"One of the first signs of Alzheimer's disease is the loss of synapses - the structures that connect neurons in the brain," - Dr Vladimir Sytnyk.
Synapse loss is a hallmark of the early stages of Alzheimer’s. New research indicates that these brain cell connections are destroyed as Alzheimer's disease spreads.
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A junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter (see image above).
It is widely accepted that the synapse plays a role in the formation of memory.
The strength of two connected neural pathways is thought to result in the storage of information that results in memory.
Synapse discovery could lead to new treatments for Alzheimer's disease
A team of researchers led by UNSW Australia scientists has discovered how connections between brain cells are destroyed in the early stages of Alzheimer's disease - work that opens up a new avenue for research on possible treatments for the degenerative brain disease like Alzeimer's.
"Synapses are required for all brain functions, and particularly for learning and forming memories. In Alzheimer's disease, this loss of synapses occurs very early on, when people still only have mild cognitive impairment, and long before the nerve cells themselves die.
"We have identified a new molecular mechanism which directly contributes to this synapse loss - a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments."The team studied a protein in the brain called neural cell adhesion molecule 2, or NCAM2 - one of a family of molecules that physically connects the membranes of synapses and help stabilise these long lasting synaptic contacts between neurons.
- Using post-mortem brain tissue from people with and without Alzheimer's, the researchers discovered that synaptic NCAM2 levels in the part of the brain known as the hippocampus were low in those with Alzheimer's disease.
- This opens a new avenue for of NCAM2 in the brain; and as a result, could lead new treatments that could prevent pr delay the onset of Alzheimer's disease.
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