The Pharmacist's Role in the Management of Alzheimer's Disease
After completing this continuing education article, the pharmacist should be able to:
- Describe the basic etiology and pathophysiology associatedwith Alzheimer's disease (AD).
- Identify the epidemiology of AD, the types, the variousstages, and risk factors associated with the developmentof AD.
- cribe the impact of AD on both patients and caregivers.
- nsel patients and their caregivers on the proper useof the pharmacologic agents.
- cribe the adverse effects associated with the use ofthese agents for the treatment of AD, as well as the criteriafor their use.
- ectively advise patients and caregivers on the managementof AD.
- Discuss the latest news, research, and clinical trials withregard to AD.
- Be able to provide information to patients and caregiversabout support groups and AD resource organizations.
Alzheimer's disease (AD) hasbeen one of the most intriguingenigmas in the medical fieldsince it was first recognized in 1906 by Dr.Alois Alzheimer. This progressive anddegenerative neurologic disorder is characterizedby a gradual decline in cognitionand behavior. In 2004, the NationalCenter for Health Statistics reported thatAD is the 7th leading cause of deathamong the elderly in the United States. Itis the most common form of dementia,accounting for >65% of all dementia inthe elderly.1,2 AD will continue to be achallenge for the elderly population,especially as the baby-boomer generationages.
It is estimated that AD now affects~4.5 million individuals in the UnitedStates?twice the number affected in1980. The disease affects ~5% of menand women aged 65 to 74 years. In addition,an estimated 50% of the population=85 years may have AD.3,4 The increase inthe number of cases may be attributedto the increase in the aging population,as well as increased awareness aboutthe disease.
Furthermore, it is estimated that, bythe year 2050, ~11 million to 16 millionindividuals will be affected by AD.4Currently, ~28 million individuals areaffected worldwide.4 More than one halfof individuals with AD are cared for athome, whereas the remainder are caredfor in various long-term care facilities.4
The increased number of AD casescontinues to have a significant impact onindividuals and families and on the healthcare industry as well, because of thecomplexity of the disease. Despite theadvances made in attempting to understandthe etiology of this disorder, manyquestions remain unanswered and muchremains to be discovered.
On average, an individual will live 8years after diagnosis of AD or as long as20 years from the onset of symptoms.3,4Caring for individuals with AD requiressignificant resources. For instance, 1 to 4family members may act as caregivers foran individual with AD. Results of a studyshowed that in 1996 the average annualcost of caring for a patient with AD was~$18,400 to $36,000, depending on theseverity of the condition.5,6 Since 1996,the costs have risen consistently. Researchsuggests that the estimatedworldwide annual cost for care ofpatients with AD and other dementia is~$248 billion.5,7 Whereas the issue of costis an important factor, the managementof AD can be both emotionally and physicallychallenging for patients, familymembers, and caregivers.
This continuing education article willreview current theories, ongoing research,and therapies available for patientswith AD. It also will provide pertinentinformation for pharmacists to utilizewhen assisting the patient with AD,as well as for family members and caregiverswho are affected by this debilitatingdisease.
Although the exact etiology of AD stillis unknown, research suggests that itcan be attributed to both inherited andenvironmental factors. The 3 standardneuropathologic features of AD includeamyloid plaques; neurofibrillary tangles;and a third factor, which has beendescribed only in the last 3 decades?synaptic and neuronal cell death thatinvolves a progressive or gradual loss ofconnections between neurons.6,8,9 Asthe death of the neurons progressesand spreads through the brain, brainatrophy occurs in the affected areas.9Whereas researchers have knownabout these features of AD for severalyears, they are still learning more aboutthem and their roles in the developmentand progression of AD. The progressionof AD often is unpredictable,and the severity varies from patient topatient.
There are 2 distinct forms of AD:(1) familial and (2) sporadic.10 Familial ADis considered very rare and typicallyoccurs before the age of 60. It also isreferred to as early-onset AD. Less than5% of the cases are early-onset, andthis form is believed to be caused bygene mutations on chromosomes 1, 14,and 21.10,11
As for sporadic AD, genes may not bethe direct cause of the disease but mayinfluence the risk of developing it.Sporadic AD also is referred to as late-onsetAD, because many cases occur inindividuals after the age of 60, with thevast majority in their 70s and 80s.10,11There are, however, exceptions to thegeneral observations regarding age atonset.
The apolipoprotein E (apo E) gene,which is found on chromosome 19, isthe best studied susceptibility gene insporadic AD.10 The apo E gene is responsiblefor the manufacturing of a proteinthat moves cholesterol and other fatsthroughout the body.10 It is postulatedthat this protein may be involved in thestructure and function of the fatty membranethat surrounds a brain cell.10 Theapo E gene occurs in many forms oralleles. The 3 forms that occur most frequentlyare apo E-II, apo E-III, and apo EIV.10-12 Furthermore, the apo E-IV genemay increase an individual's chance ofdeveloping late-onset AD. It is estimatedthat between 35% and 50% of individualswith AD carry some form of the apoE-IV gene.10
Current research indicates that ADmay be triggered by several factors,including age, genetics, serious headinjuries, and inflammation of the brain, aswell as environmental factors. Age is themost well-documented risk factor. Otherpossible risk factors include the following13-15:
- Down's syndrome
- Head injury
- Diabetes mellitus
- Family history
- Sedentary lifestyle
- Diets high in saturated fat
Signs and Symptoms
Recognizing the warning signs associatedwith the development of AD iscrucial in order to initiate early intervention,as well as to differentiate ADfrom other forms of dementia. In manycases, an individual's symptoms mayprogress gradually over time and maynot be obvious initially. Patients mayexhibit cognitive or intellectual symptoms,such as acalculia (inability to performsimple mathematical calculations),aphasia (inability to communicateeffectively), apraxia (inability toperform daily activities such as brushingteeth or combing hair), amnesia,and agnosia (loss of the ability to interpretsensory stimuli) as the disease progresses.Behavioral signs and symptoms?such as depression, apathy, andanxiety?typically are present in theearly stages, and delusions, hallucinations,and psychosis are prevalent duringthe latter stages.16,17 In the advancedstages, individuals also may presentwith extrapyramidal symptoms, such asgait disturbance, myoclonus, tremor,and urinary incontinence.16
Potential Warning Signs
Some warning signs of AD are as follows16:
- Memory loss that may affect job performance
- Difficulty in performing routine, familiar tasks
- Difficulty or problems with speech
- Decrease in judgment skills
- Difficulty with abstract thinking
- Disorientation as to time and place
- Difficulty in finding objects or misplacing items
- Changes in mood, personality, or behavior, such as agitation, aggression, and hallucinations
- Loss of initiative or motivation
- Impaired memory or thinking
- Impaired visual or spatial skills
Because AD progresses in severityover time, the disease generally is characterizedby the following stages: mild,moderate, and severe. During the mildstage, the individual may start to experiencesome memory loss, which may beinsignificant enough that others may notnotice a problem. Short-term memoryusually is affected first.
As the disease progresses from mildto moderate, the signs may becomemore noticeable to family and friends,because the patient may exhibit difficultyin self-care and in accomplishingeveryday tasks. At this stage, somebehavioral changes often are noted,such as frustration, anger, and anxiety.Usually at this stage, the need for caregiverassistance may become essentialfor the safety of the individual.
In the severe stage of AD, individualstypically are characterized as being solelydependent on the caregiver. Some patientsin this stage may experience loss ofbladder and bowel control and episodesof aggression. Table 1 lists, for each stageof AD, behavioral and cognitive changesas well as how the disease may affect theindividual's daily routine.18
To date, there is no definitive diagnostictest to ascertain whether an individualhas AD. Diagnosis, however, can bedetermined by a careful evaluation of thesymptoms manifested by the patient, acomprehensive assessment of thepatient's medical history in consultationwith family members, and a thoroughneurologic examination, possibly utilizingcomputerized tomography or magneticresonance imaging (MRI).19
In addition, the Mini Mental StateExamination (MMSE) can be used toevaluate memory, recognition, comprehension,and attention. The maximumscore that a patient can obtain is 30points. Mild dementia is suggested by ascore in the range of 20 to 24, moderatedementia is suggested by a scorerange of 13 to 20, and a score of =12indicates severe dementia. Typically, anindividual with AD has a decline of 2 to4 points per year on the MMSE.19 Today,clinicians can diagnose AD with up to90% accuracy, but a confirmation of thediagnosis can be made only at time ofautopsy.12
Because there is no definitive biologicaltest for confirming AD, the NationalInstitute of Neurological and CommunicativeDisorders and Stroke and theAlzheimer's Association combined effortsand created criteria to facilitatediagnosing of AD. The criteria also areintended to aid physicians in making adistinction between AD and other formsof dementia. Dementia typically is confirmedby the following criteria20:
- Clinical and neuropsychological examination
- Progressive worsening of memory and other mental functioning
- No disturbances of consciousness (ie, fainting)
- Symptoms beginning between ages 40 and 90
- No other disorders that might account for the dementia
As individuals get older, some will developa memory deficit greater than what isanticipated for their age group. Becauseother aspects of cognition are not affected,these individuals may not meet all theaccepted criteria for developing AD. Theseindividuals are believed to have mild cognitiveimpairment (MCI). Furthermore, it isestimated that ~40% of these individualswill develop AD within 3 years.20
Others, however, do not seem todevelop AD, at least in the time framestudied so far (up to ~6 years). Learningmore about the development and characteristicsof MCI is critical for helpinghealth care professionals to obtainknowledge for early diagnosis of AD.20
Currently there are no pharmacologicagents to halt the progression ofAlzheimer's disease. There are, however,FDA-approved agents for treating ADthat can stabilize or possibly slow theprogression of the classic symptomsassociated with the disease. It should beemphasized that these agents only slowthe progression of the disease. They areintended to assist in enhancing cognitivefunction, to delay continual cognitivedecline, and to prevent or decrease theincidence of disruptive behavior, as wellas enabling the patient to maintain a reasonablequality of life and independencefor as long as possible.12,13
To date, the FDA has approved 2 classesof drugs, acetylcholinesterase (AChE)inhibitors and N-methyl-D-aspartate(NMDA) antagonists, for treating certaincognitive symptoms of Alzheimer's disease,such as memory problems andother mental deficits.
The first AD medications to be approvedwere AChE inhibitors. Three ofthese drugs are now commonly prescribed?donepezil, approved in 1996;rivastigmine, approved in 2000; andgalantamine, approved in 2001. Tacrine,the first AChE inhibitor, was approved in1993, but it is rarely prescribed todaybecause of its associated side effects,including possible hepatoxicity.
Donepezil hydrochloride is a reversible,selective inhibitor of AChEchemically known as (+)-2,3-dihydro-5,6-dimethoxy-2-[[1-(phenylmethyl)-4-piperidinyl]methyl]-1 H-inden-1-one hydrochloride.Donepezil is believed to exert itspharmacologic action by enhancingcholinergic function. Donepezil is approvedby the FDA for the treatment ofmild-to-moderate dementia associatedwith AD.21 In 2006, the FDA also approveddonepezil for the treatment of severedementia associated with AD, therebymaking it the only pharmacologic agentapproved to treat all 3 stages of AD.22-24
The most common adverse effectsassociated with the use of donepezilinclude headache, nausea, diarrhea,anorexia, and fatigue. Dosing is 5 mg perday initially but may be increased to 10mg per day at bedtime after 4 to 6weeks. Donepezil is available in 5-and10-mg tablets as well as in an oral disintegrating-tablet formulation. Donepezilshould be administered in the eveningjust prior to bedtime and can be administeredwithout regard to food. The oraldisintegrating formulation should beallowed to dissolve on the tongue, followedby consumption of some water.
In a recent Mayo Clinic study, resultsshowed that donepezil slows the rate ofbrain shrinkage in some individuals withMCI, which is a pre-AD condition. Thestudy included 131 participants withMCI. The participants were divided into 3different groups, the members of whichtook donepezil, vitamin E, or a placebo.The participants were given a series ofMRIs to evaluate brain shrinkage. Theresults showed that brain shrinkage inindividuals treated with donepezil whowere apo E-IV carriers was 4.5% per year,compared with 6.14% for those whotook the placebo. Vitamin E had no effecton brain shrinkage in any of the studyparticipants.25
A review of 13 additional studies, usinga combined total of ~7300 participants,showed that donepezil, rivastigmine, andgalantamine seem equally effective inthe treatment of mild-to-moderate AD.26
Rivastigmine is classified as an intermediate-acting or pseudoirreversibleinhibitor of AChE that crosses theblood-brain barrier. It is approved forthe treatment of mild-to-moderatedementia of AD.27
Initial dosing is 1.5 mg twice a day. Ifthe drug is tolerated for at least 2 weeks,then the dosing may be increased to 3mg twice daily. Increases to 4.5 and 6 mgtwice a day should be attempted onlyafter at least 2 weeks at the previousdose. The maximum dose is 6 mg twicedaily. Common adverse effects includenausea, vomiting, abdominal pain, andloss of appetite.20,27
Rivastigmine is available in 1.5-, 3-,4.5-, and 6-mg capsules. It also is availablein a 2-mg/mL oral solution.
The emergence of newer therapiesmay be instrumental in the quest fortreating AD. Researchers are investigatingthe possibility of a topical drug-deliverysystem, which appears to minimizeadverse effects. The results of the IDEALstudy, which involved 1195 patients,were presented at the InternationalConference on Alzheimer's Disease andRelated Disorders in Madrid, Spain, in2006.28,29 The study included a 24-weekexperiment, with ~600 participants from21 countries. The participants ranged inage from 50 to 85 and were diagnosedwith moderate-stage AD. They weregiven a placebo or a small or large versionof the rivastigmine patch. In addition,~600 other participants with thesame criteria were administered a standarddose of rivastigmine bid in the oralformulation or a placebo.
The researchers reported that, whencomparing the placebo results withthose with the patch, the patch induced"significant benefits" with regard to thepatient's cognitive function as well as theability to perform routine daily activities.The findings further showed that the outcomesof individuals with the patch wereequivalent to those achieved by those onthe oral formulation.
The patch appeared to lessen the incidenceof adverse effects. In the studygroup, 7% of the participants with thepatch experienced nausea, whereas 23%of those taking the oral formulation experiencednausea.
The investigators found that the topicalformulation was well-tolerated.Approximately 8% of the study participantsusing this drug-delivery systemexperienced moderate-to-severe erythemaof the skin. It is possible that thispatch may be available sometime in2007, pending FDA approval.28,29
Galantamine (Razadyne; formerlyReminyl)
Galantamine hydrobromide is a tertiaryalkaloid and is a competitive andreversible inhibitor of AChE. Althoughthe precise mechanism of galantamine'saction is unknown, it is theorizedto exert a therapeutic effect by enhancingcholinergic function. This action isaccomplished by increasing the concentrationof acetylcholine through reversibleinhibition of its hydrolysis bycholinesterase.30
The manufacturer's recommendeddose is 4 mg bid with meals, titratedmonthly to 12 mg bid. Common adverseeffects associated with the use of galantaminehydrobromide include nausea,vomiting, and diarrhea.30 Galantamineshould be administered with food andwater. It is available as 4-, 8-, and 12-mgtablets and as an oral solution of 4mg/mL, as well as extended-release capsulesin 8-, 16-, and 24-mg dosages foronce-a-day dosing.
Memantine (Namenda)In October 2003, the FDA approvedmemantine for the treatment of moderate-to-severe AD. This agent is classifiedas the first NMDA receptor antagonist. Itaids in protecting nerve cells in the brainfrom an excess of glutamate, which isthe neurotransmitter that plays a role inneurodegenerative diseases such asAD.31 The presumption is that this agentexerts its action as an uncompetitiveopen-channel NMDA receptor antagonistthat binds to the NMDA-receptor-operatedcation channels.31
Clinical studies have shown thatmemantine actually may improve memoryfunction and prolong independenceand quality of life in some patients withAD.31 This agent can be used as monotherapyor in conjunction with AChEinhibitors. Research has shown that theuse of memantine in conjunction with acholinesterase inhibitor has producedimprovement with regard to the performanceof everyday functions.
Memantine is available in 5-and 10-mg tablets. The usual starting dosageregimen is 5 mg once daily, with thedosage eventually titrated up to thedesired dose of 20 mg per day. Thedosage is increased in increments of 5 to10 mg per day in 2 divided doses, then to15 mg per day (administered as 5 mg and10 mg in separate doses), then to 20 mgdaily as 10 mg bid. This agent can betaken with or without meals. The recommended minimal time interval betweendosage increases is 1 week. Followingoral administration, memantine is highlyabsorbed, with peak concentrationsreached in 3 to 7 hours.
The manufacturer cautions that, in certaincases, some agents such as carbonicanhydrase inhibitors and sodium bicarbonate,which increases urinary pH, maydecrease the urinary elimination ofmemantine, resulting in increased plasmalevels of this agent.31 The most frequentlyreported side effects includeataxia, hypokinesia, anemia, dizziness,headache, and constipation.
Pharmacists may receive inquiriesfrom patients about alternative/complementarymedications. Herbal and dietarysupplements such as ginkgo biloba, coenzymeQ, omega-3 fatty acids, or vitamin Eoften are promoted for preventing ortreating AD. To date, no scientific studieshave proven the effectiveness of the useof these agents with regard to AD.Ongoing trials are studying the effects ofginkgo biloba, coenzyme Q10, and vitaminE to determine their effects regardingAD. More information on these trials canbe found at the US National Institutes ofHealth Clinical Trials Web site atwww.clinicaltrials.gov. Pharmacists canbe instrumental in screening for potentialdrug interactions as well as possible contraindications.Pharmacists always shouldadvise patients to discuss the use ofthese agents with their primary healthcare provider prior to using them.
Recent Developments: ClinicalTrials and Ongoing ResearchStudies
Currently, >100 clinical studies arebeing conducted to explore other meansof understanding and treating AD. Theseclinical trials may one day bring relief tothe millions affected by this disease. Formore in-depth information on these clinicaltrials, visit www.clinicaltrials.gov.Examples of these clinical trials are listedin Table 2.32,33
Researchers are continually investigatingpossible causes and preventivemeasures with regard to AD. Presently,clinical trials are studying the possiblelink between AD and diabetes. One of thetrials is researching whether the diabetesagent rosiglitazone can either slowor halt the progression of AD.34 In preliminarytrials, the use of rosiglitazonedemonstrated beneficial results inpatients who did not have the apo E-IVgene.34 Because the current diabetes epidemicin the United States is largelyattributed to the growing number ofobese patients, some researchers theorizethat it is possible to utilize theincrease in obesity as an indicator in predictingincreases in cases of AD.34 Studiesalso suggest that individuals with weightissues at middle age may be at a greaterrisk for the development of AD.33,34
Geldmacher et al conducted a smallstudy on the use of the diabetes agentpioglitazone and its effects on nondiabeticswith AD. This study was conducted todetermine the safety of long-term use ofthis agent in this patient population. Theresearchers also investigated whetherthe drug could possibly slow the progressionof AD. The results suggested thatthose taking pioglitazone experiencedless worsening of the disease on someassessments. Due to the promisingresults of this effort, a more comprehensivestudy involving a larger group maybe beneficial.35,36
The results of another trial were publishedin the February 2006 issue of theArchives of General Psychiatry. Thisstudy, based on a sample of ~12,000Swedish twins, of whom 25% were identical,found that 80% of the risk of AD isdue to genetics.37,38 Thus, it appears thatgenetic factors may outweigh environmentalfactors with regard to the risk ofdeveloping AD. Furthermore, in studyingidentical twins, it was found that thedevelopment of AD in one twin did notmean that the other twin would definitelydevelop AD. In 45% of the cases, if onemale identical twin developed AD, thenthe other twin would, too. The rateamong female identical twins was60%.37,38 The differences between menand women could possibly be attributedto the fact that women tend to have alonger life span than men.
An article in the on-line July 2006 issueof Lancet Neurology reported thatincreased blood levels of specific formsof amyloid beta (A?) proteins were associatedwith an increased incidence of ADas well as other forms of dementia. In thestudy, 1756 individuals over the age of 55years were evaluated for 9 years. Duringthat time period, 392 participants developedsome form of dementia. Theresearch demonstrated that subjectswith low blood levels of A?1-42 and highlevels of A?1-40 at the start of the studyhad a greater than 10-fold risk of likelydeveloping dementia, compared withthose participants with low levels of eachprotein.39
In recent studies, researchers atNorthwestern University have developedan innovative orally administered agentthat is designed to specifically target suppressionof brain cell inflammation andneuron loss that is often associated withAD. The compound, known as MW01-5-188WH, exerts its therapeutic action byselectively inhibiting cytokines by glia.40,41Glia are integral components of the centralnervous system and are overactivatedin certain neurodegenerative diseasessuch as AD.41
In another recent study, researchersdeveloped a computer-aided analysistechnique to identify early cellular damagein patients with AD. The methodsmay enable earlier diagnosis of AD, thuspossibly slowing the progression of thedisease. The 13 study patients, with MCI,and 13 elderly control subjects underwentMRI of the brain and performedrecall tasks. On the MRI images, apparentdiffusion coefficient values were measuredin the gray and white regions byusing the computer-analysis program.The findings were compared betweenthe 2 groups. The results showed thatindividuals with MCI who seem to belikely to further progress to AD may beable to commence early treatment interventions.42
An AD Vaccine
At a recent conference on AD, researcherssuggested that they are makingprogress in the development of a vaccinefor AD. An older trial for a vaccinewas discontinued in 2002 when 6% ofthe study participants developed encephalitis,while others developed brainshrinkage.The new methods of approachdo not seem to pose these adverseevents. Currently, 2 trials in differentphases are investigating the passiveimmunization approach.41
Other Pharmacologic Agents Usedin the Management of AD
In some cases, it may be necessary forphysicians to prescribe other classes ofpharmacologic agents, such as antianxietydrugs, antipsychotics, and antidepressants.These agents may be used totreat patients with AD who are exhibitingspecific behavioral symptoms, such asdepression, agitation, hallucinations, orsleep disturbances. In these instances,the patients were not responding to nonpharmacologicbehavioral strategies.These agents are prescribed as perphysician discretion and based on specificpatient need.
Caregiver Strategies andNonpharmacologic Therapies
It is important to note that most individualswith AD do not die from the diseaseitself but rather from complicationsof a secondary illness such as pneumonia.In some cases, when patients withAD are unable to care for themselves, therisk increases of developing other healthconcerns?such as pneumonia, infections,and injuries or complications dueto falls.
A diagnosis of AD affects not only thepatient, but the caregivers as well.According to the Alzheimer's Association,approximately 1 in every 10 individualshas a family member with AD.Caregivers must learn to cope with theprogressive physical and mental changesin their loved ones and to deal with theemotional and physical stress oftenassociated with caring for such a patient.The care of a patient with AD requiressignificant time and resources and canbe demanding, difficult, and overwhelmingat times.
Because AD is a progressive disease,decisions about care need to beplanned in advance. These decisionsdepend on the home environment, theavailability of family members and/orthe ability of caregivers to provide assistancein day-to-day activities, maintainingfinancial resources, and routinemedical care.
The Role of the Pharmacist
In almost every area of pharmacypractice, pharmacists are very likely toencounter a patient with AD and/or acaregiver. Therefore, it is imperativefor pharmacists to keep abreast ofnew developments in research andpharmacologic therapies regarding thedisease.
Pharmacists can be a vital resource forboth patients and their caregivers, therebyimproving quality of life. A comprehensiveunderstanding of the etiology,pathophysiology, and stages of AD, aswell as pharmacologic therapy, is imperativeto provide effective care to thepatient.
Pharmacists can assist patients withAD through monitoring drug regimensfor potential drug interactions as well aspossible contraindications. More importantly,pharmacists always should try todemonstrate empathy toward patientswith AD and their caregivers, keepingthem informed about new developmentsin the fight against this condition andsuggesting resources of information forthem.
Caring for a patient with AD involvesmore than drug treatment. Caregiversshould be encouraged to join a local supportgroup and to take care of themselvesand seek assistance when warranted.
During counseling, pharmacists canprovide patients and their caregivers withvarious suggestions for techniques thatmay aid in the management of AD, suchas the use of memory aids or schedules.Examples of memory aids include a list ofdaily routines, important telephone numbersin case of an emergency, andinstructions on how to perform varioustasks. In addition, pharmacists can makerecommendations for creating a safeenvironment and establishing an exerciseroutine, if appropriate.44
Currently, there are no cures for AD,but progress has been made over thelast 15 years (Table 345). The prospect forpossible treatments and a cure lies in theongoing research. Maybe one day hopewill become reality and benefit the millionsof individuals affected by the disease.It is clear that, as the number of ADcases continues to increase, moreresearch is needed to solve the mysteryof this disease that affects the lives of somany individuals.
Yvette C. Terrie, BSPharm, RPh is a Clinical Pharmacy Writer based in Haymarket,Va.
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Pharmacy Times/Ascend Media Office of Continuing Professional Education is accreditedby the Accreditation Council for Pharmacy Education as a provider of continuing pharmacyeducation. This program is approved for 2.5 contact hours (0.25 CEUs) under the ACPEuniversal program number of 290-000-06-017-H01. The program is available for CE creditthrough January 1, 2010.
(Based on the article starting on page 103) Choose the 1 most correct answer.
1. Alzheimer's disease (AD) wasfirst recognized in what year?
2. Since 1980, the number of casesof AD in the United States has:
- Remained the same.
3. AD accounts for what percentageof dementia among the elderlypopulation?
4. AD affects what percentage ofindividuals over 85 years of age inthe United States?
5. What are the 2 forms of AD?
- Genetic and environmental
- Familial and sporadic
- Mild and moderate
- None of the above
6. Which of the following is themost well-documented risk factorassociated with the development ofAD?
7. A score of 21 on the Mini MentalState Examination is indicative ofwhat stage of dementia?
- None of the above
8. The apolipoprotein E (apo E) geneis found on which chromosome?
9. Between 35% and 50% of individualswith AD carry some form ofwhat gene?
- Apo-E-IV gene
- Apo-E-V gene
- Apo-E-II gene
- Apo-E-III gene
10. How many individuals areaffected by AD worldwide?
- 4.5 million
- 28 million
- 11 million
- 16 million
11. How many pharmacologicclasses are currently FDA-approvedfor treating dementia associatedwith AD?
- None of the above
12. What is the average life span ofa patient with AD following diagnosis?
- 10 to 12 years
- 1 to 5 years
- 1 to 2 years
- 8 to 20 years
13. The average cost of caring for apatient with AD is estimated to be:
- $18,400 to $36,000.
- $75,000 to $100,000.
- $20,000 to $25,000.
- $5000 to $10,000.
14. Which drug is rarely prescribedbecause of its adverse effects?
15. Memantine is classified as a(an):
- Cholinesterase inhibitor.
- N-methyl-D-aspartate (NMDA)receptor antagonist.
- Tertiary alkaloid.
- N-methyl-D-aspartate (NMDA)receptor agonist.
16. MPC-7869, r-flurbiprofen is classifiedas a (an):
- Uncompetitive NMDA receptorchannel blocker.
- Neurotrophic agent.
- Selective amyloid-loweringagent.
- ?-secretase inhibitor.
17. Which agent(s) is (are) approvedfor the treatment of severedementia?
- B and C
18. Common adverse effects suchas anemia, dizziness, and headacheare associated with the use of:
19. Which of the following agentshas been studied for a topical formulation?
20. Which of the following pharmacologicagents is available in anextended-release form?
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