenic freezing to preserve the clarity of the synapses.
Amyloi beta is present in cognitively healthy brains, but can indicate Alzheimer’s development beyond a certain threshold. The researchers plan to investigate therapies that slow buildup of the protein to delay or prevent dementia.
Compiled by Madeleine Pauker, Bruin contributor.