Scientists have made a breakthrough in the battle to beat early-onset dementia.
Using animal models, researchers have discovered how a protein deficiency may be linked to frontotemporal dementia – a form of early-onset dementia that is similar to Alzheimer’s disease.
They say the results lay the foundation for therapies that one day may benefit those who suffer from the illness and related diseases that wreak havoc on the brain.
As its name implies, FTD is a fatal disease that destroys cells, or neurons, that comprise the frontal and temporal lobes of the brain – as opposed to Alzheimer’s which mainly affects brain’s memory centres in the hippocampus.
Early symptoms of FTD include personality changes, such as increased erratic or compulsive behaviour. Sufferers later experience difficulties speaking and reading, and often suffer from long-term memory loss.
Alzheimer’s
FTD is usually diagnosed between the ages of 40 and 65, with death occurring within two to 10 years after diagnosis. No drug exists to slow, halt or reverse the progression of FTD.
The new study, led by Doctor Robert Farese, offers new hope in the fight against this and other related conditions.
Dr Farese and his team showed how a protein called progranulin prevents a class of cells called microglia from becoming ‘hyperactive.’
Without adequate progranulin to keep microglia in check, this hyperactivity becomes toxic, causing abnormally prolonged inflammation that destroys neurons over time-and leads to debilitating symptoms.
Dr Farese, who is a professor at the University of California, San Francisco, said: ‘We have known that a lack of progranulin is linked to neurodegenerative conditions such as FTD, but the exact mechanism behind that link remained unclear.
‘Understanding the inflammatory process in the brain is critical if we are to develop better treatments not only for FTD, but for other forms of brain injury such as Parkinson’s disease, Huntington’s disease and multiple sclerosis.’
