Michael Mistric, PhD, RN, FNP, BCNurse PractitionerMichael E. DeBakey VA Medical Center

Describe the demographics associated with Alzheimer’s dementia

Describe the clinical features of Alzheimer’s dementia

Describe the medical management of Alzheimer’s dementia

Describe caregiver support services for individuals with Alzheimer’s dementia

Describe caregiver’s basic social process of formulating expectations of dementia care

A syndrome that has multiple reversible and irreversible causes and requires systematic evaluation of the patient presenting with a cognitive complaint

   An acquired, persistent decline (not secondary to delirium) involving at least three of the following five domains: language, memory, visiospatial skills, executive function, and personality and mood

Cummings, Benson, LoVerme (1980) Reversible dementia. JAMA, 243(23)

Approximately 5 million Americans have Alzheimer’s disease (AD).  Unless a cure or prevention is found, that number will increase to 14 million by 2050.

An estimated 280,000 Texas have Alzheimer’s disease.

One in eight persons over 65 and nearly half of those over 85 have AD.  A small percentage of people as young as their 30s and 40s get the disease.

AD is degenerative disease of the brain from which there is no recovery.

AD is now the seventh leading cause of death in adults.

2010 Alzheimer's Disease Facts and Figures (alz.org)

Direct and indirect costs of AD and other dementia’s amount to more than $148 billion annually.

Almost 10 million Americans are caring for a person with AD or another dementia; approximately one out of three of these caregivers is 60 years or older.

In 2005, it was estimated that unpaid caregivers of people with AD and other dementias provided 8.5 billion hours of care valued at almost $83 billion dollars.  

More than half the states in the United States provide more than a billion dollars in unpaid care each year – Texas $5.8 billion.

2010 Alzheimer's Disease Facts and Figures (alz.org)

The primary pathologic features of AD are amyloid deposition, neurofibrillary tangle formation, and neuronal loss

Plaques and Tangles: The Hallmarks of AD

The brains of people with AD have an abundance of two abnormal structures:

An actual AD plaque An actual AD tangle

• beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells

• neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell

AD and the Brain

Beta-amyloid Plaques

Amyloid precursor protein (APP) is the precursor to amyloid plaque.

1. APP sticks through the neuron membrane.

2. Enzymes cut the APP into fragments of protein, including beta-amyloid.

3. Beta-amyloid fragments come together in clumps to form plaques.

1.

2.

3.

AD and the Brain

In AD, many of these clumps form, disrupting the work of neurons. This affects the hippocampus and other areas of the cerebral cortex.

Neurofibrillary Tangles

Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles.

AD and the Brain

Memory loss

Difficulty with familiar tasks

Problems with language

Disorientation to time and place

Poor or decreased judgment

Trouble with abstract thinking

Misplacing things

Changes in mood or behavior

Changes in personality

Loss of initiative

Memory impairment and 1 or more: Aphasia (language disturbance) Apraxia (inability to carry out motor activities Agnosia (failure to recognize objects) Disturbed executive function (planning,

organizing) Cognitive deficits Gradual onset, continued decline Deficits not due to another condition Deficits not exclusive to delirium

The Changing Brain in Alzheimer’s Disease

No one knows what causes AD to begin, but we do know a lot about what happens in the brain once AD takes hold.

Pet Scan of Normal Brain

Pet Scan of Alzheimer’s Disease Brain

AD and the Brain

Treat a reversible condition

Treat co-morbid conditions

Avoid exacerbation

Limit complications

Relieve symptoms

AD no longer a diagnosis of exclusion

Drugs & programming depend on staging

Caregivers can be secondary victims: provide for them as well

Providers today use a number of tools to diagnose AD:

• a detailed patient history

• information from family and friends

• physical and neurological exams and lab tests

• neuropsychological tests (MMSE, GDS, Global Deterioration Scale, Affect Balance, BEHAVE-D

• imaging tools such as CT scan, or magnetic resonance imaging (MRI), PET scans

AD Research: Diagnosing AD

Complete PE & History

Mini-Mental State Exam (MMSE) or Physical Self-Maintenance Scale (PSMS) to establish baseline cognition and functional ability

Global Deterioration Scale – useful for

staging Affect Balance or Geriatric Depression Scale Katz ADLs – IADLs BEHAVE-AD

Members of various ethnic groups, cultures, and races manifest and cope differently with the disease, care-giving, and related stresses Some Asian/Pacific Islanders view AD as a

normal part of aging

Some Hispanics view AD as a spiritual test or punishment for a past deed.

Some African Americans rely on their spiritual faith to deal with the illness and care-giving.

1st degree African American relatives have higher risk than Caucasians.

African Americans are 4 times more likely to develop AD by age 90

African Americans and Hispanics may be at higher genetic risk based on APOE-4 allele aberration

Hypertension and hypercholesterolemia each place African American at a 4 times risk for AD

http://www.ethniceldercare.net

African American family members & caregivers may not consider dementia an illness, but rather an expected consequence of aging

Some believe it is a form of mental illness May be believed to be the result of

“worriation” and behaviors may be interpreted as “spells”

First cue may be in the failure to carry out role and social functions (later than desired recognition per professional assessment)

http://www.ethniceldercare.net

Hispanics may be 2 times more likely than Caucasians to develop AD by age 90

Vascular dementia has higher prevalence than AD

http://www.ethniceldercare.net

Female family members are the designated caregivers

Dementia may be viewed as some form of mental illness

Dementia is a source of shame, embarrassment, stigma; and, therefore may be a barrier to getting help

Problem not typically shared in the cultural network

http://www.ethniceldercare.net

Dementia is a form of normal aging

Dementia is a form of mental illness

Dementia is a source of shame

Dementia is a family secret that should not be shared

Dementia is a result of fate

http://www.ethniceldercare.net

Early Dementia“All dressed up and no where to go”

Middle Dementia“I want to go with you”

Late Dementia“In his own little world”

Physical Appearance May still dress self appropriately

Awareness “Lost in Time”

Behaviors Wandering Anxious Resistance to ADLs Sleep disturbance

Preclinical AD • Signs of AD are first noticed in the entorhinal cortex, then proceed to the hippocampus.

• Affected regions begin to shrink as nerve cells die.

• Changes can begin 10-20 years before symptoms appear.

• Memory loss is the first sign of AD.

AD and the Brain

Slide 20

Eating Eats independently May need cueing Remove stimulants from diet

Toileting Needs supervision locating bathroom and

reminders to go Usually continent

Hydration Needs supervision Provide favorite beverages frequently

Dressing Needs help locating and choosing clothing

Coaxing--resistance

Personal Hygiene Needs supervision-is relatively

independent Bathing

Needs supervision

Awareness of need to bathe is variable

Physical Appearance ▪ Looks unfinished; does not want to change

clothes▪ Change in posture

Awareness ▪ May be awareness of past versus present▪ Unable to think in the abstract

Behaviors▪ Wanders, is suspicious, resistant to

caregivers, social butterfly

Mild to Moderate AD• AD spreads through the brain. The

cerebral cortex begins to shrink as more and more neurons stop working and die.

• Mild AD signs can include memory loss, confusion, trouble handling money, poor judgment, mood changes, and increased anxiety.

• Moderate AD signs can include increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements.

AD and the Brain

Slide 21

Eating Trouble using utensils, positioning, and

swallowing--precut food, use prompting/cueing

Toileting Needs assistance with mechanics--wiping,

flushing, pulling down underwear, reminders

Hydration Hydration is dependent on caregiver

attention

Dressing Assistance in dressing due to agnosia, apraxia

Personal Hygiene Assistance due to agnosia, apraxia,

Parkinsonian symptoms

Needs tasks broken down

Bathing Needs supervision

Awareness of need to bathe is dependent on

caregiver

Physical Appearance ▪ Looks abnormal, undresses, looks lost,

posture/balance deficits, loses weight, loss of 3D vision

Awareness▪ Limited to field of vision, seeks sensory

stimulation

Behaviors▪ Hyper/hypo activity, cannot

communicate needs, does not recognize self or loved ones

Severe AD• In severe AD, extreme shrinkage

occurs in the brain. Patients are completely dependent on others for care.

• Symptoms can include weight loss, seizures, skin infections, groaning, moaning, or grunting, increased sleeping, loss of bladder and bowel control.

• Death usually occurs from aspiration pneumonia or other infections. Caregivers can turn to a hospice for help and palliative care.

AD and the Brain

Slide 22

Eating Total loss in eating skills: using

utensils, position, swallowing difficulty Toileting

Total Care May resist

Hydration Unable to pour water or understand

need or mechanics of drinking water

Dressing Needs total assistance

May disrobe or fiddle with clothes

Personal Hygiene Needs total assistance.

Able to do one step tasks – e.g. washing face

Bathing Unable to comprehend bathing

May resist sponge or bed bath

All are focused on maximizing the potential of the patient and managing symptoms

▪ Support cognitive functioning

▪ Reduce and prevent functional disabilities

▪ Ameliorate and mediate behavioral disturbances

Between 70 to 90% of people with AD eventually develop behavioral symptoms, including sleeplessness, wandering and pacing, aggression, agitation, anger, depression, and hallucinations and delusions. Experts suggest these general coping strategies for managing difficult behaviors:

AD Research: Managing Symptoms

• Stay calm and be understanding.• Be patient and flexible. Don’t argue or try to convince.• Acknowledge requests and respond to them.• Try not to take behaviors personally. Remember: it’s

the disease talking, not your loved one.

Experts encourage caregivers to try non-medical coping strategies first. However, medical treatment is often available if the behavior has become too difficult to handle. Researchers continue to look at both non-medical and medical ways to help caregivers.

Still are people that accept memory loss & confusion as a natural part of aging

Cognitive impairments of any kind are not easy to admit, recognize, or discuss

Patients hide or compensate for early signs

Families deny what is being seen

Requires comparison of cognitive and physical functioning relative to a previous level of performance

Eliminate or reverse any other (vascular, metabolic, etc.) causes

Proceed by clinical criteria and protocols for radiologic & laboratory studies

Refer to neurologist and Alzheimer’s Disease Research Center

What Alzheimer symptoms are most prevalent? What significant changes have you noticed?

Memory Behavior Personality Skills Other

How have you successfully accommodated for these changes?

What caregiving challenges are you facing? What activities does your loved one still enjoy? Describe a special moment you shared with

your loved one recently.

Current treatments for Alzheimer’s are not designed to reverse the disease process totally, yet they can produce some improvements in cognition.

Existing medications can be effective in slowing the progression of the disease and helping patients remain independent for longer periods of time.

Treating symptoms effectively is valuable not only to patients but also to their caregivers and families.

Cholinesterase inhibitorsReceptor agonistsEstrogenAnti-inflammatory drugsAntioxidantsVarious experimental

agentsBehavioral controls

Cholinesterase Inhibitors Donepezil (Aricept): Mild/Moderate Dementia

▪ Start with 5 mg/day; increase to 10 mg/day in 4 weeks▪ Nausea; Diarrhea; Poor Appetite

Rivastigmine (Exelon): Mild/Moderate Dementia▪ Start with 4.6 mg/24 hour patch daily; increase to 9.5

mg/24 hour patch daily in 4 weeks▪ Nausea; Diarrhea; Poor Appetite

Galantamine (Reminyl): Mild/Moderate Dementia▪ Start with 8 mg a day; increase by 8 mg every four

weeks up to 24 mg a day▪ Nausea; Diarrhea; Poor Appetite

N-methyl-D-aspartate (NMDA) Memantine (Namenda):

Moderate/Severe Dementia Start with 5 mg a day; increase by 5 mg a week

up to 10 mg twice a day Headache; Dizziness; Confusion

Tacrine (Cognex): Not used anymore Prototypical cholinesterase inhibitor for the

treatment of Alzheimer's disease

Muscarinic receptor agonists M1-type muscarinic acetylcholine receptors play

a role in cognitive processing. In Alzheimer disease (AD) amyloid formation

may decrease the ability of these receptors to transmit their signals leading to decrease cholinergic activity.

A number of muscarinic agonists have been developed and are under investigation to treat AD.

These agents show promise as they are neurotrophic, decrease amyloid depositions, and improve damage due to oxidative stress.

Nicotinic receptor agonists Nicotine has long been known to improve cognitive

function, but its adverse effects make it problematic as a treatment for diseases of cognitive dysfunction

Recent research has revealed that certain subtypes of nicotinic acetylcholinesterase receptors (nAChRs) in the brain are involved in cognitive function

Agents that target these nAChRs have shown promise in Alzheimer’s disease

Research also suggests that these agents may not only improve cognition but also be neuroprotective

Early studies of estrogen suggested that it might help prevent AD in older women. However, a clinical study of several thousand postmenopausal women aged 65 or older found that combination therapy with estrogen and progestin substantially increased the risk of AD. Estrogen alone also appeared to slightly increase the risk of dementia in this study. Therefore, based on epidemiological correlations, the use of estrogen to prevent or treat dementia has not been supported by follow-up studies and is not recommended.http://www.medicinenet.com

Several studies have found evidence of brain inflammation in AD and researchers have proposed that drugs that control inflammation, such as NSAIDs, might prevent the disease or slow its progression and early studies of these drugs in humans have shown promising results. However, a large NIH-funded clinical trial of two NSAIDS (naproxen and celecoxib) to prevent AD was stopped in late 2004 because of an increase in stroke and heart attack in people taking naproxen, and an unrelated study that linked celecoxib to an increased risk of heart attack. Therefore, based on epidemiological correlations, the use of NSAIDs to prevent or treat dementia has not been supported by follow-up studies and is not recommended.

http://www.medicinenet.com

A recent double-blind, placebo-controlled study of Vitamin E and donepezil for the treatment of mild cognitive impairment was unable to demonstrate benefit form Vitamin E and showed only modest and short-term benefit from donepezil.

This result suggested there was no role for the use of Vitamin E in the prevention or early treatment of Alzheimer’s Dementia.

Petersen et al. (2005). New England Journal of Medicine (352)

Many researchers believe a vaccine that reduces the number of amyloid plaques in the brain might ultimately prove to be the most effective treatment for AD.

In 2001, researchers began one clinical trial of a vaccine called AN-1792.

The study was halted after a number of people developed inflammation of the brain and spinal cord.

Despite these problems, one patient appeared to have reduced numbers of amyloid plaques in the brain.

Other patients showed little or no cognitive decline during the course of the study, suggesting that the vaccine may slow or halt the disease.

Researchers are now trying to find safer and more effective vaccines for AD.

http://www.medicinenet.com

Look for concurrent illness/problems Look at medications Try non-pharmocologic alternatives Target the dominant symptom Start drugs low and go slow Look at drug with best side effect

profile Review compliance Simplify Give clear and written instructions

Respiridone (Resperdal) 0.5 - 2 mg/day in two divided doses Sedation; Parkinson's Disease symptoms

Haloperidol (Haldol) 0.25 - 2 mg/day. Gradually increase this dose. Use sparingly

only for severe agitation Parkinson's Disease symptoms; Sedation; Falling; Abnormal

Movements Quetiapine (Seroquel)

12.5 - 200 mg/day in two divided doses Sedation; Light headedness

Olanzapine (Zyprexia) 2.5 - 10 mg/day Sedation; Light headedness; Confusion; Dry Mouth;

Constipation

Citalopram (Celexa) 10 - 60 mg/day Nausea; Dry Mouth; Sedation

Mirtazepine (Remeron) 15 - 30 mg at night Sedation; Weight Gain; Dry Mouth

Sertraline (Zoloft) 50 - 200 mg/day Insomnia; Diarrhea; Tremor

People with AD usually die from complications

Without an advance directive executed while the individual was competent, a substitute decision maker makes difficult life and death decisions

End-of-life choices may include the use, limitation, withdrawal or refusal of:

procedures, treatments or technology such as tube feeding

mechanical respirators or ventilators cardiopulmonary resuscitation (CPR) surgery the use of antibioticsA hospice program offers a more humane

and compassionate option than the nursing home or hospital during the final months

Simplify - Simplify - SimplifyMedications: Start SlowLook for concurrent

illness/problemsRemember your goal:

To improve quality of life Do no harm!

Consider the caregiver and family

The specific aims were to: Elicit subjective perspectives of family

members about what constitutes quality LTC for loved-ones with dementia, and

Develop a grounded theory of shared meanings about quality dementia care that reflects the expectations of family members in various stages of giving care and relinquishing care for a loved-one with dementia

Research Question: How do family members describe their

expectations of dementia care in the LTC setting?

Stage 1: Transitions to caregiver role Sees losses

Stage 2: Takes on caregiver role Fills gaps

Stage 3: Relinquishes caregiver role Recognizes limits Acknowledges need for LTC placement Responds to relinquishment of care

Stage 4: Selects and evaluates LTC facility Makes selection Evaluates care

Stage 5: Accepts LTC resident status Accepts LTC status Justifies LTC placement

Patient Care Nutrition, hygiene,

toileting, medications, and activities

Pleasant Surroundings Resident’s room and

facility common areas Competent Staff

Ability to provide dementia care and care of individuals in LTC

Caring Staff Treat with dignity and

respect; free from neglect and abuse

Communication What is communicated

& when communication should occur

Institutional Responsiveness Staff response to

questions and concerns

The Alzheimer’s Association http://www.alz.org

Family Caregiver Alliance http://www.caregiver.org

AgeNet; follow the "Geriatric Health" link http://www.agenet.com/early_alz_guide.html

Mayo Clinic Health Oasis http://www.mayohealth.org/

Alzheimer's Disease Education and Referral Center (ADEAR Center) http://www.alzheimers.org

Alzheimer's Research Forum http://www.alzforum.org

American Academy of Neurology http://www.aan.com

National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov

Medic Alert http://www.medicalert.org

National Institute on Aging and Eldercare Locator http://www.eldercare.gov

American Health Assistance Foundation (AHAF) http://www.ahaf.org

Ethnicity and Dementia http://www.ethnicelderscare.net

Summary