- University of Minnesota team has spent 10 years analyzing the disease
- They found one enzyme appears to attack a specific neuron protein
- By focusing on this process, they restored memory deficits in lab mice
- Lead author Dr Karen Ashe said this is the closest to a cure so far
Mia De Graaf For Dailymail.com
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Scientists have reversed Alzheimer’s in mice – bringing us closer than ever to a cure for the devastating disease.
After tens years of research, a team at the University of Minnesota has finally identified what they believe disrupts the brain in sufferers.
An enzyme called Caspase-2 attacks neurons, specifically targeting a protein called tau.
By focusing on that process, the team led by Dr Karen Ashe managed to restore memory deficits.
Breakthrough? After tens years of research, a team at the University of Minnesota has finally identified what they believe disrupts the brain in sufferers – and reversed it
Dr Ashe has conducted numerous studies in the field.
But she believes this is the most concrete findings to date that could lead to a pill for humans.
‘In the past, many studies focused on the accumulation of tangles and their connection to memory loss,’ Dr Ashe, professor of neurology, said.
‘But the more we learn, the less likely it seems that they are the cause of disease symptoms.
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‘The pathological fragment of tau that we have identified resists forming tangles and can instead move freely throughout the cell.
‘Therefore, we decided to look for other mechanisms that could affect synaptic function.’
To do this, Dr Ashe’s group used fluorescent labeling to track and compare the behavior of normal and mutated tau in cultured neurons from the rat hippocampus, the brain region most associated with learning and memory.
Unlike normal tau, both mutated tau and the short fragment produced when caspase-2 cuts tau were primarily found within structures called dendritic spines, where neurons receive inputs from neighboring cells.
The overabundance of mutated tau, including the caspase-2-produced fragment, caused disruptions in synaptic function in the spines. The impact on synapses was specific, with no observed effects on the overall structure or survival of the neurons.
‘It appears that abnormally processed tau is disrupting the ability of neurons to properly respond to the signals that they receive, producing memory deficits independent of tangle formation,’ said Dr Ashe.
‘Because this effect is occurring without cell death or a loss of synapses, we have a better chance of intervening in the process and hopefully reversing symptoms of the disease.’
Dr Ashe and her team are now planning additional experiments to uncover the mechanisms by which abnormally processed mutant tau produces memory deficits.
The study was funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) and published in the journal Nature Medicine.
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