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Written By: Agencies | Published : January 20, 2014 6:32 PM IST
Researchers have claimed to have identified a protein in the brain that plays a critical role in the memory loss seen in Alzheimer's patients.
The protein Neuroligin-1 (NLGN1) is known to be involved in memory formation; this is the first time it's been linked to amyloid-associated memory loss.
In Alzheimer's disease, amyloid beta proteins accumulate in the brains of Alzheimer's patients and induce inflammation. (Read: Beware Type 2 diabetes can increase your Alzheimer's risk!)
This inflammation leads to certain gene modifications that interrupt the functioning of synapses in the brain, leading to memory loss. (Read: Why do neurons die in Alzheimer's disease?)
Using animal models, Cleveland Clinic researchers discovered that during this neuroinflammatory process, the epigenetic modification of NLGN1 disrupts the synaptic network in the brain, which is responsible for developing and maintaining memories. Destroying this network can lead to the type of memory loss seen in Alzheimer's patients.
The study has been published online in the journal Nature Neuroscience. (Read: 14 new genes that lead to Alzheimer's identified)
What is Alzheimer's?
Scientists have for the first time pinpointed the part of the brain where Alzheimer's originates, a finding that can lead to early diagnosis and better treatments for the nuerodegenerative disease. Using high-resolution functional MRI (fMRI) imaging in patients with Alzheimer's disease and in mouse models of the disease, Columbia University Medical Centre (CUMC) researchers have clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads.
In addition to advancing understanding of Alzheimer's, the findings could improve early detection of the disease, when drugs may be most effective. 'It has been known for years that Alzheimer's starts in a brain region known as the entorhinal cortex,' said co-senior author Scott A Small. (Read: Alzheimer's drug to be developed within five years)
'But this study is the first to show in living patients that it begins specifically in the lateral entorhinal cortex, or LEC. The LEC is considered to be a gateway to the hippocampus, which plays a key role in the consolidation of long-term memory, among other functions,' Small said. The study also shows that, over time, Alzheimer's spreads from the LEC directly to other areas of the cerebral cortex, in particular, the parietal cortex, a brain region involved in various functions, including spatial orientation and navigation.
The researchers suspect that Alzheimer's spreads 'functionally,' that is, by compromising the function of neurons in the LEC, which then compromises the integrity of neurons in adjoining areas.
A third major finding of the study is that LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist. 'The LEC is especially vulnerable to Alzheimer's because it normally accumulates tau, which sensitises the LEC to the accumulation of APP. Together, these two proteins damage neurons in the LEC, setting the stage for Alzheimer's,' said co-senior author Karen E Duff. The researchers used a high-resolution variant of fMRI to map metabolic defects in the brains of 96 adults. All were free of dementia at the time of enrollment.
'This study has given us a unique opportunity to image and characterise patients with Alzheimer's in its earliest, preclinical stage,' said Small. (Read: Rare mutation gene in Alzheimer's could help with early diagnosis)
Source: ANI
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