About Alzheimer’s

The Neurological Causes Of Alzheimer’s Disease

The true causes of Alzheimer’s disease remain elusive. However, researchers have made progress in understanding the neurological roots of this debilitating condition.

The disease is named after Alois Alzheimer, who was the first to identify the peculiar plaques and tangles in the brain, which is characteristic of the illness. Till the final decades of the twentieth century, Alzheimer’s could be diagnosed accurately only by a post-mortem examination.

Nowadays, scientists are beginning to uncover precisely what is happening and why those characteristic tangles and plaques crop up in the brain.

Many of the symptoms of Alzheimer’s disease are caused by neurofibrillary tangles in the brain. Microscopic filaments clog the neurons. These filaments are made up of an abnormal kind of Tau protein.

In a normal brain, Tau protein bonds into microtubules and enables transmission of messages from one neuron to another. But in an Alzheimer brain, instead of bonding into message pathways, Tau protein bonds with itself. And the neuron messages go nowhere.

Since the neurons are clogged, signals from the environment are no longer transmitted the way they should be. That is why severe cognitive impairment is one of the symptoms of Alzheimer’s disease.

Scientists speculate that Tau protein malfunction which results in neurofibrillary tangles is caused by beta amyloid protein, but this is yet to be conclusively proved.

It is beta amyloid protein that causes plaques between neurons, which is the other main damage to the brain in Alzheimer’s disease.

The plaque deposits are sticky patches in the brain which contain beta amyloid protein. Plaque blocks communication pathways between neurons, which results in the memory problems and learning inabilities associated with Alzheimer’s disease.

The degree of cognitive impairment depends on the amount of plaque present. Plaque acts by interfering with the normal functioning of acetylcholine, which helps to transmit nerve messages.

Treatment for Alzheimer’s disease involves using acetylcholinesterase inhibitors, which works by blocking enzymes that consume the acetylcholine. This medication is effective during the early stages of the disease before too much plaque has already built up.

Some research seems to indicate that plaques cause tangles. One study took proteins from mice to eliminate the plaque-causing beta amyloid. They found that the proteins got rid of the tangles as well. Similar effects have been brought about by other medications as well.

Others believe that both plaques and tangles are the result of other processes. One possible culprit is swollen axons. Axons are critical for transmitting messages between neurons. When axons swell, they may block message transmission and perhaps lead to the plaques and tangles which bring on Alzheimer’s disease.

Scientists are working hard at uncovering the causes of Alzheimer’s disease, which may sooner or later lead to a comprehensive cure for this dreaded condition.

By: Jane Peters

Article Directory: http://www.articledashboard.com

Jane Peters is a researcher and has written on several topics. For must-have articles on vitamin E treatment in Alzheimer’s disease and other facts on Alzheimer’s syndrome, see the foregoing links.

(HealthDay News) — U.S. researchers have spotted two proteins that deliver a double hit to the brain function of Alzheimer’s disease patients.

The U.S. National Institute on Aging has more about Alzheimer’s disease.
– Robert Preidt

SOURCE: University of Rochester, news release, Dec. 21, 2008P

Source: One Healthy Lifestyle

If you suspect that a loved one may be experiencing one or more symptoms associated with Alzheimer’s disease, it is important to see a doctor. He or she will find out if the symptom you are concerned about is an indicator of the disease or of another condition. While the condition is always fatal, early diagnosis allows the patient’s family to prepare for the care he or she will need as the disease progresses.

There is no litmus test that proves the existence of the disease, but a diagnosis of the condition is correct 80 to 90 percent of the time. A medical doctor will evaluate the patient’s medical history and administer a number of tests. These tests include a physical exam and blood tests to help rule out other contributing conditions. A mental test will also be administered, requiring the patient to perform simple memory and processing tasks. In some cases other specialists may be involved in the diagnosis, and brain imaging can be used to evaluate the progression of the disease.

Earlier diagnosis giving Alzheimer’s a new voice

Alzheimer’s patient Kris Bakowski attends The Alzheimer’s Association town hall meeting about the early stages of the disease, Monday, May 12, 2008, in Washington. Alzheimer’s patients now a…   Read more…

MRI scans can be used to diagnose Alzheimer’s - WorldHealth.net

“This study demonstrates that MRI brain scans are accurate enough to be clinically useful, both in diagnosing Alzheimer’s disease itself at an early stage and in identifying people at risk …   Read more…

Source Natural Health News:

While we are on this thread of natural help for dis-ease isn’t it timely that I just received this article about how "High Doses of Vitamins Fight Alzheimer’s Disease".

And now I am sharing it with you, for your education, and then you can ask your doctor why they aren’t recommending them.

Vitamin B3 is also used successfully for schizophrenia, rheumatoid arthritis, arthritis, reducing plaque of arteriosclerosis and cholesterol reduction. It has an excellent anti-inflammatory action.
(OMNS, December 9, 2008) The news media recently reported that "huge doses of an ordinary vitamin appeared to eliminate memory problems in mice with the rodent equivalent of Alzheimer’s disease." They then quickly added that "scientists aren’t ready to recommend that people try the vitamin on their own outside of normal doses." (1)

In other words, extra-large amounts of a vitamin are helpful, so don’t you take them!

That does not even pass the straight-faced test. So what’s the story?

Researchers at the University of California at Irvine gave the human dose equivalent of 2,000 to 3,000 mg of vitamin B3 to mice with Alzheimer’s. (2) It worked. Kim Green, one of the researchers, is quoted as saying, "Cognitively, they were cured. They performed as if they’d never developed the disease."

Specifically, the study employed large amounts of nicotinamide, the vitamin B3 widely found in foods such as meat, poultry, fish, nuts and seeds. Nicotinamide is also the form of niacin found, in far greater quantity, in dietary supplements. It is more commonly known as niacinamide. It is inexpensive and its safety is long established. The most common side effect of niacinamide in very high doses is nausea. This can be eliminated by taking less, by using regular niacin instead, which may cause a warm flush, or choosing inositol hexaniacinate, which does not. They are all vitamin B3.

HealthDay Reporter mentioned how cheap the vitamin is; the study authors "bought a year’s supply for $30" and noted that it "appears to be safe." Even so, one author said that "I wouldn’t advocate people rush out and eat grams of this stuff each day." (1)

The BBC quoted Rebecca Wood, Chief Executive of the UK Alzheimer’s Research Trust, who said, "Until the human research was completed, people should not start taking the supplement. . . . people should be wary about changing their diet or taking supplements. In high doses vitamin B3 can be toxic." (3)

The Irish Times reiterated it: "People have been cautioned about rushing out to buy high dose vitamin B3 supplements in an attempt to prevent memory loss . . . The warnings came today one day on from the announcement . . .Vitamins in high doses can be toxic." (4)

Their choice of words is quaint but hardly accurate. There is no wild "rush;" half of the population already takes food supplements. And as for "toxic," niacin isn’t. Canadian psychiatrist Abram Hoffer, M.D., asserts that it is actually remarkably safe. "There have been no deaths from niacin supplements," Dr. Hoffer says. "The LD 50 (the dosage that would kill half of those taking it) for dogs is 5,000-6,000 milligrams per kilogram body weight. That is equivalent to almost a pound of niacin per day for a human. No human takes 375,000 milligrams of niacin a day. They would be nauseous long before reaching a harmful dose." Dr. Hoffer conducted the first double-blind, placebo-controlled clinical trials of niacin. He adds, "Niacin is not liver toxic. Niacin therapy increases liver function tests. But this elevation means that the liver is active. It does not indicate an underlying liver pathology."

The medical literature repeatedly confirms niacin’s safety. Indeed, for over 50 years, nutritional (orthomolecular) physicians have used vitamin B3 in doses as high as tens of thousands of milligrams per day. Cardiologists frequently give patients thousands of milligrams of niacin daily to lower cholesterol. Niacin is preferred because its safety margin is so very large. The American Association of Poison Control Centers’ Toxic Exposure Surveillance System annual reports indicates there is not even one death per year due to niacin in any of its forms. (5)

One the other hand, there are 140,000 deaths annually attributable to properly prescribed prescription drugs. (6) And this figure is just for one year, and just for the USA. Furthermore, when overdoses, incorrect prescription, and adverse drug interactions are figured in, total drug fatalities number over a quarter of a million dead. Each year.

The BBC’s curious mention that we should even be "wary about changing our diets" is especially odd. More and more scientists think our much-in-need-of-improvement diets are what contribute more than anything to developing Alzheimer’s. "There appears to be a statistically significant link between a low dietary intake of niacin and a high risk of developing Alzheimer’s disease. A study of the niacin intake of 6158 Chicago residents 65 years of age or older established that the lower the daily intake of niacin, the greater the risk of becoming an Alzheimer’s disease patient." The group with the highest daily intake of niacin had a 70 percent decrease in incidence of this disease compared to the lowest group. "The most compelling evidence to date is that early memory loss can be reversed by the ascorbate (vitamin C) minerals. Greater Alzheimer’s disease risk also has been linked to low dietary intake of vitamin E and of fish." (7)

Nutrient deficiency of long standing may create a nutrient dependency. A nutrient dependency is an exaggerated need for the missing nutrient, a need not met by dietary intakes or even by low-dose supplementation. Robert P. Heaney, M.D., uses the term "long latency deficiency diseases" to describe illnesses that fit this description. He writes: "Inadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. . . Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible." (8) Where pathology already exists, unusually large quantities of vitamins may be needed to repair damaged tissue. Thirty-five years ago, in another paper, Hoffer wrote: "The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure." (9)

As there is no recognized cure for Alzheimer’s, prevention is vital. In their article, the Irish Times does admit that "Healthy mice fed the vitamins also outperformed mice on a normal diet" and quoted study co-author Frank LaFerla saying that "This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve." (4) And study author Green added, "If we combine this with other things already out there, we’d probably see a large effect."

The US Alzheimer’s Association’s Dr. Ralph Nixon has said that previous research has suggested that vitamins such as vitamin E, vitamin C and vitamin B12 may help people lower their risk of developing Alzheimer’s disease. At their website (although you have to search for it), the Alzheimer’s Association says, "Vitamins may be helpful. There is some indication that vitamins, such as vitamin E, or vitamins E and C together, vitamin B12 and folate may be important in lowering your risk of developing Alzheimer’s. . . One large federally funded study (10) showed that vitamin E slightly delayed loss of ability to carry out daily activities and placement in residential care."

But overall, at their website http://www.alz.org/index.asp the Alzheimer’s Association has strikingly little to say about vitamins, and they hasten to tell people that "No one should use vitamin E to treat Alzheimer’s disease except under the supervision of a physician." ( http://www.alz.org/alzheimers_disease_10428.asp ) "They write as if these safe vitamins are dangerous drugs, not be used without a doctor’s consent," comments Dr. Hoffer. "I have been using them for decades."

Niacin and nerves go together. Orthomolecular physicians have found niacin and other nutrients to be an effective treatment for obsessive compulsive disorder, anxiety, bipolar disorder, depression, psychotic behavior, and schizophrenia. New research confirms that niacinamide (the same form of B3 used in the Alzheimer’s research) "profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits" in animals with an illness very similar to multiple sclerosis. (11)

A measure of journalistic caution is understandable, especially with ever-new promises for pharmaceutical products. Drugs routinely used to treat Alzheimer’s Disease have had a disappointing, even dismal success rate. So when nutrition may be the better answer, foot-dragging is inexplicable, even inexcusable. Nutrients are vastly safer than drugs. Unjustified, needlessly negative opinionating is out of place. Over 5 million Americans now have Alzheimer’s disease, and the number is estimated to reach 14 million by 2050. Potentially, 9 million people would benefit later from niacin now.

"Man is a food-dependent creature," wrote University of Alabama professor of medicine Emanuel Cheraskin, M.D.. "If you don’t feed him, he will die. If you feed him improperly, part of him will die."

When that part is the brain, it is dangerous to delay the use of optimum nutrition.

SUPPLEMENTATION WITH FOLATE SEEN AS ANOTHER WEAPON IN THE BATTLE vs AGE RELATED DEMENTIA & ALZHEIMER’S DISEASE

Here is some good news for those of us on the Alzheimer’s and age related dementia front. I say good news because it confirms that there is still another thing we can do decrease our risks of developing these conditions. This time we are talking about Folate(folic acid) or Vitamin B 9.

Does anyone get enough of this key nutrient? Sadly and dangeously the answer is no almost no one gets enough from our day to day nutritional intake. That is mostly because the best sources of Folate in our diets are leafy greens, a food item that people don’t readily choose to eat at least not in sufficient quantities.

Add to that fact the fact that today’s vegetable greens are just not what they used to be. They do not offer the same nutirent punch as they once did. This is due to nutrient scarcity in the soils they are grown in.

This all leads to the real issue which is as confirmed in a Korean study there is a real measurable and direct connection between folate deficiency and the likelihood of Alzheimer’s  and age-related dementia.

Out of five hundred senior citizens age 65 or older were closely monitored for a period of 30 months 45 developed dementia 34 of those were vistims of Alheimer’s Disease. It was noted that what the members of the group that developed dementia there was a commonthread of a declination of their folate levels. This in comparison to the people in the study who did not develope dementia.

The statisticians then went to work on the findings in the study and it was concluded that people with the lower levels of folate had 3X the risk of developing dementia or Alzheimer’s Disease.

Currently it is being recommended that supplementation with 800 mcg of folate to compensate for the deficiency amnd of course to eat more leafy green vegetables such as they are.

 If you want to know more about the efficacy or start supplementing with Folate to help protect you this you must as always first discuss it with your doctor. no medical advice is part of this blog.

Null Series: B vitamins for preventing mental decline as we age

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Study Suggests Folate Deficiency Increases Dementia Risk Three …

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In a recent Email to me and others Shane Ellison a chemist who is unafraid to take on traditional approaches to medical issues including overweight and high cholesterol touched on Alzheimer’s Disease. Aware of this study I thought I would share with you this scientist’s words. I personally supplement with Acetyl L Carnitine and Alpha Lipoic Acid ever since I became aware of the findings of biochemists that indicate it might help as a mitigator of age related dementia.

There is never any medical advice in this blog. My purpose here is always to bring to your attention things that have come to my attention in the years since personal experiences brought Alzheimer’s into my focus. If this or any other blog encourages you to supplement or adopt some other behavior it should NOT. What it should do is encourage you to learn more and ask your doctor for advice in this and all such matters. Below are Shane Ellison’s emailed comments"

"Whether it’s simple forgetfulness or the all-out scourge of Alzheimer’s, the loss of mental acuity as we age ruins quality of life. To the surprise of most, studies show that this decline can be slowed or even prevented by controlling blood sugar! And with the simple, everyday use of a nutritional supplement, this is easier to do than ever.

The nutritional supplements acetyl-L-carnitine (ALCAR) and alpha-lipoic acid (ALA) work to increase our sensitivity to insulin. Insulin is the "sugar taxi." The greater sensitivity you have, the faster your sugar is escorted out of the blood and into muscle cells where it is converted into energy. This not only preserves memory but also keeps skin looking vibrantly young and preserves our heart by helping it beat forcefully without damage caused by spikes in blood sugar.

Better than FDA Approved Drugs

In addition to increasing insulin sensitivity, ALCAR increases memory-boosting neurotransmitters like acetylcholine while protecting neurons from oxidative stress. This makes the ALA/ALCAR combo a potent weapon against Alzheimer’s induced memory loss. In fact, I’d choose it over the commonly used medications, which are known technically as acetylcholinesterase inhibitors (AChEs).

Little is known about what causes Alzheimer’s, but all sufferers appear to have low levels of acetylcholine. Using AChEs, the drug industry attempts to increase this essential brain chemical by preventing the breakdown of acetylcholine within the brain. Theoretically, this would enhance or preserve memory. But if there is little or no acetylcholine to preserve, the drugs are useless. Perhaps that is why they have only marginal benefits - benefits that do not outweigh their immense risks.

Believe it or not, AChEs are synthetic copycats of naturally occurring poisons and venoms! Their use is rationalized by the "a lot kills, a little cures" mentality. But evidence doesn’t support this. Research consistently shows users to suffer short-term side effects, including diarrhea, anorexia, vomiting, and tremors. Long-term side effects include kidney damage and even cancer.

Where these drugs fail, the energizing ALA/ALCAR combo succeeds.

Once ingested, both ALA and ALCAR pass the blood-brain barrier to nourish brain cells, thereby helping them manufacture more acetylcholine - to preserve and restore life’s most precious memories as we age. "

Thanks you Shane Ellison for this informational email.

  Alpha Lipoic Acid: The Multi-Tasking Supplement

  Alpha Lipoic Acid & Acetyl L-Carnitine Anti-Aging and Energy …

Recently at an Alzheimer’s support group meeting the subject of inflammation and it’s role in Alzheimer’s Disease came up. I referred the group to an answer provided by Dr. Don Colbert about a year ago. Dr Colbert is a blender of alternative and traditional approachs to medical problems, a pretty smart guy.

The doctor was asked:

  How can simple inflammation cause such a devastating disease?

Dr. Colbert’s answer with (references below provided by the doctor in his forum):

" Plaques and tangles are indeed the hallmarks of Alzheimer’s disease. But researchers looking at the brain damage caused by Alzheimer’s have always noted the presence of inflammation wherever plaques and tangles form.¹⁰ In the past, this inflammation was thought to be simply a consequence of Alzheimer’s disease. Now scientists believe the inflammation itself starts a chain reaction ultimately contributing to the developement of Alzheimer’s disease.¹¹ When cells in the brain are disrupted by inflammation, amyloid, a protein normally found in the brain, begins to act chaotically. This chaos results in the creation of beta amyloid, protein that is toxic to cells in the brain. Sticky deposits of beta-amyloid build up and collect around the cells, making dense clumps or plaques. Because the brain can’t break the plaques down or get rid of them, they stay right where they are and slowly accumulate.^10,12,13
Tangles result when long protein fibers that act like scaffolding for brain cells begin to twist and tangle. The cell is damaged and eventually dies. But the tangled proteins remain in the brain even after the dead neuron has been cleared away.^10,14 And inflammation might be the culprit causing the long protein fibers to start tangling.¹⁵

1. Jha S, Patel R. Some observations on the spectrum of dementia. Neurol India. 2004;52:21 3-4.
2. Vas CJ, Pinto C, Panikker D, et al. Prevalence of dementia in an urban Indian population. Int Psychogeriatr 2001 ;1 3:439-50.
3. The Alzheimer’s Disease Fact Sheet. Alzheimer’s Disease Education & Referral Center. A service of the National Institute of Aging. Accessed on September 8, 2005.
4. Chandra V, Pandav R, Dodge HH, et al. Incidence of Alzheimer’s disease in a rural community in India: the Indo-US study. Neurology. 2001 ;57:985-9.
5. Ringman JM, Frautschy SA, Cole GM, Masterman DL, Cummings JL. A potential role of the curry spice curcumin in Alzheimer’s disease. Curr Alzheimer Res. 2005;2:131-6.
6. Curcuma longa (turmeric). Monograph. Altern Med Rev. 2001 ;6 Suppl:S62-6.
7. Sharma RA, Gescher AJ, Steward WP. Curcumin: The story so far. Eur J Cancer. 2005;41 :1955-68.
8. Weber WM, Hunsaker LA, Abcouwer SF, Deck LM, Vander Jagt DL. Anti-oxidant activities of curcumin and related enones. B!oorg Med Chem. 2005;1 3:3811-20.
9. Karunagaran D, Rashmi R, Kumar TR. Induction of apoptosis by curcumin and its implications for cancer therapy. Curr Cancer Drug Targets. 2005;5:1 17-
10. Curtis SM, Porth CM. Alzheimer’s disease. In: Porth CM. Pathophys!ology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa: Lippincott; 2002: 914- 917.
11. Fryer JD, Holtzman DM. The bad seed in Alzheimer’s disease. Neuron. 2005;47:167-8.
12. Kranenburg O, Bouma B, Gent YY, et al. Beta-amyloid (Abeta) causes detachment of N1E¬115 neuroblastoma cells by acting as a scaffold for cell-associated plasminogen activation. Mol Cell Neurosc!. 2005;28:496-508.
13. Morgan C, Colombres M, Nunez MT, Inestrosa NC. Structure and function of amyloid in Alzheimer’s disease. Prog Neurob!ol. 2004;74:323-49.
14. Liazoghli D, Perreault S, Micheva KD, Desjardins M, Leclerc N. Fragmentation of the Golgi apparatus induced by the overexpression of wild-type and mutant human tau forms in neurons. Am J Pathol. 2005;166:1499-514.
15. Minghetti L. Role of inflammation in neurodegenerative diseases. Curr Op!n Neurol. 2005;18:315-21.
16. Andel R, Crowe M, Pedersen NL, Mortimer J, Crimmins E, Johansson B, Gatz M. Complexity of work and risk of Alzheimer’s disease: a population-based study of Swedish twins. J Gerontol B Psychol Sc! Soc Sc!. 2005;60:P251 -8.
17. Heady JA, Kennaway EL. The increase in deaths attributed to cancer of the lung. Br J Cancer. 1949;3:31 1-20.
18. Park SY, Kim DS. Discovery of natural products from Curcuma longa that protect cells from beta-amyloid insult: a drug discovery effort against Alzheimer’s disease. J Nat Prod. 2002;65:1227-31.
19. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J B!ol Chem. 2005;280:5892-901.
20. Ono K, Hirohata M, Yamada M. Ferulic acid destabilizes preformed beta-amyloid fibrils in vitro. B!ochem B!ophys Res Commun. 2005;336:444-449.
21. Ono K, Hasegawa K, Naiki H, Yamada M. Curcumin has potent anti-amyloidogenic effects for Alzheimer’s beta-amyloid fibrils in vitro. J Neurosc! Res. 2004;75:742-50.
22. Aggarwal BB, Shishodia S. Suppression of the nuclear factor-kappaB activation pathway by spice-derived phytochemicals: reasoning for seasoning. Ann N Y Acad Sc!. 2004;1030:434-41.
23. Yang F, Lim GP, Begum AN, et al. Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. J B!ol Chem. 2005;280:5892-901.
24. Giri RK, Rajagopal V, Kalra VK. Curcumin, the active constituent of turmeric, inhibits amyloid peptide-induced cytochemokine gene expression and CCR5-mediated chemotaxis of THP-1 monocytes by modulating early growth response-1 transcription factor. J Neurochem. 2004;91 :1199-210.
25. Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosc!. 2001 ;21 :8370-7.
26. Cole GM, Morihara T, Lim GP, Yang F, Begum A, Frautschy SA. NSAID and Antioxidant Prevention of Alzheimer’s Disease: Lessons from In Vitro and Animal Models. Ann N Y Acad Sc!. 2004;1 035:68-84.
27. The Univerity of California at Los Angeles (UCLA) Alzheimer’s Disease Research Center (ADRC) Current studies: Mild to Moderate Alzheimer’s Disease and Curcumin. Information available at the ADRC Website: http://www.npistat.com/adrc/Treatment. asp.
28. Pasinetti GM. From epidemiology to therapeutic trials with anti-inflammatory drugs in Alzheimer’s disease: the role of NSAIDs and cyclooxygenase in betaamyloidosis and clinical dementia. J Alzhe!mers D!s. 2002;4:435-45.
29. What You Need to Know About Nonsteroidal Anti-Inflammatory Medications (NSAIDs). The Cleveland Clinic Health Information Center. Accessed on September 8, 2005.  Available at: http://www.clevelandclinic.org/health/h ealthinfo/ docs/0700/071 4.asp?index=490 1.

It is vital we don’t try to go it alone when dealing with the care of a loved one who has Alzheimer’s Disease. No man is an island as the saying goes. seek out support of others who know the ropes. Communal support from others who are sharing your very difficult burden may just get you through the ordeal with the least emotional pain.

Never blame yourself if you get frustrated with what may be demanded of you. You are only human. having the support of others who know these feelings is the rick

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Alzheimer’s … mer’s Patients with Meaningful Activities

Being the family or caregiver of an Alzheimer’s patient will expand your family if you make the effort to get support from and give support to others facing this challenge.