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Alzheimer’s Disease: What is its cause and prevelance?

Alzheimer’s Disease: Prevalence and Cause

Alzheimer’s Disease Prevalence

Alzheimer’s disease is the most prevalent cause of dementia, accounting for between 55% 65% of all cases of dementia. While there were fewer than 3 million cases of Alzheimer’s disease diagnosed in the United States in 1980, the Census Bureau predicts there will be more than 10 million American citizens with Alzheimer’s disease by the year 2050. The prevalence of this disease is believed to double with every five year period of time between the ages of 65 and 85 years old.

Some researchers separate Alzheimer’s disease into senile and pre-senile forms, although the two disorders actually represent the same pathological process. However, the early-onset type (onset before the age of 65) of Alzheimer’s disease is usually associated with a more rapid course of progression than the later-onset type.

Alzheimer’s disease affects women at a rate of 3 to 1 over men (although the reasons are unknown). Also, at least one study has suggested dementia, including Alzheimer’s disease, is more common in black then white American women. Interestingly enough, comparison of population studies in various countries show distinctly similar prevalence rates.

Alzheimer’s Disease Cause:

The cause and pathogenesis of Alzheimer’s disease is unknown. It is believed that multiple causative pathways are likely involved in this disorder. There have been many hypothesis regarding the cause and progression of Alzheimer’s disease including genetic factors, slow or unconventional viruses, defective membrane metabolism, endogenous toxins, autoimmune disorders, and neurotoxicity of such trace elements as aluminum and mercury.

It is known that the brains of individuals with Alzheimer’s disease contain senile plaques, neurofibrillary tangles and Hirano’s bodies. There is a deterioration of nerve cells, but the atrophy seen on neural diagnostic examination may be more the result shrinkage of neurons and the loss of dendritic spines then of the actual neuronal loss. Certain parts of the brain, such as the association cortex demonstrate the most apparent changes, with early decay in the primary motor and sensory areas being relatively spared from these changes. Cholinergic abnormalities are exhibited in the neurochemicals of the brain. There is a significant decrease in acetylcholine in most individuals along with decreased immunological activity of somatostatin and corticotropin-releasing factors. The enzyme required for acetylcholine synthesis, choline acetyltransferase, is also significantly reduced. Other studies seem to suggest involvement of the noradrenergic and serotonergic systems in later-onset Alzheimer’s disease and reduced gamma-aminobutyric acid (GABA). Although it is a well-known fact that the involvement of cholinergic transmission along the hippocampus and nucleus basalis essential to the ability to learn new information, it is believed that many of the symptoms of Alzheimer’s disease are not totally explained on the basis of cholinergic abnormalities. Investigators continue to examine a variety of other potential causative or contributing factors.

Researchers have also investigated the role of beta-amyloid protein in Alzheimer’s disease, and some even believe that this material, a significant component of all plaques, is a major contributor to the neurodegenerative changes associated with the disease, possibly both initiating and promoting the disease process. This assertion is also supported by genetic studies of families with heritable forms of presenile dementia, which seem to indicate that disease occurrence is linked to mutations involving beta-amyloid-related systems. Also, some investigators have focused on the neurofibrillary tangles and the identification of a major component of its helical filament, the tau protein. These researchers have considered the possibility that modification of tau protein, predominantly by phosphorylation, is an important feature in the development of Alzheimer’s disease.

By Paul Susic Ph.D. Licensed Psychologist

Unnecessary Medication Use Associated With Dementia Diagnosis

Introduction to the study:

A recent study conducted at the University of Sydney has found that inappropriate and unnecessary medications seem to be routinely prescribed for newly diagnosed dementia patients. This longitudinal research study of 2,500 people was conducted in collaboration with the University of Kentucky and Yale University and published in the Journals of Gerontology: Medical Sciences.

Estimates of people currently living with dementia is approximately 50 million worldwide. In Australia the estimate is approximately 425,000 costing the country more than $15 billion per year and is currently the second leading cause of death.

Study and Conclusions:

The lead author, Dr. Danijela Gnjidic, NHMRC Dementia Leadership Fellow and Senior Lecturer from the Faculty of Pharmacy and Charles Perkins Centre at University of Sydney stated that “Our study found that following a diagnosis of dementia in older people, medication use increased by 11 per cent in a year and the use of potentially inappropriate medications increased by 17 percent”. She went on to say, “These medications are typically recommended for short term use but are commonly used long term by people with dementia,”

Some of the more common unnecessary and inappropriate medications are pain pills, sleep aids, depression medications and drugs for acid reflux referred to as proton pump inhibitors

A number of reasons were given to account for this including a lack of time in the patient and physician encounters, inappropriate guidelines, difficulty in setting goals with the patient and difficulty in the communication and comprehension of the patient.
She stated, “These findings are of major concern and highlight the importance of weighing up the harms and benefits of taking potentially unnecessary medications as they may lead to increased risk of side effects such as sedation or drowsiness, and adverse drug events such as falls, fractures and hospitalization.” She felt that increased efforts need to be made to support the recognition and potential use of medications that are inappropriate to minimize harm to patients.
Finally, Dr. Gnjidic concluded that “For Australians living with dementia and their caregivers (who commonly are responsible for managing medications for people with dementia), the key is to communicate closely with general practitioners, pharmacists and other health professionals to make informed decisions and to practice good medicine management techniques to minimize the risk of side effects.” Also, she commented that “Deprescribing unnecessary medications may improve an individual’s quality of life and can reduce unnecessary healthcare cost.”

Adapted by Paul Susic Ph.D. Licensed Psychologist from article at ScienceDaily: Dementia Diagnosis Linked to Unnecessary Medication Use dated Apr. 19, 2018

Story Source:

Materials provided by University of Sydney. Note: Content may be edited for style and length.

Journal Reference:

Danijela Gnjidic, George O Agogo, Christine M Ramsey, Daniela C Moga, Heather Allore. The impact of dementia diagnosis on patterns of potentially inappropriate medication use among older adults. The Journals of Gerontology: Series A, 2018; DOI: 10.1093/gerona/gly078

Increased mortality found in Alzheimer’s patients who use benzodiazepines.


A recent research study conducted by the University of Eastern Finland found that individuals with Alzheimer’s disease may have an increase in mortality of 40% when using benzodiazepines. These findings were recently published in the International Journal of Geriatric Psychiatry.

Increased risk of mortality with benzodiazepine use:

Researchers found that the risk of death was increased at the baseline or initiation of use with these drugs (benzodiazepines) which includes such medications as Ativan, Valium and Xanax. Increased mortality was believed to be from adverse events that seem to derive directly from the use of these medications such as injuries related to falling down such as hip fractures as well as from stroke and pneumonia.

The research was conducted on persons diagnosed with Alzheimer’s disease in Finland during 2005 and 2011. Individuals who had used benzodiazepines prior to the research study were excluded from the research population including 10,380 new users of these medications. They were compared to the control group of 20,760 subjects who did not use these medications.


Although many treatment guidelines recommend nonpharmacological treatments as opposed to medications for first-line treatment of anxiety, insomnia and agitation, these medications continue to be somewhat routinely prescribed. If benzodiazepines seem to be necessary for patients with Alzheimer’s or other forms of dementia, it is recommended that they only be used on a short-term basis. These research findings encourage a more reflective approach to the use of benzodiazepines among patients with dementia and a consideration of the increased risk of mortality.

Information adapted by Paul Susic Ph.D. Licensed Psychologist from “Benzodiazepines increase mortality in persons with Alzheimer’s disease”. (Published November 20, 2017 ScienceDaily)

Story Source:

Materials provided by University of Eastern Finland. Note: Content may be edited for style and length.

Journal Reference:

Laura Saarelainen, Anna-Maija Tolppanen, Marjaana Koponen, Antti Tanskanen, Jari Tiihonen, Sirpa Hartikainen, Heidi Taipale. Risk of death associated with new benzodiazepine use among persons with Alzheimer disease: A matched cohort study. International Journal of Geriatric Psychiatry, 2017; DOI: 10.1002/gps.4821

New study shows, being unaware of memory loss may predict Alzheimer’s disease

Most clinicians and researchers are aware that while memory loss is an early symptom of Alzheimer’s disease its presence doesn’t necessarily mean that an individual has dementia. A recent research study has found that a clinically useful way to predict whether an individual will develop Alzheimer’s disease may be based upon their awareness of their memory problems according to a new study at the Centre for Addiction and Mental Health (CAMH).
The research found that people who were unaware of the loss of memory which is referred to as anosognosia were more likely to progress to a clinical diagnosis of Alzheimer’s disease according to a study published in the Journal of Clinical Psychiatry published recently. Those who are aware of their memory deficits were much less likely to develop dementia.

Unawareness and dementia

Dr. Philip Gerretsen, Clinician Scientist in CAMH’s Geriatric Division and Campbell Family Mental Health Research Institute stated that “If patients complain of memory problems, but their partner or caregiver isn’t overly concerned, it’s likely that the memory loss is due to other factors, possibly depression or anxiety.” He also went on to state that “they can be reassured that they are unlikely to develop dementia, and the other causes of memory loss should be addressed.”

On the contrary, family members or caregivers are much more likely to be distressed when the patients do not believe they have memory problems while it seems apparent they do. This lack of awareness brings upon additional burdens to family members and caregivers. Both unawareness (anosognosia) and memory loss can be assessed objectively using questionnaires.

Huge Study:

This study, believed to be the largest of its kind included data on 1062 people aged 55 to 90 years old from the Alzheimer’s Disease Neuroimaging Initiative. They also evaluated the brain’s uptake of glucose which is a type of sugar the brain cells need to function which seems to be impaired in Alzheimer’s disease patients, in order to identify which parts of the brain were affected in what has been referred to as “impaired illness awareness”.
PET brain scans show that those with “impaired illness awareness” also had reduced glucose uptake in specific brain regions even while factoring in additional factors such as age and degree of memory loss.

Future dementia research

In future research, Dr. Philip Gerretsen and colleagues will next track whether older adults with mild cognitive impairment receiving some type of intervention can prevent the development of Alzheimer’s dementia. This research will combine brain training exercises and brain stimulation using a mild electrical current to stimulate brain cells and improve learning and memory. While the main study will focus on dementia prevention, Dr. Garretson will also be assessing whether the intervention improves “illness awareness” along with preventing an individual’s progression to dementia.

Adapted by Paul Susic Ph.D. Licensed Psychologist from ScienceDaily.com article : Being unaware of memory loss predicts Alzheimer’s disease, new study shows.

Article Source:
Materials provided by Centre for Addiction and Mental Health. Note: Content may be edited for style and length.

Journal Reference:
1. Philip Gerretsen, Jun Ku Chung, Parita Shah, Eric Plitman, Yusuke Iwata, Fernando Caravaggio, Shinichiro Nakajima, Bruce G. Pollock, Ariel Graff-Guerrero. Anosognosia Is an Independent Predictor of Conversion From Mild Cognitive Impairment to Alzheimer’s Disease and Is Associated With Reduced Brain Metabolism. The Journal of Clinical Psychiatry, 2017; DOI: 10.4088/JCP.16m11367

Namenda (Memantine): A cure for Alzheimer’s Disease?

Namemda- An Introduction to one of the newest Alzheimer’s medications.

Namenda (Memantine) was approved by the FDA in October as the newest treatment option for sufferers of Alzheimer’s disease. Memantine is marketed in the United States by Forest Laboratories and will be sold under the brand name of the Namenda, for patients with moderate to severe Alzheimer’s Disease. Forest Laboratories has stated that Namenda should be on the pharmacy shelves in January, 2004. Namenda has been sold for quite some time in Germany and Canada, and many U.S. families have been purchasing it over the internet for awhile. It is estimated that approximately 4 million Americans have Alzheimer’s disease, and about one million of them are believed to suffer severe symptoms. This will be the first time in which a medication is being offered for patients in the moderate to severe stage of the disease.

How will Namenda help?

Namenda has been found to help improve the memories and thinking skills of some patients who have moderate to severe impairments in their cognition (ability to think). However for the vast majority, the drug has been found to slow the pace of deterioration, allowing some patients to maintain their abilities to function somewhat independently for a longer period of time, which may benefit the patient and caregivers in some very important ways.

How is Namenda different from other Alzheimer’s medications?

While there are a few similarities between Namenda and other Alzheimer’s medications currently on the market, there are many more differences. Namenda is similar in that like the other Alzheimer’s medications (Aricept, Exelon, Reminyl and Cognex) it does not usually improve functioning as much as it retards the deterioration, allowing individuals to maintain independent functioning for a longer period of time. The most prominent difference is that these other medications are known to only be effective in the early stages of the disease, while Namenda is the first to have demonstrated effectiveness in the moderate to severe stages of Alzheimer’s. These other drugs delay the breakdown of another brain chemical called acetylcholine, which is necessary in the communication between nerve cells. Namenda naturally blocks excess amounts of another brain chemical called glutamate, which has been found to damage or kill nerve cells. Ultimately, doctors may eventually be able to prescribe combinations of medications in the hopes of better results.

Why should we feel hopeful about Namenda?

As just mentioned, doctor’s may be able to possibly use Aricept, Exelon, Reminyl or Cognex in the early stage the disease and possibly transition to a medication such as Namenda as the disease progresses to a more severe level of disability. It is recommended by the FDA’s scientific advisors whom have evaluated the drug, to recognize that Namenda does not offer miraculous benefits, and should not be a source of false hope to families of the most severely ill patients with Alzheimer’s. However, it is just another step in the progression of the development of medications which forestall the progressive deterioration of memory, and eventually may be an avenue toward a cure.

Namenda Side Effects: Special Warnings

What Namenda side effects may occur?

Although Namenda side effects cannot be anticipated, if any develop or change in intensity you need to contact your doctor immediately. Only your doctor can determine if it is still safe to continue taking this memory drug in spite of the Namenda side effects.

The Namenda side effects may include:

Confusion, constipation, coughing, dizziness, hallucinations, headache, high blood pressure, pain, sleepiness, vomiting

Namenda side effects and special warnings:

Namenda is not recommended for patients who have severe kidney impairment. There are various disease conditions that may alter the alkaline balance of the urine, which then may cause a build up of this medication in your body. You should always tell your physician about any major dietary changes, kidney problems such as renal acidosis, or urinary tract infections.

You should always make sure your doctor has information about any history of seizures that you may have. In addition to the previously mentioned Namenda side effects, this medication has not been formally studied among people with seizure disorders.

Namenda side effects and food and drug interactions:

In addition to the Namenda side effects, this medication should not be taken with certain other drugs as the effects can either be increased, decreased or altered in some other way. It is always important to check with your physician when combining Namenda with any of the following medications:

Amantadine (Symmetrel)
Cimetidine (Tagamet, Tagamet HB)
Cough suppressants that contain dextromethorphan (usually denoted as “DM”)
Glaucoma drug such as Diamox and Neptazane
Hydrochlorothiazide (HydroDIURIL)
Ketamine (Ketalar)
Nicotine (Nicoderm patch, Nicorette gum)
Quinidine (Quinidex)
Ranitidine (Zantac)
Sodium bicarbonate (baking soda, Alka-Seltzer)
Triamterene (Dyrenium DM)
You always need to be very sensitive to the combination of medications in addition to an awareness of any Namenda side effects.

Namenda Dosage: What is the recommended amount?

Namenda dosage for adults:

The recommended Namenda dosage is 10 mg twice a day. The Namenda dosage at the initiation of therapy is usually recommended to be 5 mg once a day for seven days, and then gradually increased by 5 mg every seven days up to a maximum Namenda dosage of 20 mg.

If side effects occur, your doctor may want to wait for about a week to increase the dose. Also, people who have impaired kidney function may also require lower doses.

Namenda dosage: How do you take this memory drug?

Namenda should be taken exactly as prescribed by your physician. The usual Namenda dosage is increased gradually in one-week intervals. Most physicians wait at least one week before increasing the dose. Dosages above the recommended amount have no additional benefit. This medication may be taken with or without food.

If you miss your dose…
You should take your forgotten dosage as soon as you remember, however, if it is almost time for your next dose, you should skip the missed one and continue on your regular schedule. You should never take two doses of Namenda at the same time.

Storage instructions…

You should always store this medication at room temperature.

Namenda Overdosage:

If your Namenda dosage is taken in excess of the recommended amount it may have serious consequences. If you suspect that you have taken too much, you should seek emergency treatment immediately.

Symptoms of Namenda overdosage may include…

Hallucinations, loss of consciousness, psychosis, restlessness, sleepiness, stupor

Taking the correct Namenda dosage is absolutely essential for the effective treatment of Alzheimer’s disease.

By Paul Susic Ph.D. Licensed Psychologist

Aricept Medication: Is this really a memory drug?

Brand name: Aricept

Generic name: Donepezil hydrochloride

Aricept medication: Why is this drug prescribed?

Aricept medication is one of only two drugs that have been found to provide some relief from symptoms of early Alzheimer’s disease. Aricept medication does not stop the progress of the underlying disease but may improve brain function in some sufferers of early Alzheimer’s disease. Alzheimer’s disease causes physical changes in the brain that interfere with the flow of information and disrupts memory, thinking and results in behavioral changes. These changes seem to be temporarily improved with the use of Aricept medication.

Aricept medication: Important information to know

In order to gain the benefits and maintain any improvement, Aricept must be taken on a regular basis. If it is stopped or taken irregularly, its benefits may be reduced or lost. You must also have some patience when starting this medication as it may take up to three weeks for any positive effects.

When should the Aricept medication not be prescribed?

Most geriatric doctors believe that there are least two main reasons to avoid Aricept: if you have an allergic reaction to the medication, or an allergic reaction to the group of antihistamines that includes Claritin, Allegra, Atarax, Periactin, Optimine, Nolahist and Hismanal.

Aricept medication: What if you’re pregnant or breast-feeding?

Since Aricept medication has not been prescribed for women of childbearing age it has not been tested among women who are pregnant or breast-feeding. Also, it has not been studied whether Aricept medication appears in breast milk and is therefore a threat to a feeding infant.

Aricept Side Effects and Special Warnings

What are some of the Aricept side effects that I may expect?

While specific Aricept side effects should not really be anticipated, if any develop or increase in intensity you need to contact your physician immediately. Only your doctor can determine if it is safe to continue this Alzheimer’s medication in spite of your or your loved one’s Aricept side effects.

Aricept side effects are usually more likely in higher doses and include diarrhea, fatigue, insomnia, loss of appetite, muscle cramps, nausea and vomiting. These are some of the more common side effects of this medication. When these side effects occur they are usually relatively mild and frequently get better as your treatment continues.

Other Aricept side effects may include:

Abnormal dreams, arthritis, bruising, depression, dizziness, fainting, frequent urination, headache, pain, sleepiness, weight-loss

Aricept side effects and special warnings:

This medication can increase the risk of seizures and aggravate asthma and other problems that you may have with your breathing. It can also cause fainting in people with heart conditions and may possibly slow your heartbeat. Obviously, you should always contact your physician if any of these problems occur. For individuals who take nonsteroidal anti-inflammatory drugs such as Aleve, Advil, or Nuprin, or for individuals who have had stomach ulcers, Aricept can possibly make your stomach side effects worse. You should always be cautious when taking this or any drug, and report all Aricept side effects to your doctor.

Aricept side effects and food and drug interactions:

In addition to the Aricept side effects, this medication may increase the effects of certain anesthetics. You should always make sure your doctor is aware that an individual is on Aricept prior to any surgeries. Aricept may also increase, decrease or otherwise alter the effects of other drugs. It is especially important to check with your doctor when taking Aricept with any of the following medications:

• Antispasmodic drugs such as Bentyl, Cogentin, and Pro-Banthine
• Bethanechol chloride (Urecholine)
• Carbamazepine (Tegretol)
• Dexamethasone (Decadron)
• Ketoconazole (Nizoral)
• Phenobarbital
• Phenytoin (Dilantin)
• Quinidine (Quinidex)
• Rifampin (Rifadin, Rifamate)

Although the above list of special precautions is fairly comprehensive, it does not include every possible Aricept side effect. You should always contact your physician if you experience any problematic concerns or any other medication related side effect that appears to be out of the ordinary.

Aricept dosages: How much is too much?

Aricept dosages: How is this medication taken?

Your Aricept dosage should be taken once a day, just before bedtime. It is very important to understand however, that your Aricept dosage must be taken every day. If Aricept is not taking regularly it will not work. This memory drug can be taken either with or without food.

If you miss your Aricept dosage…

You should take it as soon as you remember. However, if it is relatively close to the time for your next dose, you should skip the one that you missed and get back to your regular dosage schedule. You should never double your dose. Aricept should always be stored at room temperature.

Recommended Aricept dosage:


The usual starting Aricept dosage is 5 mg. once a day at bedtime, for a period of at least four to six weeks. You should not increase your dosage through this period of time unless you’ve been directed to do so by your physician. If it is warranted, your doctor may increase your Aricept dosage to as high as 10 mg.


Aricept has not been tested among children for either safety or effectiveness.

Aricept overdosage:

Any medication taken in excess of the recommended amount can be dangerous to your health. If you suspect an overdosage of Aricept you need to contact your doctor immediately or seek medical attention.

Symptoms of Aricept overdosage include:

Collapse, convulsions, extreme muscle weakness (possibly ending in death), low blood pressure, nausea, salivation, slowed heart rate, sweating, vomiting

Taking your Aricept dosage as prescribed is incredibly important. The only way to receive the benefits of this effective Alzheimer’s medication is consistently and accurately taking your Aricept dosage.

By Paul Susic Ph.D. Licensed Psychologist

Alzheimer’s Care: 9 Ideas That Really Work

Alzheimer’s care for the patient and the caregiver:

Alzheimer’s care is available for both the patient and the caregiver. Obviously, proper Alzheimer’s care is only available when educating yourself and following through on the recommendations of available professionals. The following 9 suggestions should help both yourself and those that you love in providing Alzheimer’s care.

(1) Be informed. You need to become as informed as possible. The more you know about Alzheimer’s disease and other dementing illnesses, the more effective and helpful you can be for your loved ones in devising strategies to manage behavioral problems.

(2) Share your concerns with the Alzheimer’s patient. You may share your concerns with the Alzheimer’s patient if they are mildly to moderately impaired. At that stage they may be able to take some part in managing their problems. They may be able to hear your worries and grief and together devise memory aids that may help him/her to remain independent. Also, mildly impaired individuals may benefit from counseling to help them accept and adjust to their limitations.

(3) Getting enough rest. One of the more difficult things family members frequently have to deal with is that the caregiver may not get enough rest or have the opportunity away from their caregiving responsibilities. This can make the Alzheimer’s caregiver less patient and unable to tolerate irritating or frustrating behaviors. If things feel like they are getting out of hand, you should ask yourself if this may be happening to you. If so, you should try to find ways to get more rest or take more frequent breaks from your caregiving responsibilities.

(4)You should use your common sense and imagination. Your common sense and imagination are your best tools along with your ability to adapt. If something can’t be done one way, ask yourself how else it could be done or if it must be done at all. For example, if an individual with Alzheimer’s can eat with her/his fingers but not with a fork, why waste your time resisting the inevitable. Simply serve as many finger foods as possible. If they insist on sleeping with his/her hat on and this is not harmful, you probably should just go along with it.

(5) Hold on to your sense of humor.
If you hold onto your sense of humor, it can get you through many crises. A person with Alzheimer’s disease is still a person and may still need to and be able to enjoy a good laugh. Also, sharing your experiences with other Alzheimer’s families may be helpful. Frequently, these other families find these shared experiences funny as well as sad.

(6) Try to establish environments with as much freedom as possible, while also maintaining structure. You need to establish a regular, predictable, and simple routine for meals, medication, exercising, bedtime and other activities. You should try to do things the same way at the same time every day. Through having an established regular routine, the Alzheimer’s individual will gradually learn what to expect. You should change routines only when they are not working. Keep the person’s surroundings reliable and very simple. Always leave furniture in the same place and put away any clutter.

(7) Remember to talk to the patient with Alzheimer’s disease.
You should make it a point to speak slowly, calmly and gently. You should also make it a point of telling the Alzheimer’s patient in simple steps exactly what you are doing and why. Always let him/her be a part of deciding as many things as possible. You should always avoid talking about him/her in front of them to others and ask others to avoid this also.

(8) Have an ID necklace or bracelet made for the confused person.
You should include on the bracelet, the nature of the disease (e.g. memory impaired) and your telephone number. This is probably one of the most important things you can do for an individual with Alzheimer’s disease who gets confused. Many confused people wander away or get lost at one time or another and an ID bracelet can save you from hours of frantic worry.

(9) Keep the impaired person active and then try not to upset them.
Families of Alzheimer’s patients often ask if retraining, reality orientation, or keeping active will slow down or stop the course of the disease process. Some individuals with dementing illnesses like Alzheimer’s disease become listless, apathetic or depressed. Families often wonder whether encouraging them to do things will help the Alzheimer’s individual to function better.

At the present time however, the relationship between activity and its effect on Alzheimer’s is not clear. Researchers continue to assess this issue. It is known that activity is beneficial in effecting and preventing other conditions and illnesses and helps the person with this dementing illness to continue to feel like they are involved in the family and that their life has meaning.

It is also well-known that individuals with Alzheimer’s cannot learn as well because the brain is damaged or parts of it had been destroyed. It would be unrealistic to expect these individuals to learn new skills. However, some individuals can learn simple tasks if they are repeated often enough and if the dementia is in the earlier stages. On the other hand, it is important to understand that too much stimulation or activity or pressure to learn may actually upset the confused person and accomplished little to nothing. The most important fact is that you should maintain balance:

1. You should accept that the lost skills are gone forever (woman who has lost the ability to cook will not be able to do so). You should also know that by gently giving information that is within the person’s abilities, it may help them to function more comfortably (an individual going into a new health care setting may be able to learn where they are with frequent reminders).

2. Always remember that even small amounts of excitement such as visitors, laughter and other changes can upset the confused person. However, you should always remember to make things interesting and stimulating within their capabilities such as walking or visiting an old friend.

3. Look for ways to simplify activities so that the individual can continue to be involved within the limits of their capabilities (a woman who can no longer cook may still be able to peel the potatoes).

4. Focus on the things that they can still do. An individual’s intellectual abilities are not all lost at once. They will benefit by careful assessment of their abilities in an attempt to keep them involved as much as possible.

5. You may consider having a trained person come into your home to visit the Alzheimer’s patient, or try a group program such as a day care program. Day care programs often offer the ideal level of stimulation for some individuals with Alzheimer’s disease as well is giving you some time off.

By Paul Susic Ph.D. Licensed Psychologist (Geriatric Psychologist)

Alzheimer’s Medications and Vitamin E

Alzheimer’s Medication and treatment overview:

Currently there is no Alzheimer’s medications or treatment that can prevent or halt the mental decline associated with Alzheimer’s disease. Many drugs have been tested, but most have been abandoned, or found to be ineffective or even toxic in their use as an Alzheimer’s treatment. Most of the more effective Alzheimer’s medications have focused on preventing the destruction of neurons, with the ultimate goal of preventing the decline of memory functioning for as long as possible.

One theory that drives research in the area of Alzheimer’s treatment involves the belief that memory deficits in Alzheimer’s disease are in part a deficiency in the neurotransmitter acetylcholine. Medical scientists have continued to try to boost the amount of acetylcholine in the brain by administering substances containing it, and by stimulating the brain to manufacture it in increasing amounts, or by preventing the breakdown of the limited quantities of acetylcholine that the brain is able to make on its own. Lecithin and Choline, which are substances that appear naturally in many foods, are used by the body to produce acetylcholine. Both Lecithin and Choline have been given in supplement form to Alzheimer’s patients in the hope of improving their mental functioning, but have had very disappointing results at the present time.

Alzheimer’s Medication – Cholinesterase Inhibitors:

Some of the more recently reported Alzheimer’s mediations include the cholinesterase inhibitors, which were the first drugs approved by the U.S. Food and Drug Administration (FDA). These medications include tacrine (Cognex), donezepil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl) and most recently memantine (Namenda) which slow the breakdown of acetylcholine. While they may reduce some the mild symptoms associated with Alzheimer’s disease, they do not prevent or in any way halt its progression. They merely delay the progression of the disease. According to guidelines published by the American Academy of Neurology in 2001, these medications are consistently better than placebo, but the average benefit is relatively small and the disease continues to progress despite the treatments.

Alzheimer’s treatment and Vitamin E:

The New England Journal of Medicine published an article in 1997 related to the study of the antioxidant properties of vitamin E. It was found in that research that patients with moderately severe Alzheimer’s disease received a daily dose of 2000 IU of vitamin E, 10 mg a day of selegeline, (a medication used for Parkinson’s disease treatment), both, or a placebo. Vitamin E or selegeline seem to slow the time to institutionalization and increase survival by approximately 7 months. The number of individuals losing their ability to do daily activities such as bathing or handling money was cut by one quarter. Combining vitamin E with selegeline did not improve the results.

The American Academy of Neurology concluded that based upon the study that there is good evidence to support the use of vitamin E in an attempt to slow the progression of the Alzheimer’s disease process. The evidence for selegiline to do the same was found to be weaker and there is no real advantage to using selegiline if vitamin E is already being used in an individual’s Alzheimer’s treatment.

An important fact to note in the use of vitamin E as an Alzheimer’s treatment is that while it is generally safe, large doses have been associated with bleeding in some individuals.

A Final Comment on the use of Alzheimer’s Medications.

While Alzheimer’s medication and treatment have limited effectiveness, they may delay the progression for some time and provide you some additional time to spend with your love ones before the inevitable decline in activites of daily living.

By Paul Susic Ph.D.. Licensed Psychologist (Geriatric Psychologist)

See Related Posts:

Alzheimer’s Diagnosis: How do you know for sure?

Alzheimer’s Diagnosis Overview:

Currently there are no definitive tests to determine an Alzheimer’s diagnosis, except for an autopsy which may be performed after death. Instead, the current approach for establishing an Alzheimer’s diagnosis basically involves a process of elimination, ruling out other conditions which may mimic or exacerbate memory conditions such as depression, Huntington’s disease, or hypothyroidism. An Alzheimer’s diagnosis is essentially made based upon data from the patient’s history, mental status exams and interviews with the patient, family members and friends over a period of time. Studies have indicated that a diagnosis of Alzheimer’s disease based upon such clinical features are accurate in about 90% of the cases.

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM- IV), among other things, a combination of memory impairment and other cognitive deficits, such as difficulty communicating which is severe enough to affect social and job functioning must be found as well as a memory decline which is determined to be gradual in onset.

Although slightly less important than clinical features in making an Alzheimer’s diagnosis, laboratory imaging studies are also useful in providing additional information. Laboratory tests look for certain proteins or genes associated with Alzheimer’s disease while imaging techniques examine the brain for shrinkage. There is no foolproof test currently available including having a genetic predisposition to Alzheimer’s disease. Genetic predisposition does not mean that a specific individual will develop the disease and coincidentally many normal brains exhibit shrinkage.

Laboratory tests for an Alzheimer’s disease diagnosis:

Recently, two new tests have been developed called the ADmark Assays. One of these assays measures beta-amyloid and tau protein in the spinal fluid (requiring a spinal tap). The other assay considers the probability that an individual’s dementia is due to Alzheimer’s disease based upon whether the specific form of the gene that makes APOE (designated as e4) is present in the individual’s system. This test is usually discouraged in asymptomatic individuals, however. According to a panel of experts assembled by the National Institutes of Health, testing for this APO e4 gene should not be performed currently because there is presently no cure for Alzheimer’s disease as well as no treatment that has been recommended to lower the risk of developing it. It is believed that knowledge of the gene’s presence could produce unnecessary anxiety in an individual and can lead to discrimination by employers or health insurance companies.

Alzheimer’s diagnosis and imaging studies:

Imaging studies may eventually aid in the Alzheimer’s disease diagnosis before the onset of symptoms. Positron emission tomography (PET), single photon emission computer tomography (SPECT) and magnetic resonance imaging (MRI) scans are all currently used to examine brain structure or function in Alzheimer’s disease patients. Currently however, the scans are not routinely used in Alzheimer’s diagnosis, although they can rule out other possible causes of dementia.

Some information from The Johns Hopkins Medical Guide to Health After 50

By Paul Susic Ph.D. Licensed Psychologist

Alzheimer’s Brain: What are some of the degenerative changes?

Alzheimer’s brain: Changes do occur.

In the Alzheimer’s brain nerve cells stop functioning, lose connections with each other and ultimately die. The death of neurons in key parts of the Alzheimer’s brain causes those areas to shrink and results in substantial abnormalities in memory, thinking and behavior.

The Alzheimer’s early symptoms are derived from the destruction of neurons in particular parts of the Alzheimer’s brain controlling memory, especially the hippocampus (which is why the early signs of Alzheimer’s are related to memory impairment). As nerve cells in the hippocampus of the Alzheimer’s brain break down, short-term memory fails and the ability to do familiar tasks begin to decline as well.

The disease begins to attack the cerebral cortex which is responsible for some of the higher memory functions, such as language, reasoning, perception and judgment. Sometimes, unwarranted emotional outbursts (known as catastrophic reactions), and disturbing behaviors such as wandering and episodes of extreme agitation may appear after the early symptoms of Alzheimer’s appear.

Tangles and plaques in the Alzheimer’s brain:

Amyloid plaques and neurofibrillary tangles are some of the hallmarks of the changes that take place in the Alzheimer’s brain. Although, these changes may only be confirmed at autopsy, they are found in virtually every patient with Alzheimer’s disease. At the present time, it is not clear whether these abnormal deposits are the cause or byproduct of the disease process in the Alzheimer’s brain, although researchers have now come to understand how plaques and tangles are formed. The increasing knowledge in the area of Alzheimer’s disease has helped with new attempts to block the underlying disease process that may lead to their buildup. The eventual success of these strategies may ultimately provide the basis for prevention or treatment in the future, if these plaques and tangles are determined to be the cause of Alzheimer’s disease.

Amyloid plaques are known to develop in areas of the Alzheimer’s brain related to memory, and are believed to be a mixture of abnormal proteins and nerve cell fragments. They may develop from beta-amyloid, a protein that breaks off from a larger amyloid precursor protein. Beta-amyloid is formed when the amyloid precursor protein that is embedded in the cell membrane is broken down for disposal. Enzymes called secretases split the protein in two and form the beta-amyloid fragment in the Alzheimer’s brain.

Cleaving Enzymes?

Research into the Alzheimer’s brain has recently identified secretases as one of the “cleaving” enzymes. They are believed to cut amyloid precursor proteins in a place that cause beta-amyloid to become insoluble and form deposits in the brain of the Alzheimer’s patient. Investigators are now beginning to suspect that by blocking the activity of beta secretases you may prevent the production of undesirable forms of beta-amyloid. Current experiments are now underway to prove this hypothesis. It is still a mystery however of what happens to the beta-amyloid segment once it separates from the amyloid precursor protein, and why it may lead to these changes in the Alzheimer’s brain.
Neurofibrillary tangles are the other major pathological change characteristic of Alzheimer’s disease. These tangles are composed mostly of the protein tau, and are twisted, hair-like threads that remain after the collapse of the neuron’s internal support structure, which are referred to as microtubules. In healthy neurons, microtubules carry nutrients from one destination to another similar to railroad train tracks. Tau seems to serve as supporting “railroad ties”, but in the Alzheimer’s brain the protein becomes hopelessly twisted and disrupts the function of the microtubules. This defect is believed to clog communication within nerve cells, and eventually lead to cell death.

What is the deal with Pinl?

Alzheimer’s researchers are not sure why tau goes awry, but some of the more recent findings are beginning to state that Pin1 may play an important role in keeping the tau intact. When Pin1 binds to an altered tau in experiments, the protein begins to function as it should and microtubule assembly is restored. Also, researchers have began to find substantially lower levels of Pin1 in Alzheimer’s brains as contrasted to healthy subjects. While the significance of these findings is not certain, the presence of an enzyme such as Pin1 may help to maintain or restore the proper function of tau, and prevent the formation of neurofibrillary tangles. This possibility raises the hope that therapies might be developed in the future to keep tau functioning in the Alzheimer’s brain.

Neurotransmitters in the Alzheimer’s brain.

Another characteristic of the Alzheimer’s brain is a reduction in the level of certain neurotransmitters that are necessary for healthy brain functioning. Acetylcholine is produced in the brain by cholinergic neurons, which is a neurotransmitter that is believed to be crucial to memory and learning. These neurons are in abundance in the hippocampus and the cerebral cortex, which are two regions of the Alzheimer’s brain most ravaged by the disease. (As is true for the plaques and tangles, it is not known currently whether neuronal loss in these parts of the brain is a cause or an effect of Alzheimer’s disease.)

As the disease continues to progress in the Alzheimer’s brain, acetylcholine levels drop dramatically and dementia becomes more pronounced. The levels of serotonin, norepinephrine, somatostatin, and GABA, which are neurotransmitters involved in many aspects of brain functioning become diminished in at least half of the patients with Alzheimer’s disease. Such imbalances may lead to depression, aggression, insomnia and other mood and personality changes.

Some information from The Johns Hopkins Medical Guide to Health After 50

Additional information and webpage by Paul Susic Ph.D. Licensed Psychologist