MEDICAL CONDITIONS
Alzheimer's Disease Medical Author: Yuri Bronstein, M.D.
Medical Editor: Stefan M. Pulst, M.D.
What is Alzheimer's disease?
Alzheimer's disease (AD) is a progressive disease of the brain that is characterized by impairment of memory and a disturbance in at least one other thinking function (for example, language or perception of reality). Many scientists believe that AD results from an increase in the production or accumulation of a specific protein (beta-amyloid protein) that leads to nerve cell death. Loss of nerve cells in strategic brain areas, in turn, causes deficits in the neurotransmitters, which are the brain's chemical messengers.
Alzheimer's disease is not a normal part of aging and is not something that inevitably happens in later life. Rather, it is one of the dementing disorders, which are a group of brain diseases that result in the loss of mental and physical functions.
Who develops Alzheimer's disease?
The main risk factor for AD is increased age. As the population ages, the frequency of AD continues to increase. 10 % of people over age 65 and 50 % of those over 85 have AD. The number of individuals with AD is expected to be 14 million by the year 2050. In 1998, the annual cost for the care of patients with AD in the United States was approximately $40,000 per patient.
There are also genetic risk factors for AD. The presence of several family members with AD has suggested that, in some cases, heredity may influence the development of AD. A genetic basis has been identified through the discovery of mutations in several genes that cause AD in a small subgroup of families in which the disease has frequently occurred at relatively early ages (beginning before age 50). Some evidence points to chromosome 19 as implicated in certain other families in which the disease has frequently developed at later ages.
Studies of aging and dementia (general mental deterioration) in the general population have identified three groups of subjects; persons who are not demented, those who are demented, and individuals who cannot be classified because they have a cognitive (thinking, memory) impairment, but do not meet the criteria for dementia.
What are the symptoms of Alzheimer's disease?
The onset of AD is usually very slow and gradual. Over time, however, it follows a progressively more serious course. Among the symptoms that typically develop, none is unique to AD at its various stages. It is important that suspicious changes be thoroughly evaluated before they become inappropriately or negligently labeled AD.
Ten Warning Signs of Alzheimer's Disease
The Alzheimer's Association has developed the following list of warning signs that include common symptoms of AD. Individuals who exhibit several of these symptoms should see a physician for a complete evaluation. - Memory loss that affects job skills
- Difficulty performing familiar tasks
- Problems with language
- Disorientation to time and place
- Poor or decreased judgment
- Problems with abstract thinking
- Misplacing things
- Changes in mood or behavior
- Changes in personality
- Loss of initiative
Problems of memory, particularly recent or short-term memory, are common early in the course of AD. For example, the individual may, on repeated occasions, forget to turn off the iron or fail to recall which of the morning's medicines were taken. Mild personality changes, such as less spontaneity, or a sense of apathy and a tendency to withdraw from social interactions, may occur early in the illness.
As the disease progresses, problems in abstract thinking or in intellectual functioning develop. The person may begin to have trouble with figures when working on bills, with understanding what is being read, or with organizing the day's work. Further disturbances in behavior and appearance may also be seen at this point, such as agitation, irritability, quarrelsomeness, and a diminishing ability to dress appropriately.
Later in the course of the disorder, affected individuals may become confused or disoriented about what month or year it is, be unable to describe accurately where they live, or be capable of correctly naming a place being visited. Eventually, patients may wander, be unable to engage in conversation, seem inattentive and erratic in mood, appear uncooperative, and lose bladder and bowel control. In extreme cases, persons may become totally incapable of caring for themselves, if the final stage is reached. Death then follows, perhaps from pneumonia or some other problem that occurs in severely deteriorated states of health. The average course of the disease from the time it is recognized to death is about 6 to 8 years, but it may range from under 2 to over 20 years. Those who develop the disorder later in life may die from other illnesses (such as heart disease), before AD reaches its final and most serious stages.
Mild cognitive impairment
In recent years, more attention has turned to the transitional period of cognitive (thinking, memory) impairment between normal aging and early AD. This condition is referred to as mild cognitive impairment. Affected individuals have problems with memory but are otherwise able to function well. The criteria for mild cognitive impairment are as follows: - Memory complaint, preferably corroborated by a family member.
- Objective memory impairment (as determined by a formal test of memory).
- Normal general cognitive function (Abilities to think and function are normal.)
- Intact activities of daily living.
The importance of early detection and ability to treat mild cognitive impairment and thus delay the progression of this condition to AD would be of great benefit. Several studies have recently addressed this issue and estimated the risk of progression from mild cognitive impairment to AD as being between 6% and 25% per year. This means that between 6% and 25% of those with mild cognitive impairment will develop AD in any given year.
Patients with mild cognitive impairment should be recognized and monitored for cognitive and functional decline due to their increased risk for subsequent dementia (general mental deterioration).
What are the causes of Alzheimer's disease?
With the exception of rare cases of familial AD, in whom the disease is caused by mutations (changes in the DNA) of a single gene, most cases of AD are probably caused by a variety of factors acting together. Cases without a family history are called "sporadic." The study of familial AD, however, has uncovered several proteins that are not only important for familial, but also for sporadic AD. These are the amyloid precursor protein (APP) and two presenilins. APP is a major component of plaques (abnormal deposits of proteins in the brain).
The break-down (faulty cleavage) of APPs likely increases their propensity to combine (aggregate) in plaques. Presenilins, on the other hand, are involved in the splitting (cleavage) of APP. Mutations in the genes that encode APPs and the presenilins can cause AD. This means that individuals carrying these mutations have a very high probability of developing AD.
Changes in other genes may not cause AD, but they may increase the risk of developing AD. The best-studied "risk" gene is the one that encodes apolipoprotein E (apoE). Certain forms (alleles) of this gene can increase the risk for AD. This effect is particularly striking in the setting of a positive family history for AD.
The apoE gene has three different forms (alleles) -- apoE2, apoE3, and apoE4. ApoE3 is the most common form in the general population. However, apoE4 occurs in approximately 40 % of all late-onset AD patients. People who inherit two apoE4 alleles (one from the mother and one from the father) are several times more likely to develop AD than those who have two of the more common E3 version. The least common allele, E2, lowers the risk of AD. People with one E2 and one E3 gene have only one-fourth the risk of developing Alzheimer's as do people with two E3 genes.
Since the 1970's, abnormalities in the brain's chemical messengers, called neurotransmitters, have been identified in patients with AD. Acetylcholine is a critical neurotransmitter in the process of forming memories. This chemical messenger is abundant in the nerve cells of the hippocampus and cerebral cortex, the regions that are devastated by AD. Levels of acetylcholine fall sharply in people with AD. Other neurotransmitters have also been implicated in AD. For example, serotonin, somatostatin, and noradrenaline levels are lower than normal in some Alzheimer's patients. Deficits in these substances may contribute to the memory and behavioral abnormalities in AD.
In addition to the known risk factors of age and family history, several other possible risk factors have been identified. Some studies have found that AD occurs more often among people who suffered traumatic head injuries earlier in life. Women may have a higher risk of the disease, although their higher rates may only reflect the effects of age, because women have longer life spans on average than do men. In addition, lower educational levels may increase the risk. It is not know whether this reflects a decreased "cognitive reserve" or other factors associated with a lower educational level.
How is the diagnosis of Alzheimer's disease made?
Clinical Features of Alzheimer's Disease
The "clinical" features of AD, as opposed to the "tissue" changes, are threefold: - Dementia - general mental deterioration, including the significant loss of intellectual abilities, such as memory capacity, that are severe enough to interfere with social or occupational functioning;
- Insidious (gradual and subtle) onset of symptoms - subtle, progressive, and irreversible course with documented deterioration over time; and
- Exclusion of all other specific causes of dementia by history, physical examination, laboratory tests, psychometric, and other studies (see below).
The essential feature of dementia is impairment in short and long-term memory that is associated with deficits in abstract thinking, impaired judgment, or personality change. Theses disturbance are severe enough to interfere significantly with work, usual social activities, or relationships with others.
Diagnosis By Exclusion
Based on these criteria, the clinical diagnosis of AD has been referred to as a "diagnosis by exclusion," and one that can only be made in the face of clinical deterioration over time. There is no specific clinical test or finding that is unique to AD. Hence, all disorders that can exhibit similar symptoms must be systematically excluded or ruled out. This explains why diagnostic workups of individuals at-risk for AD can be so frustrating for the patient and family alike. They are not told that AD has been specifically diagnosed, but that other possible diagnoses have been dismissed, leaving AD as the likely diagnosis by the process of elimination.
What other conditions should be screened for?
There are many conditions that affect the brain and result in intellectual, behavioral, and psychological dysfunction. These disorders represent a broad grouping of diseases and include AD. Some of these disorders that can cause clinical problems similar to those of AD may be reversible or controlled with proper diagnosis and treatment. These other conditions include: - Side effects of medications: Unusual reactions to medications, too much or too little of prescribed medications, and combinations of medications which, when taken together, can cause adverse side effects.
- Psychiatric disorders: Severe forms of depression can cause problems with memory and concentration that initially may be indistinguishable from the early symptoms of AD. Sometimes, these conditions, referred to as pseudodementia, can be reversed. Other psychiatric problems can similarly masquerade as AD, and, like depression, respond to treatment. Studies have shown that persons with depression and coexistent cognitive (thinking, memory) impairment are highly likely to have an underlying dementia when followed for several years.
- Substance Abuse: Abuse of legal and/or illegal drugs and alcohol abuse.
- Metabolic Disorders: Thyroid problems, nutritional deficiencies such as vitamin B 12 deficiency, anemias, etc.
- Circulatory Disorders: Heart problems, strokes, etc.
- Neurological Disorders: Normal-pressure hydrocephalus , multiple sclerosis , etc.
- Infections: Especially viral or fungal infections of the brain.
- Trauma: Injuries to the head.
- Toxic Factors: Carbon monoxide, methyl alcohol, etc.
- Tumors: Any type within the skull, whether originating or metastasizing there.
- Syphilis: Screening for this disease in a patient with dementia is only recommended if the patient has some specific risk factor or evidence of a prior syphilitic infection, or if the patient resides in one of the few areas in the U.S. with high numbers of syphilis cases (i.e., southern states and Midwest).
The Importance of Comprehensive Clinical Evaluation
Because of the many other disorders that can be confused with AD, a comprehensive clinical evaluation is essential in arriving at a correct diagnosis of symptoms that resemble those of AD. Such an assessment should include at least three major components; (1) a thorough general medical workup, (2) a neurological examination, and (3) a psychiatric evaluation that may include psychological and memory testing. The family physician can be consulted about the best way to get the necessary examination.
The American Academy of Neurology recently published guidelines to include imaging of the brain in the initial evaluation of patients with dementia. These studies are either a noncontrast CT scan or an MRI scan. Other imaging procedures that look at the function of the brain (functional neuroimaging), such as SPECT, PET, and fMRI, may also be helpful.
Despite many attempts, identification of a blood test to diagnose AD has remained elusive. There has been intense interest in developing markers for AD in the blood and particularly in the cerebrospinal fluid (CSF) (the fluid surrounding the brain and the spinal cord). CSF b-amyloid 1-42, CSF tau, CSF AD7C-NTP have all been studied, but are currently not routinely recommended in determining the diagnosis of AD at this time.
What is the prognosis for a person with Alzheimer's disease?
Though the changes just described represent the general range of symptoms for AD, the specific problems, along with the rate and severity of decline, can vary considerably in different individuals. Indeed, most persons with AD can function at a reasonable level and remain at home far into the course of the disorder. Moreover, throughout much of the course of the illness, individuals maintain the capacity for giving and receiving love, sharing warm interpersonal relationships, and participating in a variety of meaningful activities with family and friends.
A person with AD may no longer be able to do math, but still be able to read a magazine with pleasure for months or years to come. Playing the piano might become too stressful in the face of increasing mistakes, but singing along with others may still be satisfying. The chessboard may have to be put away, but playing tennis may still be enjoyable. Thus, despite the many exasperating moments in the lives of Alzheimer patients and their families, many opportunities remain for positive interactions. Challenge, frustration, closeness, anger, warmth, sadness, and satisfaction may all be experienced by those who work to help the person with AD.
The reaction of an individual to the illness, and his or her capacity to cope with it, also vary and may depend on such factors as lifelong personality patterns and the nature and severity of stress in the immediate environment. Depression, severe uneasiness, paranoia, or delusions may accompany or result from the disease, but these conditions can often be improved by appropriate treatments. Although there is no cure for AD, treatments are available to alleviate many of the symptoms that cause suffering.
Some people have the disease only for the last 5 years of life, while others may have it for as many as 20 years. The most common cause of death in AD patients is infection.
What treatment and management options are available for Alzheimer's disease?
The management of AD consists of medication-based and non-medication based treatments. Treatments aimed at changing the underlying course of the disease (delaying or reversing the progression) have so far been largely unsuccessful. Medicines that restore the deficit (defect), or malfunctioning, in the chemical messengers of the nerve cells (neurotransmitters), such as the cholinesterase inhibitors, have been shown to improve symptoms. Finally, medications are available that deal with the psychiatric manifestations of AD.
Various other agents have been tried in an attempt to modify the course of AD, including ginkgo biloba, anti-inflammatory agents, and prednisone . However, the use of these agents is so far not supported by adequate available evidence. Estrogen should not be routinely prescribed to treat AD.
Cholinesterase inhibitors (ChEIs)
ChEIs are the only agents that are approved by the FDA for the treatment of AD. ChEIs are medicines that restore the defect, or malfunctioning, in the chemical messengers of the nerve cells. These chemical messengers are referred to as neurotransmitters. ChEIs impede the action of an enzyme that inactivates the chemical messengers. Therefore, in the presence of ChEI medicines, more chemical messengers are available to transmit the messages of the nerves in the brain.
Four ChEIs have been approved; tacrine (Cognex), donepezil hydrochloride (Aricept) , rivastigmine , and galantamine . Significant treatment effects have been demonstrated indicating that this class of agents is consistently better than a placebo. However, the disease eventually continues to progress despite treatment and the average effect on mental functioning has only been modest.
ChEIs have effects on many aspects of daily living. Head-to-head comparative trials evaluating the relative usefulness of ChEIs have not been conducted. Available data do not suggest major differences in the effectiveness among different ChEIs, although side-effects may vary slightly.
The principal side effects of ChEIs involve the gastrointestinal system and include nausea, vomiting, cramping, and diarrhea . Tacrine is the only agent that is associated with liver toxicity and the use of this agent requires close hematologic (blood test) monitoring, including liver function tests every other week during the period of dose escalation and every 3 months thereafter. Rivastigmine has been associated with weight loss and the monitoring of the patient's weight is recommended when using this drug.
The occurrence of side effects for ChEIs is related to the rate of dose increase. Therefore, doctors gradually increase the dose at intervals until the optimal therapeutic dosage has been reached. The interval between dose increases may be extended or the dose step size may be reduced accordingly if side effects occur. Between 75% and 90% of patients will tolerate therapeutic doses of ChEIs.
Initiating, Maintaining, and Terminating Treatment
Treatment with ChEIs should be initiated at the time the diagnosis of AD is established. In other words, treatment should not be delayed until more severe deterioration has occurred. Evidence from studies in which the start of treatment has been delayed suggests that such delay reduces the maximum possible response to ChEIs. Patients should be treated for 3 to 5 years until the severity of clinical deficit is such that little therapeutic benefit is likely. Treatment trials using ChEIs in patients residing in nursing homes demonstrate that patients with moderately severe dementia continue to show cognitive and behavioral responses. The placement of the patient in a nursing home or the emergence of moderately severe dementia are not in themselves reasons for discontinuing ChEIs. Interruptions in ChEIs therapy should be minimized. There is evidence that the response following reinitiation of ChEIs after a period without therapy is less that obtained with the first start of treatment.
When continuing benefit is in doubt or when the family or medical practitioner desires to discontinue treatment with ChEIs, the agent should be withdrawn with close observation. The therapeutic dose can be reduced by 50% every 2 weeks. The patient should be monitored at the time of dose reduction. If there is deterioration in cognition, behavior, or function, thereby suggesting that the patient is continuing to benefit from the treatment, then an optimal dosage should be restored.
Switching from one ChEI to another has not been well studied. The prescribing of two ChEIs at the same time is not recommended because there may be side effects. Doctors' experience with many different patients indicates that those who fail to respond to one ChEI may respond to another.
There is substantial individual variability in a patient's response to ChEIs and predictors of this variability are being actively investigated. Patients with low MMSE (mental exam) scores have larger cognitive responses (ability to think), and patients with more severe behavioral disturbances also demonstrate a greater benefit when treated with ChEIs.
Recent clinical trials have begun to include additional features, such as secondary effects on caregivers, delay to nursing home placement, pharmacoeconomic outcomes (cost of drug treatments), and impact on quality of life, as measures for the potential use of ChEIs. These studies may further influence the use of ChEIs in clinical practice.
Treatment of psychiatric symptoms
The principal treatable neuropsychiatric disturbances in AD are: - Agitation
- Depression
- Psychosis
- Anxiety
Patients with AD may respond well to antipsychotics, antidepressants, anticonvulsants, and other psychopharmacological (medicines for the treatment of psychiatric disturbances) agents. Target symptoms should be clearly specified and documented and the treatment response should be evaluated regularly.
Agitation occurs in as many as 70% of patient with AD and is more common as the disease progresses. Classes of agents used to treat agitation include antipsychotics, mood-stabilizing anticonvulsants, trazodone , anxiolytics, and beta-blockers. Available evidence suggests that antipsychotics, trazodone , or anticonvulsants have the greatest effectiveness in reducing agitation. Atypical antipsychotic agents such as clozapine , risperidone , olanzapine , quetiapine , and ziprasidone appear to have advantages over the older antipsychotic agents based on their side effect profiles and the patients' ability to tolerate them.
Psychosis is common in AD, with a frequency of about 50% over the lifetime of an AD patient. Atypical antipsychotics are the treatment of choice. Risperidone and olanzapine have an established benefit in this regard and quetiapine and ziprasidone may be useful. Sedation (dullness, calmness) is the most common side effect noted in patients receiving antipsychotics.
Depressive symptoms are frequent in AD and occur in as many as 50% of patients. Major depression is more unusual. The treatment of depressive symptoms commonly consists of selective serotonin reuptake inhibitors (SSRIs), such as sertraline , citalopram , or fluoxetine . Full doses of the SSRIs are generally tolerated in the elderly, which is unlike most other psychotropic agents wherein lower doses are typically used. Alternatively, tricyclic antidepressants with few anticholinergic (dry mouth, constipation , memory problems) side effects, such as nortriptyline , or combined noaradrenergic and serotonergic reuptake inhibitors, such as venlafaxine , have been used.
Anxiety is a common symptom in AD and affects 40% to 50% of patients at some point in the course of the illness. Most patients do not require medicines for the treatment of their anxiety. For those requiring medicines, benzodiazepines are best avoided because of their potential adverse effects on the thinking process. Nonbenzodiazepine anxiolytics, such as buspirone or SSRIs, are preferred.
Difficulty sleeping (insomnia) occurs in many patients with AD at some point in the course of their disease. Agents that are useful in treating insomnia in AD patients include moderately short-acting benzodiazepines, such as temazepam , nonbenzodiazepine sedative hypnotics, such as zolpidem or zaleplon , or sedating antidepressants, such as trazodone. Sleep improvement measures, such as sunlight, adequate treatment of pain, and limiting nighttime fluids, should also be implemented.
Potential and future therapies for AD
Advances in our understanding of the brain abnormalities that occur in AD will provide the framework for new targets of treatment that are more focused on altering the course of the disease. Many compounds, including anti-inflammatory agents, are being actively investigated. Clinical trials using specific cyclooxygenase inhibitors (COX-2), such as rofecoxib and celecoxib , are underway.
Preliminary animal experiments using immunization with beta-amyloid antibodies (amyloid vaccine) have shown very promising results. Clinical trials for patients with AD are underway and results will be highly anticipated.
Caring for the caregiver and Alzheimer's disease resources
Caring for the caregiver is an essential element of managing the patient with AD. Caregiving is a distressing experience. On the other hand, caregiver education delays nursing home placement of AD patients. The 3Rs - Repeat, Reassure, and Redirect - can help caregivers reduce troublesome behaviors and limit the use of pharmacological (medicines) intervention. The short-term educational programs are well liked by family caregivers and can lead to a modest increase in disease knowledge and greater confidence among caregivers. Educational training for staffs of long-term care facilities can decrease the use of antipsychotics in AD patients.
Caregivers should be directed to support services, particularly the Alzheimer's Association (1-800-272-3900, www.alz.org/chapter/). - Alzheimer's disease is a brain disease of unknown cause that leads to dementia.
- Most patients with Alzheimer's disease are over 65 years of age.
- There are 10 classic warning signs of Alzheimer's disease: memory loss that affects job skills, difficulty performing familiar tasks, problems with language, disorientation to time and place, poor or decreased judgment, problems with abstract thinking, misplacing things, changes in mood or behavior, changes in personality, and loss of initiative.
- Patients with symptoms of dementia should be thoroughly evaluated before they become inappropriately or negligently labeled Alzheimer's disease.
- Although there is no cure for Alzheimer's disease, treatments are available to alleviate many of the symptoms that cause suffering.
- The management of AD consists of medication-based and non-medication based treatments organized to care for the patient and family. Treatments aimed at changing the underlying course of the disease (delaying or reversing the progression) have so far been largely unsuccessful. Medicines that restore the defect, or malfunctioning, in the chemical messengers of the nerve cells have been shown to improve symptoms. Finally, medications are available that deal with the psychiatric manifestations of AD.
Sources Of Help
State Agencies on Aging
These agencies coordinate services for older Americans, providing information on services, programs, and opportunities. (*In-State Toll Free Number)
Services within the United States:
Alabama
Executive Director, Alabama Commission on Aging
770 Washington Avenue, Suite 470
RSA Plaza
Montgomery, Alabama 36130
(205) 242-5743
Alaska
Executive Director, Older Alaskans Commission
P.O. Box 110209
Juneau, Alaska 99811-0209
(907) 465-3250
Arizona
Administrator, Aging and Adult Administration
Department of Economic Security
1789 West Jefferson - 950A
Phoenix, Arizona 85007
(602) 542-4446 *1-(800) 352-3792
Arkansas
Director, Division of Aging and Adult Services
Arkansas Department of Human Services
1417 Donaghey Plaza South
P.O. Box 1437, Slot 1412
Little Rock, Arkansas 72201-1437
(501) 682- 2441
California
Director, California Department of Aging
1600 K Street
Sacramento, California 95814
(916) 322-5290
Colorado
Director, Aging and Adult Services
Department of Social Services
1575 Sherman Street, 10th Floor
Denver, Colorado 80203-1714
(303) 866-5905
Connecticut
Director, Division of Elderly Services
25 Sigourney Street, 10th Floor
Hartford, Connecticut 06106-5033
(860) 424-4966
Delaware
Director, Delaware Division on Aging
Department of Health and Social Services
1901 North Dupont Highway - Second Floor
New Castle, Delaware 19720
(302) 577-4791 *1-(800) 223-9074
District Of Columbia
Director, District of Columbia Office on Aging
Executive Office of the Mayor
441 - 4th Street, N.W., 9th Floor - South
Washington, D.C. 20001
(202) 724-5622
Florida
Secretary, Department of Elder Affairs
Building B - Suite 152
4040 Esplanade Way
Tallahassee, Florida 32399-7000
(850) 414-2000
Georgia
Director, Division of Aging Services
Department of Human Resources
2 Peachtree Street, N.E., 18th Floor
Atlanta, Georgia 30303
(404) 657-5258
Hawaii
Director, Hawaii Executive Office on Aging
250 South Hotel Street, Suite 109
Honolulu, Hawaii 96813-2831
(808) 586-0100
Idaho
Administrator, Idaho Commission on Aging
P.O. Box 83720
Boise, Idaho 83720-0007
(208) 334-3833
Illinois
Director, Illinois Department of Aging
421 East Capitol Avenue
Springfield, Illinois 62701
(217) 785-2870 *1-(800) 252- 8966
Indiana
Director, Bureau of Aging and In-Home Services
Division of Disability, Aging and Rehabilitative Services
Family and Social Services Administration
420 W. Washington Street, #W454
P.O. Box 7083
Indianapolis, Indiana 46207-7083
(317) 232-7020
Iowa
Executive Director, Department of Elder Affairs
Clemens Building, 3rd Floor
200 Tenth Street
Des Moines, IA 50309-3609
(515) 242-3333
Kansas
Secretary, Department of Aging
New England Building
503 S. Kansas Ave.
Topeka, KS 66603-3404
(785) 296-4986
Kentucky
Director, Division for Aging Services
Cabinet for Human Resources
Department for Social Services
275 East Main Street
Frankfort, Kentucky 40621
(502) 564-6930
Louisiana
Director, Governor's Office of Elderly Affairs
4550 North Boulevard, P.O. Box 80374
Baton Rouge, Louisiana 70806
(504) 925- 1700
Maine
Director, Bureau of Elder and Adult Services
Department of Human Services
State House - Station 11
Augusta, Maine 04333
(207) 626-5335
Maryland
Director, Maryland Office on Aging
301 West Preston Street
Baltimore, Maryland 21201
(301) 225-1102 *1-(800) 338-0153
Massachusetts
Secretary, Massachusetts Executive Office of Elder Affairs
1 Ashburton Place, 5th Floor
Boston, Massachusetts 02108
(617) 727-7750 *1-(800) 882-2003
Michigan
Director, Office of Services to the Aging
611 W. Ottawa, N. Ottawa Tower, 3rd Floor
P.O. Box 30676
Lansing, MI 48909
(517) 373-8230
Minnesota
Executive Secretary, Minnesota Board on Aging
444 Lafayette Road, 4th Floor
St. Paul, Minnesota 55155-3843
(612) 296-2770 *1- (800) 652-9747
Mississippi
Director, Division on Aging and Adult Services
Department of Human Resources
750 North State Street
Jackson, Mississippi 39202
(601) 359-4925 *1-(800) 948-3090
Missouri
Director, Division of Senior Services
Department of Health and Senior Services
615 Howerton Court
Jefferson City, Missouri 65102-1337
(573) 751-8687
Montana
State Aging Coordinator, Senior & Long Term Care Division
Department of Public Health & Human Services
111 Sanders, Room 211
Helena, Montana 59620
(406) 444-4077
Nebraska
Director, Department on Aging; 301 Centennial Mall South
P.O. Box 95044
Lincoln, Nebraska 68509-5044
(402) 471- 2306
Nevada
Administrator, Division for Aging Services
Department of Human Services
State Mail Room Complex
3416 Goni Road, Building D-132
Carson City, NV 89706
(775) 687-4210
New Hampshire
Director, Division of Elderly and Adult Services
State Office Park South
129 Pleasant Street, Brown Bldg. #1
Concord, New Hampshire 03301
(603) 271-4680
New Jersey
Asst. Commissioner, Dept. of Health and Senior Services
New Jersey Division of Senior Affairs
P.O. Box 807
Trenton, New Jersey 08625-0807
(609) 943-3436
New Mexico
Director, New Mexico State Agency on Aging
La Villa Rivera Building, Ground Floor
224 East Palace Avenue
Santa Fe, New Mexico 87501
(505) 827-7640 *1-(800) 432-2080
New York
Director, New York State Office for the Aging
Agency Building #2
Empire State Plaza
Albany, New York 12223-0001
(518) 474-5731 *1-(800) 342-9871
North Carolina
Director, Department of Health and Human Services
Division of Aging
2101 Mail Service Center
Raleigh, NC 27699-2102
(919) 733-3983
North Dakota
Director, Aging Services Division
North Dakota Department of Human Services
600 South 2nd Street, Suite 1C
Bismarck, ND 58504
(701) 328-8910 *1-(800) 451-8693
Ohio
Director, Ohio Department of Aging
50 West Broad Street - 9th Floor
Columbus, Ohio 43215
(614) 466-5500
Oklahoma
Division Administrator, Aging Services Division
Department of Human Services
312 N.E. 28th Street
P.O. Box 25352
Oklahoma City, Oklahoma 73125
(405) 521-2327
Oregon
Administrator, Senior and Disabled Services Division
Department of Human Resources
500 Summer Street, N.E., 2nd Floor
Salem, Oregon 97310-1015
(503) 378-4728
Pennsylvania
Secretary, Pennsylvania Department of Aging
Commonwealth of Pensylvania
Forum Place
555 Walnut Street, 5th Floor
Harrisburg, Pennsylvania 17101-1919
(717) 783-1550
Rhode Island
Director, Department of Elderly Affairs
160 Pine Street
Providence, Rhode Island 02903
(401) 277-2858 *1-(800) 322-2880
South Carolina
Deputy Director, Office of Senior & Long Term Care Services
Department of Health and Human Services
P.O. Box 8206
Columbia, South Carolina 29202-8206
(803) 898-2501
South Dakota
Administrator, Office of Adult Services and Aging
Richard F. Kneip Building
700 Governors Drive
Pierre, South Dakota 57501-2291
(605) 773-3656
Tennessee
Executive Director, Commission on Aging and Disability
Andrew Jackson Building, 9th Floor
500 Deaderick Street
Nashville, Tennessee 37243-0860
(615) 741- 2056
Texas
Executive Director, Texas Department on Aging
4900 North Lamar, 4th Floor
Austin, Texas 78751-2316
(512) 424-6840
Utah
Director, Utah Division of Aging &
Adult Services
120 North 200 West, Room 401, P.O. Box 45500
Salt Lake City, Utah 84145- 0500
(801) 538-3910
Vermont
Commissioner, Department of Rehabilitation and Aging
103 South Main Street
Waterbury, Vermont 05671-2301
(802) 241-2400 *1- (800) 642-5119
Virginia
Commissioner, Virginia Department for the Aging
1600 Forest Avenue, Suite 102
Richmond, Virginia 23229
(804) 662-9333
Washington
Assistant Secretary, Aging and Adult Services Administration
Department of Social and Health Services
P.O. Box 45050
Olympia, Washington 98504-5050
(206) 586-3768 *1-(800) 422-3263
West Virginia
Director, West Virginia Office of Aging
State Capitol Complex - Holly Grove
1900 Kanawha Boulevard
Charleston, West Virginia 25305- 0160
(304) 558-3317 *1-(800) 642-3671
Wisconsin
Director, Bureau on Aging & Long Term Care Resources
Department of Health and Family Services
1 West Wilson Street, Room 450
Madison, Wisconsin 53707-7850
(608) 266-2536
Wyoming
Administrator, Division on Aging
Wyoming Department of Health
6101 Yellowstone Road, Suite 259B
Cheyenne, Wyoming 82002-0710
(307) 777-7986
International Sources:
American Samoa
Director, Territorial Administration on Aging
Government of American Samoa
Pago Pago, American Samoa 96799
(684) 633-1251
Commonwealth Of The Northern Mariana Islands
Director, CNMI Office on Aging
P.O. Box 2178
Commonwealth of the Northern Mariana Islands
Saipan, Mariana Islands 96950
(670) 233-1320
Guam
Administrator, Division of Senior Citizens
Department of Public Health and Social Services
P.O. Box 2816
Government of Guam
Agana, Guam 96910
(671) 734-2942
Puerto Rico
Executive Director, Puerto Rico Office of Elderly Affairs
Call Box 50063
Old San Juan Station, Puerto Rico 00902
(809) 721-0753
Republic Of Palau
Director, State Agency on Aging
Department of Social Services
Republic of Palau; Koror, Palau 96940
Virgin Islands
Commissioner, Virgin Islands Department of Human Services
Knud Hansen Complex, Building A
1303 Hospital Ground
Charlotte Amalie, Virgin Islands 00840
(809) 774-1166
Alzheimer's Association, Inc.
919 North Michigan Ave., Suite 1000
Chicago, Illinois 60611
(312) 335-8700 *1-800-272-3900 (Illinois)
*1-800-621-0379 (National) (Provides support through AA Chapter Family Support Groups; educational and patient care materials; information about local resources and services)
Alzheimer's Disease Education And Referral Center
P.O. Box 8250
Silver Spring, Maryland 20907- 8250
(301) 495-3311 *1-800-438-4380 (A service of the National Institute on Aging, the center distributes information on Alzheimer's disease, on current research activities, and on services available to patients and family members).
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