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THE LANCET Neurology Vol 2 July 2003 http://neurology.thelancet.com 391

Newsdesk

The foundation stone of the firstSpanish centre specialising in the long-term rehabilitation of patients withmultiple sclerosis (MS) was laid onMay 19 in Madrid. The centre, whichwill open in the summer of 2004, will employ about 40 professionals,including neurologists specialising inrehabilitation, speech therapists, occu-pational therapists, and psychologists.The centre will offer training coursesfor health professionals involved in thecare of patients with MS and will alsosupport clinical and epidemiologicalresearch.

The Centre for the IntegralRehabilitation of MS patients will bemanaged by the Spanish Association ofMultiple Sclerosis (AEDEM). “We havereceived an unconditional grant fromMadrid’s City Council”, says AEDEMspokeswoman Amparo Mínguez. Thecity council has donated a 3000 m2 plotto AEDEM to construct the centre nearthe Ramón y Cajal Hospital. The ObraSocial Caja de Madrid foundation will

donate €1·5 million to build the centre, and ONCE, a Spanish nationalorganisation for the blind, will providethe equipment, including twogymnasiums.

AEDEM is a 20-year-old, non-profit organisation made up of 48 localassociations. It provides informationto newly diagnosed patients. “Bypositively modifying our mind andbehaviour, MS will become a journeycompanion and not an unknown

enemy—that’s our message topatients”, says Mínguez.

Francisco Alcázar, a rehabilitationdoctor at the nearby hospital, says theinitiative, although isolated, is “greatnews” because patients with MS arenot currently given sufficient long-term care. After a relapse, he says,patients “are transferred to a short-term rehabilitation centre and then gohome until another relapse occurs”.Rehabilitation and psychologicalsupport are essential for bothrelapsing–remitting and progressiveMS, notes Alcazar.

Luis Gangoiti, a member ofAEDEM’s advisory medical board,who also heads the Madrid-basedCentre for Brain Damage, applaudsthe rehabilitation centre and notes thatin addition to increased resources forpatients with MS, the initiative willprovide doctors with an opportunityto receive specialised training inrehabilitation.Xavier Bosch

Spanish centre for rehabilitation of multiple sclerosis to be built

New findings may help resolve thedispute on whether therapy forAlzheimer’s disease (AD) should targetoverproduction of tau protein foundin neurofibrillary tangles or amyloid-�peptide (A�) in plaques. The answer,suggest researchers from University ofPennsylvania School of Medicine(Philadelphia, PA, USA), may be toinhibit an enzyme involved in bothprocesses, which can be achieved withlithium—at least in an animal model.

Previously, the team led by PeterKlein discovered that lithium inhibitsglycogen synthase kinase-3 (GSK-3),which phosphorylates tau, and alsointeracts with presenilin. Mutatedpresenilin leads to increased A�production. “We wanted to testwhether GSK-3 might be involved inthis process”, says Klein. “Weinhibited GSK-3 with lithium andfound that it indeed reducedproduction of A� in vitro and in micethat overproduce A�”. This effect wasalso seen with another inhibitor ofGSK-3, while increased and decreased

expression of another isoform,GSK-3�, increased and decreased A�production, respectively.

Together, the studies indicate thatGSK-3� is required for the processingof amyloid precursor protein (APP)into A� by regulating �-secretase, saysJames Woodgett (Ontario CancerInstitute, Toronto, Canada), who co-authored a commentary on theresearch. “The effect of the kinase onAPP processing is selective in that�-secretase activity towards Notch,another substrate of the secretase, isunaffected by inhibition of GSK-3”, heexplains. This led Klein’s team toconclude that GSK-3� offers anattractive target for pharmacologicalagents aimed at reducing theformation of amyloid plaques andneurofibrillary tangles (Nature 2003;423: 392–93, 435–50).

Retrospective analysis of AD risk inpeople treated with lithium for bipolardisorder could provide furthersupportive evidence. But Woodgettbelieves that there is now justification

to assess whether lithium treatment ofpatients predisposed to AD can act as aprophylactic for plaque formation andretard progression of the disease.“What isn’t known”, he says, “iswhether clinically established dosagesof lithium used in the treatment ofbipolar disorder will be sufficient toprevent APP processing and plaqueformation in people.”

Since certain non-steroidal anti-inflammatory drugs similarly reduceA� production, but via a differentmechanism, combination therapymight further reduce amyloidaccumulation. “Several companieshave been developing small-moleculeinhibitors of GSK-3”, Woodgett toldThe Lancet Neurology. These agents arenot selective for � or � isoforms, but“since both forms of GSK-3 areimplicated in the generation ofhyperphosphorylated tau, this may bea good thing”, he says. Klein’slaboratory will now start searching forregulators of GSK-3�.Kelly Morris

Mood metal makes two-pronged attack on Alzheimer’s disease

MS centre will open in the summer of 2004

AED

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