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Lithium: a medication for Alzheimer's disease?
According to scientists Alzheimer’s disease, a condition which leads to the size of the brain decreasing faster than ageing, could be treated by lithium, a naturally occurring element that is extremely inexpensive and already in use for other psychiatric disorders.
Lithium has been in use to treat bipolar affective disorders and now, researchers at Sao Paulo University in Brazil, led by Dr Orestes Forlenza have discovered that the pills slowed down memory loss in the elderly, reducing their cognitive decline. They also noted that there was a decrease in build-up of tangles of damaging proteins called phospho- tau in people’s cerebrospinal fluid which characterized Alzheimer’s disease.
For the study the team examined 41 people over the age of 60 with mild cognitive impairment, out of whom 21 took low doses of lithium every day for a year. All went through tests of memory and attention and a sample of their brain fluid was analyzed for tau concentrations. Although all the participants showed a decline in memory function over the year, those taking lithium showed less of a decline than those taking the placebo. Those taking lithium also had less of a form of the tau protein, pTau – a hallmark of Alzheimer’s disease – in their cerebrospinal fluid. The findings are published today in the British Journal of Psychiatry. The researchers now want to see larger studies to investigate whether lithium could have potential as a preventative treatment for Alzheimer’s.
Professor Allan Young, a psychiatrist from Imperial College London, described the study as “encouraging” – and particularly presents a value therapeutic opportunity, because no pharmaceutical company has a patent on lithium, meaning it is very cheap to prescribe. He added, “This trial adds to the increasing evidence that lithium may have beneficial effects on the brain and begs to be replicated in further randomised trials.”
Regarding dementia – it's the tau, stupid!
Tau is implicated in a number of different forms of dementias.
A new study is looking at the earliest events associated with neurodegenerative diseases characterized by abnormal accumulation of tau protein. The research, published the prestigious journal Neuron, reveals how tau disrupts nerve-to-nerve communication at synapses and may help to guide development of therapeutic strategies that precede irreversible nerve damage.
Tau normally contributes to the supportive framework of proteins in the cell. It is meant to form the structural skeleton of the cell. It is well established that abnormal tau sometimes clumps into neuron-damaging filament deposits and that aggregates of tau with multiple phosphate groups attached are the defining feature of neurodegenerative disorders called “tauopathies”, which include Alzheimer’s disease and other dementias. Dr. Ashe and colleagues investigated how tau induces early memory deficits and disrupts communication between nerves, before actual obvious neuron damage. The researchers found that early accumulation of hyperphosphorylated tau in dendrites and dendritic spines disrupted communication coming in from other nerve cells.
Whether it’s the tau or the amyloid (a different protein) that is causing all the problems will be a focus of much research into Alzheimer’s disease and its treatment, as usual, in 2011.
