Thinking preventively about dementia: a review

INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY

Int J Geriatr Psychiatry 2002; 17: 895–906.

Published online in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/gps.707

Thinking preventively about dementia: a review

Brian Cooper*

Institute of Psychiatry, London

SUMMARY

Background The dementias of late life now constitute a major public health challenge to our society.Objective To examine the contributions of neuroscience, clinical treatment and health-care policy to the building of anational programme for preventive approaches to dementia.Method Critical review of the literature, making use of international databases (Medline, Embase, Psychlit) and Britishofficial publications.Results Recent developments in a number of research fields afford prospects for advances in primary and secondary pre-vention. These include findings from case-control and cohort studies of associations with earlier head injury and vasculardisease, possibilities of pharmacological protection for persons at high risk for Alzheimer’s disease, and the use of moreeffective anti-dementia drugs in the mild to moderate stages of severity. Research aimed at tertiary prevention is laggingbehind, but there are some indications that the worst features of late-stage decline could already be mitigated by improve-ments in community support services and nursing-home care.Conclusions Containment of the growing social and economic burdens of dementia calls for a national policy to ensurethat new research findings can be translated into practice and applied to the benefit of all old people who stand in need. Forthis purpose the most appropriate conceptual framework is supplied by a preventive model, broadly similar to those alreadydeveloped for some other forms of chronic degenerative disease. Copyright # 2002 John Wiley & Sons, Ltd.

key words— dementia; Alzheimer disease; preventive medicine; neuroprotective agents; health services research

That the proverbial ounce of prevention is worth apound of cure would no doubt hold true for late-lifedementia, if only one knew where to find that preciousquantum. At the present stage of knowledge, however,it has to be sought over a wide terrain. There are nowquite elaborate neuroscience and clinical-diagnosticframeworks for research in this field, but as yet nocomparable public-health framework. The aim of thisshort review is not to consider the various approachesin depth, but rather to incorporate them into a concep-tual system for thinking preventively about dementia.

THE PUBLIC-HEALTH CHALLENGE

The longstanding public-health neglect of dementiadisorders had several grounds. Although these are

lethal conditions, their excess mortality is concen-trated among the very old, and the impact on totallife-expectancy therefore small. Most affectedpersons being past working age, the economicconsequences are less conspicuous than for manyother diseases. Above all, a knowledge base forrational preventive action has been lacking.

Today, however, the public health challenge is atlast being confronted. To begin with, these arecommon conditions of late life. In England and Walesa diagnosis of dementia can be assigned in over 6% ofover-65-year olds, including more than half of allcare-home residents (Medical Research Council,1998). At 65, the mean expectation of life withdementia is 0.7–0.9 years for men and 1.3–1.8 yearsfor women (McNamee et al., 2001). Clinical demen-tia is the single biggest cause of dependency amongpersons aged over 75 (Aguero-Torres et al., 1998),while the burden on family caregivers is itself a factorof mental ill-health (Donaldson et al., 1997).

Received 18 February 2002Copyright # 2002 John Wiley & Sons, Ltd. Accepted 29 April 2002

*Correspondence to: Dr B. Cooper, Section of Old Age Psychiatry,Institute of Psychiatry, De Crespigny Park, London SE5 8AF, UK.E-mail: [email protected]

Dementia-related service costs for England, adaptedto 1998/99 prices, are estimated at £1.85 billion andtotal costs at over £6 billion annually (Audit Commis-sion, 2000). Over the next 50 years, population ageingwill double the case numbers, mainly due to theincrease in over-80-year olds (Melzer et al., 1997),while health-care costs will continue to rise as newtreatments raise public expectations (Knapp et al.,1998).

Despite recent advances in neuroscience, however,many doubts remain (Gilleard, 2000). What is thescope for preventive action in this field? Can the ben-efits of these advances be made widely available toelderly populations? If so, what is the likely impacton dementia incidence and course?

PREVENTIVE APPROACHES TO DEMENTIA

In order to protect the people’s brains and mental lifewe must proceed according to the same public healthprinciples as we do to protect the people from all dis-orders: we must prevent what we can prevent, termi-nate what we can terminate, and mitigate what wecannot prevent and cannot terminate (Gruenberg,1980).

One may start from two postulates, the first ofwhich is set out above. Here the terms prevent, termi-nate and mitigate correspond to the public-healthusage of primary, secondary and tertiary prevention,now recognized in psychiatric teaching (RoyalCollege of Psychiatrists, 1993). Primary preventionreduces disease in a population by lowering exposureto causal agents or promoting host resistance, itsimpact on dementia being measurable by a fall inage-specific incidence rates or a rise in the meanage of onset. Secondary prevention limits progressionand recurrence of disease by early case-detection,diagnosis, and treatment; hence it reduces totalprevalence in a population. Tertiary prevention ame-liorates the consequences of disease by containingdisability and dependency, and maintaining an accep-table quality of life. Each of these three stages will beconsidered in turn, though in respect of dementia theygradate imperceptibly one into another.

The second postulate is simply that the dementiasare stamped by causal heterogeneity, even withindiagnostic categories. Such differences exist betweenvascular dementia (VaD) and the primary neurode-generative forms, including Alzheimer’s disease(AD), and are to be expected also among these latter.Hence preventive programmes probably will have toinclude a number of different components.

PRIMARY PREVENTION

Of the two broad approaches to prophylaxis (Rose,1985), the whole population strategy seeks to lowergeneral levels of pathogenic exposure, whereas thealternative high-risk group strategy leaves exposurelevels unchanged but seeks to protect persons atincreased risk, by reducing their vulnerability.

Whole-population strategy

So far epidemiological research has supplied fewpointers to possible whole-population measures, fieldstudies having yielded little information on environ-mental risk factors. Incidence rates have not beenshown to vary geographically, apart from some lowestimates in East Asian countries which may be arte-factual (Jorm and Jolley, 1998). Currently the mostpromising environmental leads are focused on cranio-cerebral trauma and neurotoxic exposures, both pos-sibly interacting with genetic vulnerability, and onsocial factors that influence the risk of brain insult.

Cranio-cerebral traumaA number of early case-control studies included headinjury with loss of consciousness as a putative riskfactor for AD. Analysis of pooled data from sevenstudies (Mortimer et al., 1991) reported a mean oddsratio of 1.82, though the association held good onlyfor men and for cases with no family history. Sincethen further evidence has accumulated (Table 1).

Although case-control studies have continued tofind associations with head injury, there is still widevariation and most findings are of low statisticalpower. The one exception, a large-scale internationalcollaboration (Guo et al., 2000), reported the biggestincrease in risk, but here the exposure rate amongcontrols was so low as to suggest unreliability in theestimates. Findings of longitudinal research arealmost equally variable. However, the cohort studyby Plassman et al. (2000) carries weight because itwas based on hospital documentation rather thaninformant interviews. In a follow up of World WarII servicemen, those hospitalised for non-penetratinghead injury were compared to controls admitted forother reasons. Hazard ratios for AD were 4.5 insevere, and 2.3 in moderate head injury, and thosefor all dementias combined 4.5 and 2.4 respectively.

On balance, serious head injury should now beregarded as a risk factor for dementia, in males atleast, though its relative importance has yet to beestablished. What are the implications for prevention?First, success in reducing rates of head injury by

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Copyright # 2002 John Wiley & Sons, Ltd. Int J Geriatr Psychiatry 2002; 17: 895–906.

highway speed limits, use of seat-belts and crash hel-mets, drink-drive and vehicle licensing laws, etc, willtend to reduce dementia incidence. Secondly, follow-up studies of cerebral trauma should be extended tothe long-term consequences, including cognitivedecline. Thirdly, treatment and rehabilitation ofhead-injury cases could have special relevance inpersons at increased risk, such as those homozygousfor apolipoprotein E4 (Nicholl et al., 1995).

Environmental neurotoxinsMetallic neurotoxins came under suspicion whenaluminium was found to cause encephalopathy in

patients on renal dialysis, and this was reinforced bydetection of aluminium in senile plaques. Furtherresearch was, however, inconclusive, and reviewersof the field took opposing positions. While McLachlanet al. (1991) considered that mean exposure levelsshould be reduced below 3 mg daily, Doll (1993) con-cluded that aluminium probably is not a cause of AD,although the possibility cannot be ruled out until rela-tive risks are known for persons with prolonged highexposure levels. The fact that aluminium absorptionmay be affected by fluoride content in water couldconfound survey research findings (Forbes et al.,1991).

Table 1. Head trauma and risk for Alzheimer’s disease: more recent epidemiological studies

a. Retrospective case-control studies

Study Place Exposure frequencies Adjusted 95% confidenceodds ratio interval

Cases Controls

van Duijn et al., 19921,2 Rotterdam, 22/197 17/197 1.6 0.8–3.4Netherlands

Fratiglioni et al., 19933 Stockholm, 4/88 25/257 0.3 0.1–1.2Sweden

Mayeux et al., 19931 New York, USA 18/138 10/193 3.7 1.4–9.7CSHA, 1994 Canada 35/184 60/453 1.7 1.0–2.8

(18 centres)Salib and Hillier, 1997 Warrington, UK 53/198 23/176 2.4 1.4–4.1O’Meara et al., 19971 Seattle, USA 32/349 16/342 2.1 1.1–3.8

Guo et al., 20001 USA, Canada, 184/2,176 30/2,443 9.9 6.5–15.1Germany (spouses)(18 centres) 88/12,159 4.0 2.9–5.5

(parents and sibs)

b. Cohort/longitudinal studies

Study Place Exposure history Adjusted Samplerel. risk statistic

Positive Negative

Incident cases of AD: 95% CISchofield et al., 19971 New York, USA 4/19 34/271 4.1 1.3–12.7Mehta et al., 19971,4 Rotterdam, 6/91 788/6,516 0.8 0.4–1.9

NetherlandsLauner et al., 19991 Four European centres 27/306 2,466/25 796 1.0 0.7–1.5Luukinen et al., 19995 N. Finland 6/31 31/586 3.7 1.7–8.4Plassman et al., 20001 USA 17/546 18/1,228 4.5 1.8–11.5

(veterans study)Median interval to AD onset: p value

Nemetz et al., 19986 Rochester MA, USA 10 yr. 18 yr. — 0.015

1Head trauma with loss of consciousness.2Early-onset AD (< 70 yr.).3Population aged 75 yr.þ.4Population aged 55 yr.þ.5No clinical diagnosis; MMSE score decline of 5 or more points.6Patients aged 40 yr.þ at last contact.

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More recent work has done little to clarify thesituation. An eight-year cohort study in South-WestFrance found in high-aluminium areas an approxi-mate doubling of risk (adjusted ratios being 2.0 fordementia and 2.1 for AD), but no clear dose-responserelationship (Rondeau et al., 2000). In the 1990s othermetallic salts came under suspicion, following areport that oral zinc supplementation had caused rapidadverse effects in Alzheimer patients (Bush et al.,1994). The possibility that a number of metallic com-pounds can combine with genetic susceptibility toincrease risks for neurodegenerative disorder moregenerally makes a good case for further research,though not yet for preventive action.

Social risk factorsProspective studies have reported inverse correlationsbetween educational attainment and dementia risk,though with some inconsistencies. Two surveys foundassociations with ‘non-AD’ (predominantly vascular)dementia but not with AD (Bickel and Cooper, 1994;Cobb et al., 1995), whereas two other projectsrestricted to AD also reported inverse associations(Stern et al., 1994; Letenneur et al., 2000): in thelatter instance for women only. The discrepanciesmay be due to a halo effect in studies restricted toAD; e.g. Stern et al. (1994) made this diagnosis in95 per cent of all emergent dementia cases in theircohort. There are also indications that low occupa-tional status is linked to dementia risk (Bickel andCooper, 1994; Stern et al., 1994).

Here again, we have no clear lead to preventiveaction. It has been suggested that early mental stimu-lation protects against AD by promoting neocorticalsynaptic density and so increasing ‘brain reserve’.Lack of stimulation is, however, only one of the risksto which socially deprived children are exposed. In aCanadian study of dementia cases that came toautopsy (Del Ser et al., 1999), the only differencebetween low and high educational attainment groupswas that the former had more cerebrovascular lesions:a finding which suggests a brain insult rather than abrain reserve explanation for the social gradient. Ifthis finding is confirmed, one may need to look intothe influence of class-related nutritional, traumatic,or other noxious exposures in earlier life.

Reducing risk in vulnerable groups

Elderly persons may be considered at high riskbecause on testing they are found to have mild cogni-tive deficits which could be prodromal signs of adementing process. Prospective studies have shown

that most individuals who develop the clinical condi-tion have minor memory impairments at least two tothree years beforehand (Braekhus et al., 1995; Cooperet al., 1996). Such deficits are, however, too commonin old age, and the proportion of ‘false positives’ fartoo high, for pre-clinical diagnosis yet to be useful ina preventive context. Hence, selective and opportunis-tic screening are better regarded currently as aspectsof secondary prevention (see below). More directlyrelevant as risk indicators are a strongly positivefamily history and the presence of medical conditionsknown to be associated with brain pathology.

Genetic counselling and family planningFamilial predisposition being, apart from age itself,the best-attested risk factor for AD, the question ofrisk reduction must be considered in relation tofamilies, as well as to individuals. Practical measuresto reduce genetic transmission are currently restrictedto counselling and family planning where indicated.While genetic counselling provides a valuable serviceto affected families, its scope as a public-health strat-egy is bound to be limited. ‘Familial’ is an impreciseconcept and one difficult to apply to the elderly inoperational terms. In practice, family planning willbe most effective when the pattern of occurrencepoints to an autosomal dominant transmission. Thefrequency of such cases in the 40–60 year range hasbeen put at just over five per 100 000 (Campion et al.,1999), corresponding to a total of about 600 personsin England and Wales (Liddell et al., 2001). Hence theimportance of counselling services cannot be gaugedin terms of total incidence rates. For the at-riskpopulation as a whole, phenotypic approaches toprevention seem likely to remain paramount.

Treatment of medical and psychiatric risk factorsA variety of medical conditions have been consideredas possible risk factors, but most research findings havebeen inconclusive, no doubt partly due to weakness ofmethod. In the EURODEM re-analysis of case-controlstudies, a history of hypothyroidism or epilepsyappeared to increase risk (Breteler et al., 1991), thoughthe latter association could have been partly due to late-life seizures. Individual studies, as well as the EURO-DEM collaboration (Jorm et al., 1991) have found anexcess of dementia among old people with a historyof medically treated depression. This association maynot, however, be specific to depression, but shared withother functional mental disorders (Cooper and Holmes,1998). Whether the underlying link is a direct patholo-gical one or is mediated by some forms of psychiatrictreatment remains unclear.

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On present evidence, however, pride of placeamong the medical risk factors must go to vasculardisease. A decade ago Hachinski (1992) called foraction against the vascular dementias as ‘preventablesenility’ and distinguished between three successivestages. For the brain-at-risk stage, which includedelderly hypertensives, heavy smokers, diabetics andcardiac patients, he advocated life-style measures(smoking cessation, graduated exercises and reducingdiet), with selective treatment (anti-hypertensives,oestrogen replacement, lipid-lowering agents, etc) asindicated. At the pre-dementia stage of establishedcerebrovascular disease, specific treatments such asanti-thrombotic medication, calcium channel block-ers or carotid endarterectomy are required, and lastlythe stage of cognitive decline calls in addition for theuse of anti-dementia drugs.

Hachinski’s paper was a plea for more systematicdiagnosis and treatment of vascular disease, withprotection of brain function as one important benefit.His argument has since been strengthened by evi-dence of the links between vascular disease and AD,supplied in part by epidemiological research (cf.Table 2). Thus the Finnish cohort study (Kivipeltoet al., 2001) indicates that two potentially treatablerisk factors in mid-life, hypertension and hypercho-lesterolaemia, are linked to the development of AD.

Recent progress in stroke prophylaxis, based on useof the newer anti-hypertensive drugs (calcium-channelblockers and angiotensin-converting enzyme inhibi-tors, or ACEIs), may therefore have implications fordementia prevention generally. The Systolic Hyper-tension in Europe (Syst-Eur) trial (Forette et al.,1998), has already reported a lower two-year inci-dence of dementia among elderly patients on thecalcium-channel blocker nitrendipine than in amatched comparison group (11 cases, or 3.8 per1000 patient-years, vs 21 cases, or 7.7 per 1000patient-years). This is an encouraging result, thoughthe resulting claim that prescribing of anti-hyperten-sives could by itself reduce dementia incidence byup to 50 per cent seems over-optimistic. In addition,recent case-control studies suggest that use of statins(HMG-coenzyme A reductase inhibitors) in strokeprophylaxis could reduce dementia risk (Jick et al.,2000).

SECONDARY PREVENTION

Although interest in ‘reversible dementia’ has waned,recent developments, including progress in cell biol-ogy and genetic techniques, research into pharmaco-logical protection, and advances in clinical treatment, T

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are encouraging the notion of secondary preventionmore generally and underlining the importance ofearly diagnosis.

‘Reversible dementia’

The notion that some cases of apparent dementiamight be reversible goes back to the 19th century,but re-emerged following successful penicillin treat-ment of neurosyphilis. Clarfield (1988), reviewingpublications from the 1970s and 1980s, found over30 relevant studies, mostly from specialist centres.The mean proportion of cases classed as potentiallyreversible was 13.2%, but in 11 studies that includedfollow-up only 3% were reported to be fully, and afurther 8% partially recovered. Surgically treatableconditions such as subdural haematoma, carotidstenosis and normal-pressure hydrocephalus werecomparatively rare. The commonest reversible causeswere given as drug abuse, depression and metabolicdisorder, suggesting that ‘reversible dementia’ as thendefined included many cases of confusion andpseudo-dementia. More recent reviews (Weytinghet al., 1995; Philpot and Pereira, 2002) indicate thatthe proportion of cases classed as potentially reversi-ble has declined over the years, and that only a frac-tion of these are found to be recovered at follow up. Inconsequence, interest is now focused less on identify-ing a reversible sub-group than on ways of postponingclinical onset and retarding progression more gener-ally.

Progress in cell biology and genetic techniques

Can advances in genetics and cell biology open upnew avenues to secondary prevention? In addition towork on possible genetic interventions, a new avenuehas been opened up by the experimental use ofso-called ‘DNA vaccines’.

Gene therapy approachesIn gene therapy research, techniques now being testedinclude positional cloning to identify disease-relatedmutations, use of ‘anti-sense’ nucleotides and ribo-zymes to reduce abnormal gene expression, and directbrain implantation either of genetically-engineeredstem cells to replace mutated genes, or of embryonicneural tissue to repair transmitter systems (Carter andSchuchman, 2001). Animal experimentation hasraised hopes that pluripotent or neural stem cellscultivated from human embryos can be integrated intothe adult brain, replacing damaged or lost neurons in anumber of neurodegenerative disorders, including

AD. The need for great caution in proceeding toclinical applications, have been demonstrated forParkinson’s disease, where dopamine tissue trans-plants resulted in severe, intractable worsening insome patients (Greene et al., 1999).

Immunization against the Alzheimer cascadeTransgenic mice injected repeatedly with Amyloid-beta42 (A�) peptide developed an antigenic response,and showed reduction of amyloid deposition andneuritic changes in comparison with controls (Schenket al., 1999). Repeated intraperitoneal injection ofantibodies to A� also reduced neuropathologicalchanges in the transgenic strain (Bard et al., 2000).In other words, both active and passive immunizationprocedures seemed effective to some degree. There isalso evidence that reduction of the amyloid plaqueburden reduces cognitive dysfunction in transgenicmice without, however, lowering total levels ofA� in the brain (Janus et al., 2000). Currently, aninternational Phase 2A clinical trial of one immuno-agent (AN-1792) has been suspended because ofadverse reactions among patient volunteers(www.biospace.com/news, 1 March 2002).

Pharmacological protective measures

Interest in possible pharmaco-protective effects hasbeen focused on anti-inflammatory drugs, oestrogenpreparations and related substances, whose prescrip-tion is reportedly associated with a reduced occur-rence or slowed progression of AD. For the presentany such effects are better placed under the head ofsecondary prevention.

Non-steroidal anti-inflammatory drugsA number of retrospective studies have found a loweruse of anti-inflammatory drugs (NSAIDs, aspirin andH2 receptor antagonists) among persons who developdementia than in age-sex matched controls (e.g.Beard et al., 1998; Anthony et al., 2000). In a long-term prospective study, the Rotterdam group observedno reduction in AD incidence among short-termusers, but a relative risk of only 0.20 among thoseprescribed NSAIDs for two years or longer (Baset al., 2001). Among autopsy-verified cases, on theother hand, no differences in plaque frequency werefound between users and non-users of NSAIDs(Mackenzie and Munoz,1998; Halliday et al., 2000).

Oestrogen replacement therapySeveral studies suggest that post-menopausal oestro-gen replacement improves cognitive performance

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and might help to prevent dementia, or slow itsprogression (Yaffe et al., 1998), though life-styledifferences between oestrogen users and non-userscould confound these findings. A case-control studydrawing on the UK General Practice Research Data-base (Seshadri et al., 2001) found no reduction in riskeven among patients who had taken oestrogens forfive years or longer. The Alzheimer Disease Co-operative Study, a US multi-centre clinical trial, con-cluded that oestrogen replacement therapy for oneyear did not retard progression of AD or improveoutcome (Mulnard et al., 2000).

Anti-oxidantsAny protective effects of anti-inflammatory drugs andoestrogens have been attributed to their anti-oxidantaction, sparking interest in other compounds whichshare this property. Here the research findings havebeen conflicting. The Alzheimer Disease Co-operativeStudy reported that selegiline and vitamin E, singly ortogether, may slow disease progression (Sano et al.,1997), whereas two population surveys found no dif-ferences in cognitive function between anti-oxidantusers and non-users after adjustment for age, sex andeducation (Jama et al., 1996; Mendelsohn et al.,1998).

In summary, a case has built up for controlled clin-ical trials; in particular of anti-inflammatory drugs.However, the evidence is not strong enough to justifyprophylactic prescribing, and advocacy for the use ofsuch drugs in earlier life, to protect persons identifiedas genetically vulnerable (Caracabelos et al., 1999),lacks any sound scientific basis.

Advances in clinical treatment

The mental deterioration in AD appears to be directlyrelated to cholinergic deficits, and clinical trials haveshown improvement among patients taking acetyl-cholinesterase inhibitors. In Britain the National Insti-tute for Clinical Excellence (2001) has recommendedthat three of these preparations—donepezil (Aricept),rivastigmine (Exelon) and galantamine (Reminyl)—should be made available under the National HealthService to people with mild to moderate AD, at anestimated cost of £42 millions annually.

The trials can, however, be criticized on severalgrounds. Research criteria have excluded co-morbiditysuch as cardiovascular, pulmonary, gastro-intestinaland endocrine disease from which so many old peoplesuffer. Tests of cognitive performance have shownonly small differences between treatment and placebogroups, restricted to the trial period, while effects on

patients’ behaviour and everyday activities remainunclear. Serious bias, moreover, could arise from sup-pression of unfavourable trial results.

A fundamental question in assessing the preventiverole of medication lies in deciding whether it slowsprogression of the disease pathology, or provides atbest a temporary relief of clinical symptoms. Inrespect of acetylcholinesterase inhibitors, this ques-tion is unresolved, despite a government press state-ment that currently prescribed substances ‘providesome improvement of symptoms in Alzheimer’s dis-ease, but they do not affect the underlying diseaseprocess’ (Department of Health, 2001a). Other poten-tial lines of treatment, such as cobalamin and folatereplacement in mild to moderate dementia (Nilssonet al., 2001) are still in the early stages of clinicalassessment.

Selective and opportunistic screening

As more effective treatments emerge, so early diagno-sis will gain in importance. While there is no case forprescriptive screening, good opportunities can beafforded in general practice; e.g. by regular surveil-lance of over-75-year-old registered patients. Briefcognitive tests can achieve good accuracy in a clinicalsituation, but in unselected samples of the elderlyyield many false positives (Flicker et al., 1997). Givencontact with family members, an informant question-naire on cognitive decline, such as the IQCODE(Jorm et al., 2000), can provide a valuable comple-ment or alternative to brief screening tests. In allsuspected cases, careful diagnostic evaluation mustprecede any intervention.

TERTIARY PREVENTION

Tertiary preventive measures are intended to postponedisablement and dependency, and maintain an accep-table quality of life. The value of ‘anti-dementia’medication as judged by these criteria is not yet clear.Clinical trials restricted to the mild to moderate stagescan supply only partial evidence, and most claimsmade for the drugs have relied on inferences aboutdisablement drawn from cognitive test results(Knapp et al., 1998). Reports from industry-sponsored research that long-term care admissioncan be delayed by drug treatment require independentconfirmation. It is thus understandable that interest intertiary prevention has centred on the provision andquality of care services. Table 3 summarizescontrolled experiments to test the effectiveness of



community support and innovations in long-stay care.Here only studies based on samples of 60 or morepersons are included.

Community support

Research design and method have varied so widelythat few direct comparisons can be made between stu-dies. In general, community programmes that includesupport for caregivers seem more effective than thosetargeted solely on patients. Two randomised trials(Mittelman et al., 1996; Brodaty et al., 1997) reportedthat caregiver support groups delayed institutionalplacement by a mean of 12–18 months: economicallya significant gain. Measures of practical help, in con-trast, have seldom been evaluated, though thedemands imposed by housework and personal carerank high as causes of stress, and assistance with thesetasks may be crucial. There is a strong case foraccepting both caregiver support groups and

affordable home help as integral components of com-munity care.

Long-term residential care

Concern has been aroused by excessive geriatric-home use of tranquillising drugs as a substitute forskilled, labour-intensive nursing. To achieve bettercare, however, changes in drug usage must go handin hand with improvement of nursing standards, asexercises in ‘dementia care mapping’ indicate(Ballard et al., 2001). Studies included in Table 3 sug-gest that innovations in home care can lower relianceon chemical and physical restraints, and afford somerelief of clinical symptoms.

Prevention and service infrastructures

Evaluative research thus highlights the importance ofnational service infrastructures and their cost-bearingmechanisms. In British settings up to half of all cases

Table 3. Controlled evaluative studies of community support and long-term care programmes for dementia

Study Sample Intervention Period of Effects ofsize assessment intervention

Community supportEngedal 19891 77 Day-care provision One year Time in hospital reduced (30 vs 50 days)*Wimo et al., 1993 55 v. 44 Day-care provision One year Institut. admissions reduced (24% vs 44%)*Lawton et al., 1989 642 Formal respite care One year Institut. admissions delayed

(mean of 22 days)Mohide et al., 19901 60 Caregiver training and 6 months No difference in institut. admissions

supportMittelman et al., 19961 206 Caregiver counselling Variable, up Home admisson delayed (mean of 47 wks.)

and support to 3.5 yearsBrodaty et al., 19971 96 Caregiver group 8 years Home admission delayed (mean

training and support of 20 months)Ostwald et al., 19991 94 Caregiver group training 5 months Caregiver burden and negative

sessions responses decreased*Gitlin et al., 20011 171 Caregiver individual 6 months Less decline in IADL and self-care scores*

training at homeLong-term care programmesRitchie et al., 1992 110 v. 242 Small-group homes Cross-sectional Reduction in:

as alternative to hospital physical dependency**wards depression**

Ray et al., 1993 194 v. 184 Staff training in behaviour 4 months Reduction in:treatment antipsychotics

(72% vs 13%***)physical restraints(36% vs 5%***)

Rovner et al., 19961 118 AGE programme 6 months Reduction in behaviourdisorders (27% vs 51%*)

Hopman-Rock1 et al., 1999 134 Psychomotor activation 6 months Less decline in cognitive scores*programme

1randomized trial design; IADL¼ instrumental activities of daily living; AGE programme¼Activities; Guidelines on medication;Educational rounds.*p< 0.05; **p< 0.01; ***p< 0.001

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known to services will be in care-homes within 2–3years of referral, and up to three-quarters in the lastperiod of life (Holmes et al., 1995). At current levelsof provision, NHS continuing care units can cope withonly a fraction of the demand, and most long-staybeds are now outside the clinical sector. Mountingprofessional disquiet over this situation led to the set-ting up of a Joint Working Party (Royal College ofPhysicians, 2000), which noted the paradox that‘ . . . older people with the greatest needs for consis-tent, creative and effective care now live in carehomes denied the traditional essence of interdisciplin-ary geriatric care’.

Development of a preventive approach to dementiais hampered in three ways. First, transfer of care to theprivate sector means that there is now little incentivefor building bridges to community services, and evenless for evaluative research. Secondly, local authori-ties, faced with huge increases in support costs, mustpare down their services to patients who still liveat home. Thirdly, imposition of means testing hascreated perverse incentives for old people and theirfamilies to delay in seeking help.

The recent Royal Commission Report (1999), inrecommending that personal care should be paid forfrom general taxation, subject to assessment of need,reckoned the public cost of their proposal as £800 mat baseline, rising to £1.7 bn after 10 years, £3.4 bnafter 20 years and £6.0 bn after 50 years, and pointedout that these sums would amount to only around one-quarter of private expenditure under the existingsystem. However, the Government’s response rejectedthe proposal as it applied to England and Wales,arguing that to make personal care free would notbe the best use of existing resources (NHS Plan,2000). How sharply in practice it will be possible todemarcate nursing from personal care for thedementing elderly remains to be seen.

DISCUSSION

To meet the growing public health challenge ofdementia, we have to start thinking preventively. Cen-tral to this issue is the need to incorporate researchendeavours, health-care policy and medical practiceguidelines into a conceptual framework, and this inturn has implications for each of the component parts.The research agenda must include investigation ofrisk factors for the dementias, and their interactionsone with another. Here both genetic studies andenvironmental epidemiology are called for.

Disease-specific data will be necessary to constructmore rational health policies, and in the case of

dementia will have to cover the whole course ofillness, including the later stages. This predicates awidened concept of NHS continuing care, and ofthe role of specialist services (geriatric medicineand old age psychiatry) within it. A National CareCommission, as proposed in the Royal Commission’sreport, may prove valuable if it pays due regard tothese aspects.

With advances in knowledge medical-practiceguidelines can become more preventively oriented.The recently-published National Service Frameworkguidelines on stroke (Department of Health, 2001b)provide a useful model, though clearly both confu-sional states and dementia will require their ownpriorities and targets.

Are the means for concerted public-health actionwithin our national resources? Optimistic forecastsof a compression of morbidity into the final stagesof life (Fries, 1996) stand in sharp contrast to predic-tions that modern medical treatment will result in amassive increase in disabled survivors: the ‘failuresof success’ (Gruenberg, 1977). Data for the UK arenot in fact consistent with either of these opposingscenarios. Population ageing, although its impact willbe buffered only partially by increase in disability-free life expectancy, is not thought to pose a majorthreat to the affordability of national health care.Indeed, a recent consultative document (Wanless,2001) argues that demographic trends alone are unli-kely to add more than 1% annually to NHS real costs.While the report in question fails to take account ofnursing and personal care costs outside the presentremit of the NHS, it seems probable that these toocould be supported by the public sector, given thenecessary political will (Royal Commission, 1999).

ACKNOWLEDGEMENT

I am grateful to Dr M. Philpot and Professor A.Macdonald for their helpful comments on an earlierdraft of this paper.

KEY POINTS

* Prospects for a preventive approach to dementiaare beginning to improve

* Research programmes, health-care policy andpractice guidelines should be incorporated intoa basically preventive framework

* The means for concerted public-health actionon dementia lie within British nationalresources



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