A new study, funded in part by Cure Alzheimer’s Fund, is shedding more light on amyloid beta’s (Aβ) impact on Alzheimer’s disease.
If you regularly read our blog, you know that studies suggest that Aβ contributes to the early stages of Alzheimer’s (Aβ plays a key role in early synaptic failure which is commonly associated with memory dysfunction), but very little is known about Aβ’s effect on the plasticity of dendritic spines.
The plasticity of dendritic spines is important because these spines provide memory storage and transmit signals across the brain, actions which require the ability to change and grow.
The study, led by Cure Alzheimer’s own Dr. Robert Malinow, found that Aβ affects structural and functional plasticity — preventing synapses from growing bigger and stronger. In fact, if Aβ is over-produced, its destructive effects can affect thousands and thousands of synapses.
Malinow and his team discovered that a continuous release of Aβ is needed to prevent plasticity so even a short period of time without Aβ secretion is enough to allow plasticity to occur — a positive sign if scientists learn how to stop the secretion of Aβ at synaptic sites.
Want to learn more about this study? Check out Science Daily for additional details: