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Look Up > Conditions > Alzheimer's Disease
Alzheimer's Disease
Risk Factors
Signs and Symptoms
Differential Diagnosis
Physical Examination
Laboratory Tests
Other Diagnostic Procedures
Treatment Options
Treatment Strategy
Drug Therapies
Complementary and Alternative Therapies
Patient Monitoring
Other Considerations


Alzheimer's disease (AD) is the most common cause of dementia in the elderly, affecting at least three to four million people in the United States. AD is defined as memory loss with at least one other area of cognitive impairment (e.g., language, attention, orientation, self-monitoring, judgment, motor skill, inability to perform daily activities). Memory loss typically begins at about age 65 and slowly progresses to severe impairment over 8 to 10 years, but it may present sooner and advance at a different rate. Language deficits are prominent, including word finding (especially nouns), comprehension, repetition, and fluency. Social graces, which may remain surprisingly intact for years, eventually deteriorate to a loss of inhibition with periods of aggression or withdrawal. Personality and behavioral changes as well as problems in judgment occur with increasing severity. Death usually occurs from malnutrition, heart disease, or infection. Clinical diagnosis cannot be definitively confirmed without autopsy.


The etiology of AD is unknown. Speculative causes include viruses, autoimmune disorders, accelerated aging process, and environmental contaminates, notably aluminum and aluminum-containing products.

Risk Factors
  • Family history—especially of epsilon 4 apolipoprotein (Apo) E gene on chromosome 19
  • Advanced age (20% to 40% of those with fully developed symptoms of Alzheimer's disease are over age 85)
  • Female > male
  • Possibly head trauma, low education level, and environmental factors, or insults not fully understood
  • Down syndrome
  • Oxidative stress > antioxidant reserve
  • Glutamate excess
  • Aluminum and mercury toxicity may contribute
  • Physical inactivity

Signs and Symptoms
  • Memory loss—eventually includes loss of personal information and inability to recognize family
  • Temporal and spatial disorientation
  • Inability to perform daily activities
  • Aphasia—language deficits include fluency, comprehension, word naming/finding
  • Accusatory behaviors
  • Problems with sequential motor tasks
  • Cortical blindness
  • Denial of symptoms
  • Hallucinations, delusions, psychosis
  • Aggression, agitation, anxiety, restlessness
  • Withdrawal, apathy
  • Insomnia or disturbances in sleep/wake patterns
  • Muscle rigidity
  • Weight loss
  • Extrapyramidal dysfunction
  • Incontinence
  • Seizures
  • Depression

Differential Diagnosis
  • Depressive disorders
  • Delirium through other causes
  • Multi-infarct dementia
  • Vitamin deficiency
  • Brain tumor
  • Drug intoxication, alcoholism
  • Huntington's disease
  • Pick's disease
  • Stroke
  • Creutzfeldt-Jakob disease
  • Advanced syphilis
  • Thyroid disease
  • Hydrocephalus
  • Parkinson's disease
  • Lewy body dementia
  • Sleep disorders

Physical Examination

AD is diagnosed on clinical grounds and by ruling out all other possible causes. A thorough evaluation includes neuropsychologic testing, EEG, chest radiograph, and a CBC.

Laboratory Tests

Tests are normal with AD. Complete blood count (e.g., for vitamin B12 or folate deficiency), chemistry battery (e.g., for chronic renal or liver failure), thyroid function tests, and other tests are given to rule out differential diagnoses. Testing of beta amyloid precursor protein levels in blood is still investigational but appears promising.

  • Diffuse atrophy of the cerebral cortex; secondary enlargement of the ventricular system
  • Neurofibrillary tangles (first noted by Alzheimer) in neuronal cytoplasm
  • Neuritic plaques—containing A beta amyloid and Apo E; accumulate in the cerebral blood vessel walls; testing of Apo E is controversial, however Apo E epsilon 4/4 homoozygotes diagnose AD at about 97% accuracy
  • Levels of acetylcholine and A beta amyloid decrease and tau protein increases in CSF
  • Cholinergic transmitter deficiency and continual loss of cholinergic cells
  • Amyloid angiopathy common

  • Imaging is used to exclude other diagnoses such as neoplasms, hematomas, or infarcts
  • MRI or CT—detect diffuse cortical atrophy, including the hippocampus seen particularly as disease progresses; enlargement of sulci
  • EEG—normal or nonspecific slowing
  • Positron emission tomography (PET)—shows early metabolic changes in parietal cortex

Other Diagnostic Procedures
  • Electroencephalogram and lumbar puncture—especially for rapid onset with delirium to rule out other causes
  • Sleep study—to rule out sleep disorders
  • Mini Mental State Examination—measure of cognitive function

Treatment Options
Treatment Strategy

As there is no cure for AD, treatment focuses on managing neurologic and behavioral symptoms and supporting patients and caregivers. In early stages, memory aids are useful. Living areas must be kept predictable and safe to reduce falls and avoid contact with potentially dangerous objects. It is important to remove triggers or stop behaviors that provoke agitation. Regular breaks are necessary for caregivers to reduce their own psychological and physical exhaustion. Social workers can inform families of community support services.

Drug Therapies
  • Tacrine—FDA-approved in 1993; inhibits cholinesterase, increases acetylcholine; 10% to 20% of early-onset patients show positive response, no benefit in late-stage AD; severe side effects include dose-related nausea, vomiting, diarrhea, and hepatotoxicity; delirium-like withdrawal effect; 10 to 40 mg qid.
  • Donepezil—FDA approved in 1997; slows progression of AD; 30% to 50% of patients show positive response; inhibits acetylcholinesterase, the cholinesterase found in the brain, with 1,200 times more selectivity than tacrine, significantly reducing side effects even at high doses; no hepatotoxicity; 5 to 10 mg at bedtime
  • SSRIs or tricyclic antidepressants with low anticholinergic side effects—for depression (e.g., sertraline 50 to 100 mg/qid)
  • Benedryl—for insomnia
  • Phenothiazines, benzodiazepines, haloperidol—for agitation, psychosis, and insomnia; side effects include sedation, confusion, adventitious movement; use lowest possible dose (e.g., haloperidol 0.5 to 2 mg bid)

Complementary and Alternative Therapies

Herbs and nutrients provide excellent support in the treatment of Alzheimer's by improving cerebral circulation, addressing contributing factors, and slowing the progression of the disease. A well-rounded diet is important in providing optimal nutrition, minimizing hypoglycemia, and reducing inflammation. An exercise program that improves circulation and increases flexibility is valuable. Aromatherapy can potentially influence positive behavior, as olfactory nerve is resistant to degenerative insult.

  • Eliminate alcohol, nicotine, and food additives (especially monosodium glutamate and aspartame). Limit saturated fats (e.g., animal products) and refined foods. Include whole grains, fresh vegetables, fruits, and anti-inflammatory oils (e.g., cold-water fish, nuts, and seeds).
  • Vitamin E (400 to 800 IU/day), vitamin C (1,000 mg tid), and coenzyme Q10 (50 mg tid) protect against oxidative stress.
  • Acetyl-L-carnitine (1,000 to 1,500 mg/day) improves energy metabolism of brain tissue and neurotransmitter activity.
  • Phosphatidyl serine (100 mg bid to tid) facilitates membrane receptor activities and improves cognition and mood.
  • NADH (10 mg/day) stimulates biosynthesis of dopamine and noradrenaline.
  • Vitamin B12 (1,000 mcg/day) and folic acid (800 to 1,000 mcg/day) may improve cognitive function even in the absence of abnormal serum values. Vitamin B1 (300 to 2,000 mg daily) and zinc (45 mg daily) are also beneficial.
  • Melatonin—investigational for insomnia; 1 to 2 mg before bed, or 3 to 10 mg daily
  • Antioxidants—vitamin E (1,000 IU bid) and selegiline (not FDA approved for Alzheimer's) may slow progression of AD


Herbs may be used as dried extracts (pills, capsules, or tablets), teas, or tinctures (alcohol extraction, unless otherwise noted). Dose is 1 heaping tsp. herb/cup water steeped for 10 minutes (roots need 20 minutes).

  • Ginkgo biloba (120 mg bid, standardized to 24% ginkgo flavone glycosides and 6% terpene) increases cerebral circulation and regulates platelets. Monitor carefully with concurrent use of anticoagulants.
  • Combine the following in equal parts to enhance peripheral circulation and improve mood: gotu kola (Centella asiatica), rosemary (Rosemarinus officinalis), hawthorn (Crataegus monogyna), prickly ash bark (Xanthoxylum clava-herculis), passionflower (Passiflora incarnata), and lavender (Lavendula angustifolia). For anxiety, substitute kava kava (Piper methysticum) for lavender. For depression, substitute St. John's wort (Hypericum perforatum) for lavender. Take 30 to 60 drops tincture bid to tid, or drink one cup of tea tid.


An experienced homeopath would consider the individual's constitution. Some of the most common acute remedies are listed below. Acute dose is three to five pellets of 12X to 30C every one to four hours until symptoms resolve. Remedies to consider include the following.

  • Alumina for mental dullness with slowed speech and loss of identity
  • Argentum nitricum for poor memory with impulsivity, anxiety, depression, and compulsive thoughts or behavior
  • Cocculus for slowed mentation with grief and vertigo
  • Conium for progressive mental deterioration with emotional flatness
  • Helleborus for stupefaction with indifference to the outside world alternating with anguish and incomprehension
  • Zincum for confusion with slowed speech, use of incorrect words, and suicidal thoughts
  • Anacardium for cruel behavior, cursing, memory loss
  • Hyocyamus for sexual behavior, undressing, touching of genitals, lewd language


May help ameliorate imbalances and support overall well-being.


Stimulates peripheral circulation. Many elderly are deprived of touch and respond well to massage therapy.

Patient Monitoring

Frequent patient monitoring is necessary to monitor medication, determine course of disease, and screen for complications, including malnutrition.

Other Considerations
  • NSAIDs—very preliminary studies indicate they may lower risk; potentially serious side effects at necessary doses and duration
  • Estrogen use for women—trials indicate it may lower risk of getting AD; potentially serious side effects
  • Reducing aluminum and mercury exposure may be helpful. Chelation for aluminum with desferrioxamine slows progression compared to controls.

  • Patient inflicting harm on self or others
  • Falls
  • "Sundowning," or increase in withdrawal and/or agitation in evening
  • Suicide
  • Malnutrition
  • Infection
  • Compromised support due to caregiver burnout


As there is no cure for AD, patients' symptoms slowly worsen despite treatment. Death may occur in 2 to 25 years, but typically in 8 to 10 years.


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Copyright © 2000 Integrative Medicine Communications

This publication contains information relating to general principles of medical care that should not in any event be construed as specific instructions for individual patients. The publisher does not accept any responsibility for the accuracy of the information or the consequences arising from the application, use, or misuse of any of the information contained herein, including any injury and/or damage to any person or property as a matter of product liability, negligence, or otherwise. No warranty, expressed or implied, is made in regard to the contents of this material. No claims or endorsements are made for any drugs or compounds currently marketed or in investigative use. The reader is advised to check product information (including package inserts) for changes and new information regarding dosage, precautions, warnings, interactions, and contraindications before administering any drug, herb, or supplement discussed herein.