Rember: Alzheimer

a new drug, hailed as a major breakthrough in the treatment of Alzeimer's disease, could be delayed for treatment because of the health service's economic assessment.

Early trials have suggested that the new drug, called rember, can bring the worst affected parts of the brain back to life.

If further tests of rember are successful researchers predict that the drug could be available within four to five years, when it will then be assessed by the National Institute for Health and Clinical Excellence (Nice), the Government's drugs watchdog, to decide if the drug, which is likely to be around £2.50 a day per patient, it is "cost effective" for the NHS.

Chief executive of the Alzheimer's Research Trust, said that Nice's calculations may improve by taking into account the £17 billion a year that caring for Alzheimer's patients costs the economy every year.

Other criteria, such as the impact the drug could have on a sufferer's quality of life, were difficult to put a price on, she added.


......"Nice remit needs to be take into account the wider benefits of treatments to society and the way the drugs can save money in other areas such as social care."

More than 400,000 people in Britain suffer from Alzheimer's, a figure which is expected to soar in coming decades as the population ages.



Ref: Daily Telegraph




Parkinson’s disease, Alzheimer’s disease and motor neurone disease: identifying a common mechanism

S. Greenfield and D. J. Vauxb


It is noteworthy that all global neurones contain acetylcholinesterase (AChE) (Smith and Cuello, 1984). At first glance, the presence of this familiar enzyme, responsible for the hydrolysis of acetylcholine (ACh), might not seem remarkable. After all, the most specific medication to date for Alzheimer’s disease has been to inhibit the catalytic activity of AChE with tacrine or, more recently, donepezil in an attempt to potentiate the deficient cholinergic transmission at one time thought to be responsible for the dysfunction. Yet the simple form of the ‘cholinergic hypothesis’ for Alzheimer’s disease can readily be discounted, due to a double dissociation. First, not all cholinergic cell groups in the brain are lost in Alzheimer’s disease, more specifically the posterior Ch5 and Ch6 neuronal groups of the pedunculopontine nuclei are spared ( Smith and Cuello, 1984). Conversely, not all neurones lost in Alzheimer’s disease are cholinergic: the global neurones comprise not only the cholinergic neurones of the basal forebrain, but also include the serotonergic cells of the raphe nuclei, the noradrenergic cells of the locus coeruleus, and the dopaminergic cells of the midbrain. Even though there is little of its conventional substrate, there are large amounts of AChE co-stored with these amines ( Holmes et al., 1997). Just such a disparity has prompted the question whether AChE might have a novel function, completely independent of its conventional enzymatic role in cholinergic transmission.



C. Holmes, S.A. Jones, T.C. Budd and S.A. Greenfield , Non-cholinergic, trophic action of recombinant acetylcholinesterase on mid-brain dopaminergic neurons. J. Neurosci. Res. 49 (1997), pp. 207–218.

Science Direct;

http://www.ncbi.nlm.nih.gov/pubmed/12150769