Natural Herbs and Nutrients for Alzheimer's Disease treatment by Ray Sahelian, M.D.
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Twice a month we email a brief abstract of
several new studies on various supplements and natural medicine topics and their
practical interpretation by Ray Sahelian, M.D.
We will mention research updates on natural options for Alzheimer's disease treatment.
Alzheimer's disease, the most common form of dementia, is a progressive disorder
characterized by widespread loss of brain cells called neurons, beta-amyloid deposits in the cerebral blood
vessels, development of plaques and the presence of neurofibrillary tangles.
These changes, occurring in the association area of the cerebral cortex, the hippocampus
and the middle and temporal lobes, are accompanied by decreased concentrations of the
neurotransmitter acetylcholine. In my opinion, it appears that a deficiency in
antioxidant status may accelerate the progression of Alzheimer's
disease, and making an effort through diet or supplements to have adequate
antioxidant status can reduce the risk for Alzheimer's disease.
Alzheimer's statistics : More than 5 million people in the US have Alzheimer's disease. Recent US census figures suggest that by 2050, the number of people with Alzheimer's disease will triple. Americans are living longer, healthier lives and only the mortality rate from Alzheimer's disease is increasing among the top 10 causes of death, the U.S. federal government reported on Wednesday. Alzheimer's disease moved to seventh place from eighth place among the leading causes of death in 2004, passing influenza and pneumonia.
Natural options for Alzheimer’s Disease
treatment - Alternatives to Alzheimer's Medication
While scientists have not fully determined the actual causes of Alzheimer’s
disease, a number of treatment options have been proposed or tried over the years.
Although much more research needs to be done in order to find out the role of
these supplements in Alzheimer's disease treatment, I think it is appropriate to give them
a try since this condition currently has no cure or effective treatment. You are
not likely to find this information in any official Alzheimer's disease
association or Alzheimer's foundation. Some natural options for Alzheimer's
disease treatment or prevention include (discuss with your doctor first):
It is nearly impossible to know which of the above nutrients or herbs, or combinations thereof are helpful as a treatment, prevention, or alternative Alzheimer's disease medication. It may be a trial and error process until the right combination or dosage is found. It is also very difficult to predict how these supplements interact with Alzheimer's medication prescription drugs. One has to be cautious with some of these supplements, particularly galantamine and huperzine since they can be quite potent. Also, when taking multiple supplements, make sure to reduce the dose of each one since they add on to each other and one could have insomnia or feel overstimulated.
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Alpha lipoic acid and
Alzheimer's disease
Alpha-lipoic acid as a new treatment option for Alzheimer's disease--a 48
months follow-up analysis.
J Neural Transm Suppl. 2007. Department of Medical Rehabilitation
and Geriatrics, Henriettenstiftung, Hannover, Germany.
Oxidative stress and neuronal energy depletion are characteristic
biochemical hallmarks of Alzheimer's disease. It is therefore conceivable
that pro-energetic and antioxidants such as alpha-lipoic acid might delay
the onset or slow down the progression of the disease. In a previous
study, 600mg alpha-lipoic acid was given daily to nine patients with
Alzheimer's disease (receiving a standard treatment with choline-esterase
inhibitors) in an open-label study over an observation period of 12
months. The treatment led to a stabilization of cognitive functions. In this report, we have
extended the analysis to 43 patients over an observation period of up to
48 months. In patients with mild dementia, the disease progressed
extremely slowly, in patients with moderate dementia at approximately
twice the rate. However, the progression appears dramatically lower than
data reported for untreated patients or patients on choline-esterase
inhibitors in the second year of long-term studies. Despite the fact that
this study was not double-blinded, placebo-controlled and randomized, our
data suggest that treatment with alpha-lipoic acid might be a successful neuroprotective
therapy option for Alzheimer's disease.
Melatonin and morning sun exposure
Sun exposure or bright light along with an evening dose of
melatonin helps normalize the sleep-wake cycle in elderly adults with
Alzheimer's disease. Patients with Alzheimer's commonly have disrupted
sleep at night and nap frequently during the day. Researchers looked at
whether light therapy -- alone or along with melatonin supplements --
could restore a more natural sleep-wake cycle. Dr. Glenna A. Dowling, of
the University of California, San Francisco, and her colleagues randomly
assigned 50 nursing home patients with Alzheimer's to one of three groups
for a period of ten weeks. Patients in the first group were given light
therapy for one hour. The light therapy consisted of either natural light
alone, or additional artificial light when needed. Patients in the second
group received both morning light therapy as well as a dose of melatonin a
few hours before bedtime. Those in the third group were exposed to only
normal indoor light and were not given melatonin. The combination of light
therapy and melatonin reduced daytime sleepiness and increased patients'
activity during the day. Light therapy alone, however, was not enough to
be helpful. Journal of the American Geriatrics Society, February 2008.
Comments: The ideal long term melatonin dosage for patients with
Alzheimer's disease is not clear but my thought is that half or 1 mg every
other night or every third night is a good option.
Melatonin and bright-light treatment
for rest-activity disruption in institutionalized patients with
Alzheimer's disease.
J Am Geriatr Soc. 2008 Feb. Dowling GA, Burr RL, Van
Someren EJ, Hubbard EM, Luxenberg JS, Mastick J, Cooper BA. Department of
Physiological Nursing, University of California at San Francisco, San
Francisco, California 94143
Alzheimer's disease subjects received 1 hour of morning light
exposure (> or = 2,500 lux in gaze direction) Monday to Friday for 10
weeks and 5 mg melatonin or placebo in the evening. Control subjects
received usual indoor light (150-200 lux). Light treatment alone did
not improve nighttime sleep, daytime wake, or rest-activity rhythm. Light
treatment plus melatonin increased daytime wake time and activity levels
and strengthened the rest-activity rhythm.
Exercise and Alzheimer's
disease
Walking, gardening and generally being physically
active after age 65 appears to ward off dementia, including Alzheimer's disease.
Alzheimer Prevention with
Juices
Drinking fruit and vegetable juices frequently could help reduce the risk
of Alzheimer's disease in individuals at risk for developing the disease. There
is evidence from both lab and animal studies that high levels of reactive oxygen
species -- harmful byproducts of normal metabolism -- may be involved in the
development of Alzheimer's disease. While vitamins and polyphenols contained in
plant foods exert antioxidant effects and thus blunt the action of oxidants,
certain ways of preparing these foods can deplete their nutrient content.
Juicing, however, can preserve much of the antioxidant content of fruits and
vegetables. The American Journal of Medicine, September 2006.
Alzheimers medication -
Alzheimer's treatment
Several Alzheimer's
medication drugs are available including cholinesterase inhibitors such as donepezil, rivastigmine,
and galantamine. I am not convinced an Alzheimer medication of this sort offers a
long term effective treatment, solution, or cure for Alzheimer's disease.
Antipsychotics and benzodiazepines, especially in combination, hasten mental
decline in Alzheimer's patients.
Alzheimer's symptom and sign
- Diagnosing Alzheimer's Disease
There are several symptoms of Alzheimer disease. The common
symptoms of Alzheimer's disease include: trouble remembering things...at first, only short-term memory
may be affected. The individual may forget an appointment or the name of a new
acquaintance. A person may also forget where they left things. Eventually,
long-term memory is also impaired. Difficulty identifying common smells such as
lemon, banana and cinnamon may be the first sign of Alzheimer's disease.
Mood or personality changes are also symptoms of
Alzheimer's disease. A person may
suddenly become angry or sad for no apparent reason. Or someone who was social
and outgoing may become withdrawn.
Trouble completing ordinary tasks is an annoying symptom of
Alzheimer's disease. Simple tasks that once caused no difficulty may become much
more challenging. For example, the individual may forget how to dress, use the
oven, etc.
Difficulty expressing thoughts and disorientation. We
all know what it's like to be driving and momentarily forget where you are
going. But those with Alzheimer's disease may get lost in their neighborhood.
They may also lose track of dates and the time.
Unusual behavior. The individual may wander, become
agitated, hide things, wear too few or too many clothes, become overly
suspicious, or engage in unsafe behaviors.
Weight loss may accelerate before the onset of clinical
signs and symptoms of Alzheimer's disease.
Cause of Alzheimers Disease
There is a very high genetic cause for Alzheimer's
disease. In addition to genetics as a cause of Alzheimer's disease, many
environmental factors including diet are to be considered.
Nerve signals travel across synapses with the help
of chemicals known as "neurotransmitters," including one called acetylcholine.
Nerve cell destruction causes a reduction in acetylcholine, leading to impaired
transmission of nerve signals and poor communication between nerve cells called
neurons. In addition to acetylcholine, the brain of Alzheimer’s disease patients
have areas of abnormal protein called "plaques" and "tangles," the names
reflecting what these abnormalities in the brain look like under the microscope.
The underlying cause of Alzheimer's – what actually triggers the changes in the
brain – is still not fully known but could partly be due oxidation and damage to
nerve cells over time. It is likely that no single factor is responsible, but
rather that it is due to a variety of factors, which may differ from person to
person. People whose parents or brothers and sisters develop the disease appear
to be at greater risk of developing it themselves, so there may be a genetic
component. However, no straightforward pattern of inheritance has been found. It
is known that head injury is a risk factor, and also that Alzheimer’s disease
often affects people with Down’s syndrome. Some researchers have suggested that
people who exercise their brains (for example, doing crosswords and other mental
agility exercises) are less likely to develop the disease. And Omega 3 fatty
acids, contained in oily fish such as mackerel and salmon may, also help to
prevent dementia. But there is no completely solid evidence to show how
environmental factors influence the chance of getting Alzheimer’s.
Australian scientists say they have identified a toxin
that may play a key role as a potential cause of Alzheimer's disease. The toxin, called quinolinic acid, kills nerve cells in the brain, leading to dysfunction and
death. Quinolinic acid may not be the main cause of Alzheimer's disease, but it plays
a key role in its progression.
Researchers have shown that a common anesthetic gas can cause
fragments of a normal brain protein called amyloid-beta to clump together, which
is thought to be the main problem underlying Alzheimer's disease. Intravenous
anesthetics have less of an effect, the team reports in the journal
Biochemistry.
Anesthetics used in long surgery, such as inhaled anesthetics
isoflurane and halothane, may be another cause of Alzheimer's disease.
Scientists conducted a series of lab experiments using nuclear magnetic
resonance to investigate the reaction of amyloid-beta peptides to the inhaled
anesthetic isoflurane and the intravenous anesthetics propofol and thiopental.
They found that the peptides aggregated together after 10 to 30 hours' exposure
to isoflurane, depending on the concentration of the gas and the size of the
protein fragments. The effect was seen with propofol after exposure for 48
hours, but no clumping was seen with thiopental. Biochemistry, January 23, 2007.
Amyloid, Obesity, and Alzheimer's Disease
As body fat increases, so do blood levels of a protein fragment linked to
Alzheimer's disease, which may explain the reported association between
obesity and the
brain-wasting disease. Obesity by itself, even in otherwise healthy middle-aged
people, is associated with elevated levels of the amyloid peptide that builds up
and causes Alzheimer's. Amyloid is normally made all throughout the body at
various lengths. Researchers at Edith Cowan University in Joondalup, Western
Australia investigated whether levels of the peptide, plasma amyloid-beta
42,were related to body mass index (BMI) or fat mass in 18 healthy adults. As
BMI rose, so did amyloid-beta 42 blood levels. The same was true for fat mass.
But there was no relationship between BMI or fat mass and another peptide,
amyloid-beta 40, which is not associated with disease. Obesity-linked conditions
like diabetes and heart disease may also increase Alzheimer's risk, but when the
team adjusted the data for levels of insulin, cholesterol, and inflammation in
an attempt to account for their influence, the fat-amyloid-beta 42 relationship
remained. This suggests that it's the fat itself -- not the diseases that excess
weight can cause -- that may be increasing levels of the dangerous protein. To
learn more about
amyloidosis.
Neurofibrillary tangles and
Gait
Brain lesions known as neurofibrillary tangles, such as those seen in
Alzheimer's disease, are also associated with impaired gait in older subjects
with or without dementia. The more tangles an older person had in the substantia
nigra - an area of the brain associated with Parkinson's disease -- the more
problems there is with gait. In addition to, or even instead of, problems with
memory, persons with Alzheimer's disease may have problems with walking and
balance.
Alzheimer's Test
Can there eventually be a helpful Alzheimer's test? Concentrations of three proteins in the fluid that bathes the brain and
spine are associated with the initial stages of Alzheimer's disease in people
with mild cognitive impairment. Researchers measured levels of three proteins
related to Alzheimer's disease -- AB42, T-tau, and P-tau181 -- in cerebrospinal
fluid samples from 137 patients with mild cognitive impairment and 39 controls.
During 4 to 6 years of follow-up, 56 of the subjects with mild cognitive
impairment remained cognitively stable, 3 died, 57 developed Alzheimer's
disease, and 21 progressed to other forms of dementia. According to the
investigators, baseline concentrations of T-tau and P-tau181 were significantly
higher, and AB42 significantly lower, among patients who developed Alzheimer's
disease compared with controls, cognitively stable patients with mild cognitive
impairment, and patients who developed other forms of dementia.
Alzheimer's Disease Research Update
- Alzheimer's Clinical Trial
Curcumin inhibits formation of Abeta oligomers and fibrils, binds plaques and
reduces amyloid in vivo.
J Biol Chem. 2004 Dec 7. Yang F, et al. University of California Los
Angeles, North Hills, CA
Alzheimer's disease involves amyloid (Abeta) accumulation, oxidative damage and
inflammation, and risk is reduced with increased antioxidant and
anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has
potent anti-inflammatory and antioxidant activities and can suppress oxidative
damage, inflammation, cognitive deficits, and amyloid accumulation. These data
suggest that low dose curcumin effectively disaggregates Ass as well as prevents
fibril and oligomer formation, supporting the rationale for curcumin use in
clinical trials preventing or treating Alzheimer's disease.
Atypical antipsychotic drugs used to treat Alzheimer's disease and other types of dementia for relatively brief periods, less than 8 to 12 weeks, may be associated with a small increased risk of death.
A high concentration of silica in drinking water seems to protect against Alzheimer's disease.
Consuming a diet rich in the omega-3 fatty acid docosahexanoic acid (DHA) may help prevent or treat Alzheimer's disease. In the study, reported in The Journal of Neuroscience, mice that ate DHA-enriched chow showed less beta-amyloid build-up in the brain than mice fed regular chow. Beta-amyloid is a protein that forms the characteristic brain plaques seen in patients with Alzheimer's disease." These results suggest that dietary DHA could be protective against beta-amyloid production, accumulation, and potential downstream toxicity," senior author Dr. Greg M. Cole, from the University of California at Los Angeles, and colleagues note. Research has linked high levels of DHA in the diet with a reduced risk of Alzheimer's disease. Still, the studies have shown an association, but don't prove that eating a diet high in DHA actually reduces amyloid levels and prevents Alzheimer's disease. To show this, animal studies are often needed. Cole's team used a mouse model of Alzheimer's disease and fed the animals low- or high-DHA chow or regular chow. The animals were fed the assigned diet until 22.5 months of age, at which point brain tissue was obtained and tested for amyloid build-up. The high-DHA diet reduced total amyloid level by 70 percent compared with the other diets. Moreover, brain plaques were reduced by 40 percent.
Britain's agency charged with assessing whether
drugs and procedures are worth their cost has issued a preliminary ruling
against all of the four main drugs licensed for treating Alzheimer's disease.
The National Institute for Clinical Excellence (NICE) said that Aricept, Exelon,
Reminyl, and Ebixa should not be reimbursed by the national health service. It
advised that people taking the drugs "may be continued on therapy until it is
considered appropriate to stop," the institute said in preliminary
recommendations. Some 52,500 patients are taking the medicines in Britain.
Although not a cure, clinical trials have shown that they can slow the progress
of symptoms of the illness. The recommendations follow an unfavourable review of
the four drugs' clinical effectiveness and cost effectiveness by NICE's
appraisals' committee. The committee said the clinical gains with the drugs
called acetylcholinesterase inhibitors were small and the evidence on outcomes
of importance to patients and caregivers, such as quality of life and time to
institutionalisation, was "limited and largely inconclusive." It also concluded
that the evidence for the clinical effectiveness of memantine, which is licensed
for more severe Alzheimer's disease, was "insufficient."
Relation of the tocopherol forms to incident Alzheimer disease and to cognitive
change.
American Journal of Clinical Nutrition, Vol. 81, No. 2, 508-514,
February 2005
High intake of vitamin E (tocopherol) from food, but not from
supplements (which usually contain -dl-tocopherol), is inversely associated with
Alzheimer disease. Objective: We examined whether food intakes of vitamin E, -tocopherol
equivalents (a measure of the relative biologic activity of tocopherols and
tocotrienols), or individual tocopherols would protect against incident
Alzheimer disease and cognitive decline over 6 y in participants of the Chicago
Health and Aging Project. Design: The 1993–2002 study of community residents
aged 65 y included the administration of 4 cognitive tests and clinical
evaluations for Alzheimer disease. Dietary assessment was by food-frequency
questionnaire. Results: Tocopherol intake from food was related to the 4-y
incidence of Alzheimer disease determined by logistic regression in 1041
participants who were clinically evaluated (n = 162 incident cases) and to
change in a global cognitive score determined by mixed models in 3718
participants. Higher intakes of vitamin E and -tocopherol equivalents were
associated with a reduced incidence of Alzheimer disease in separate
multiple-adjusted models that included intakes of saturated and trans fats and
docosahexaenoic acid. - and -Tocopherol had independent associations. In
separate mixed models, a slower rate of cognitive decline was associated with
intakes of vitamin E, -tocopherol equivalents, and - and -tocopherols.
Conclusion: The results suggest that various tocopherol forms rather than -
tocopherol alone may be important in the vitamin E protective association with
Alzheimer disease.
Researchers at Mount Sinai School of Medicine have found that a low carbohydrate diet that reduced total caloric intake by 30% prevented the development of a fundamental feature of Alzheimer's disease in mice genetically engineered to develop the disease. The study is the first to demonstrate that a change in diet can slow and possibly prevent Alzheimer's diseases.
Pharmacotherapeutic approaches to the prevention of Alzheimer's disease.
Am J Geriatr Pharmacother. 2004 Jun;2(2):119-32.
Alzheimer's dememtia (Alzheimers disease) is the most common cause of
cognitive impairment in older patients and is expected to increase greatly in
prevalence. Interventions that could delay disease onset would have a major
public health impact. The objective of this article is to review
evidence from epidemiologic studies and controlled trials addressing whether Alzheimers disease can be prevented. Data were gathered through a comprehensive,
systematic search of MEDLINE using focused search criteria and spanning a 6-year
period from January 1998 through January 2004; a hand search of reference lists
from these studies and reviews; a review of the Cochrane Database of Systematic
Reviews; and a hand search of relevant journals. Selection of articles was based
on the clinical focus. Preventive interventions for Alzheimers disease
include vitamins, nonsteroidal anti-inflammatory drugs, and agents that protect
the endothelium (eg, statins). Good control of hypertension with angiotensin-converting
enzyme inhibitors and long-acting dihydropyridines also confers neuroprotective
benefits. CONCLUSIONS: The paradigm that Alzheimers disease is pharmacologically
unresponsive is shifting as more effective pharmacotherapies for prevention and
treatment rapidly emerge. Our understanding of the molecular mechanisms of
neurodegeneration will soon allow us to more specifically target and interrupt
the processes that contribute to this progressive dementia.
Alzheimer's disease, oxidative injury, and
cytokines.
J Alzheimers Disease. 2004 Dec;6(6):651-657.
Alzheimer's disease is infrequently a genetically driven disease. Rather
it is the product of free radical injury inflicted over decades after an initial
insult to the central nervous system (CNS). The brain is uniquely sensitive to
oxidative injury. A variety of insults to the CNS are now associated with
Alzheimer's disease. These include hypertension, diabetes, and head trauma.
These then cause a cytokine cascade and microlocalized inflammation in the CNS,
that in time results in clinical Alzheimer's disease. By the ninth decade of
life over half of the population manifests Alzheimer's disease. Prevention or
reversal of Alzheimer's disease will lie in administration of effective
antioxidant therapy with specific treatments when etiologies are known.
Docosahexaenoic acid protects from dendritic pathology in an
Alzheimer's disease mouse model.
Neuron. 2004 Sep 2;43(5):633-45.
Learning and memory depend on dendritic spine actin assembly and docosahexaenoic
acid (DHA), an essential n-3 (omega-3) polyunsaturated fatty acid (PFA). High
DHA consumption is associated with reduced Alzheimer's disease risk, yet
mechanisms and therapeutic potential remain elusive. Here, we report that
reduction of dietary n-3 PFA in an Alzheimer's disease mouse model resulted in
80%-90% losses of the p85alpha subunit of phosphatidylinositol 3-kinase and the
postsynaptic actin-regulating protein drebrin, as in Alzheimer's disease brain.
The loss of postsynaptic proteins was associated with increased oxidation,
without concomitant neuron or presynaptic protein loss. n-3 PFA depletion
increased caspase-cleaved actin, which was localized in dendrites
ultrastructurally. Treatment of n-3 PFA-restricted mice with DHA protected
against these effects and behavioral deficits and increased antiapoptotic BAD
phosphorylation. Since n-3 PFAs are essential for p85-mediated CNS insulin
signaling and selective protection of postsynaptic proteins, these findings have
implications for neurodegenerative diseases where synaptic loss is critical,
especially Alzheimer's disease.
Drinking tea appears to affect the brain in a similar way as drugs prescribed for Alzheimer's disease, UK researchers report. The team, based at Newcastle University's Medicinal Plant Research Centre, investigated the properties of green and black tea, as well as coffee, in a series of laboratory experiments. The results showed that both types of tea inhibited the activity of enzymes associated with the development of Alzheimer's disease. Coffee, however, had no significant effect, according to a report in theOct, 2004 edition of Phytotherapy Research. The teas inhibited the activity of acetylcholinesterase -- the same mechanism of action used by drugs such as Novartis' Exelon and Pfizer's Aricept. The teas also hindered the activity of the butyrylcholinesterase, which has been found in senile plaques in the brains of Alzheimer's disease patients. Green tea obstructed the activity of beta-secretase, which also plays a role in the production of senile plaques.
The benefits and risks associated with cholinesterase inhibitor
therapy in Alzheimer's disease.
Expert Opin Drug Saf. 2004 Sep;3(5):425-40.
The 'second-generation' cholinesterase inhibitors (ChEIs), donepezil,
galantamine and rivastigmine, are a class of medications that are
currently approved for the treatment of mild-to-moderate Alzheimer's
disease (Alzheimer's disease). These medications have proven efficacy in
improving cognition, behaviour, activities of daily living, and global
functioning in mild-to-moderate Alzheimer's disease. They have also been
shown to reduce caregiver stress and to delay time to nursing home
placement. Two separate meta-analyses have indicated that ChEIs confer a
modest but significant therapeutic benefit in the treatment of Alzheimer's
disease, despite higher rates of treatment discontinuation and side
effects than placebo. There is growing evidence to support their efficacy
in treating moderate-to-severe Alzheimer's disease. ChEIs are generally
well-tolerated, with side effects that tend to be dose-related and are
most problematic during dose titration. The most common adverse effects,
related to cholinergic stimulation in the brain and peripheral tissues,
include gastrointestinal, cardiorespiratory, extrapyramidal,
genitourinary, and musculoskeletal symptoms, as well as sleep
disturbances. Few clinically significant drug-drug interactions with ChEIs
have been identified. Three head-to-head disease trials of ChEIs in the
treatment of Alzheimer's disease have been published to date, but are
limited due to their open-label design, rates of titration, and the drug
dosage levels utilised. Further study is needed to examine other
indications for ChEIs, as well as their combination with newer treatments,
such as memantine.
Alzheimer's fact : People who spent most of their lives in jobs that involve little brain work appear more likely to eventually develop Alzheimer's disease.
A recent report suggests high copper levels
in tap water may play a role in causing Alzheimer's disease. Those at risk for
Alzheimer's (i.e. family history) may consider drinking distilled water.
For women, maintaining high levels
of "good" HDL cholesterol may be one of the most effective strategies for
fending off Alzheimer's disease, according to new research.
Data from the ongoing Women's Health Study indicate that women with the highest HDL levels -- ranging from 60 to 75 -- have half the risk of becoming mentally impaired as those with the lowest levels.
Alzheimer's fact : High intake of niacin, particularly from food sources, may reduce the risk of Alzheimer's dementia disease and age-related cognitive decline.
Drugs for early Alzheimer's disease, which pharmaceutical companies and campaigners have lobbied the UK government to provide to large numbers of elderly patients with Alzheimer's dementia across the country at a cost of over £39m a year, have little effect on their memory and do not stop the distressing deterioration of their lives or preventing Alzheimer's disease progression, according to an important study published July 2004. The five-year study, paid for by the NHS and not the drug companies, found that the drugs are a waste of the scarce resources available for the condition, said the lead re searcher Roger Gray, director of Birmingham University's clinical trials unit. alzheimers disease information
Estrogen pills appear to slightly increase the risk of Alzheimer’s disease and other forms of dementia in postmenopausal women, a study found, echoing recent findings involving estrogen-progestin supplements. The findings contradict the long-held belief that estrogen pills can help keep older women’s minds sharp. The results came from a government study called the Women’s Health Initiative and were published in The Journal of the American Medical Association. The research involved nearly 3,000 women, ages 65 to 79, who had had hysterectomies and had taken daily estrogen-only pills, sold by Wyeth Pharmaceuticals as Premarin, for an average of about five years. alzheimers care
Clinical efficacy and safety of huperzine Alpha in treatment of mild to moderate
Alzheimer disease, a placebo-controlled, double-blind, randomized trial
Zhonghua Yi Xue Za Zhi. 2002 Jul 25;82(14):941-4.
To evaluate the clinical efficacy and safety of huperzine Alpha in
treatment of patients with mild to moderate Alzheimer disease METHODS: Two
hundred and two patients with the diagnosis of possible or probable Alzheimers
disease from 15
centers the nationwide were randomly divided into two groups: huperzine Alpha
group (n = 100, given huperzine Alpha 400 micro g/day for 12 weeks) and placebo
group (n = 102 ). RESULTS: In comparison with the baseline data, there was an
improvement of 4.6 points in cognition; an improvement in behavior and mood with
59.2% of the Alzheimer disease patients being on the mend clinically. CONCLUSION: A safe and effective
medicine, huperzine Alpha remarkably improves the cognition, behavior, ADL, and
mood of Alzheimer disease patients.
A high concentration of silica in drinking water seems to protect against
Alzheimer's disease
Blue Green Algae
has a cholinesterase inhibitor
Alzheimer's disease info emails
Q. I just got your Mind Power Rx for my mother,
who has early stage Alzheimer's disease. Then today I noticed your article on galantamine
as an Alzheimer's medication. Would it be OK to give her both supplements together, or do they
have the same basic function?
A. Mind Power Rx
does not contain a cholinesterase inhibitor like galantamine or huperzine.
However, if your doctor decides to combine them, half a capsule of each would be
preferable as a starter. Alzheimer's medications can have potentially serious
side effects.
Email from a doctor who says: I have a patient who was
not doing well on the Alzheimer's medications Aricept and Namenda until we added nicotine patch and sage
extract. He is my poster child! Sage contains several cholinesterase inhibitors
and could help Alzheimer's disease.
Saw
Palmetto has important phytosterols
AHCC
Q. Are insulin and Alzheimer's disease related? Any info would
be helpful.
A. I don't see a direct link between insulin and
Alzheimer's disease. I am not sure if those with diabetes have a higher
incidence of Alzheimer's.
Q. What are your suggestions on prevention of
Alzheimer's disease? I have a family history of Alzheimer's disease. My mom has
it and my grandmother died from the disease.
A. Leading a healthy lifestyle with a good diet,
exercising, keeping the mind busy, getting good sleep, and perhaps taking low
doses of antioxidants could all be helpful.
Q. Are Alzheimer's disease medications of any help? I
read in a book that they weren't.
A. According to Alzheimer's articles in medical
journals, these pharmaceutical Alzheimer's medications do not appear to be worthwhile,
whether in the early stage of Alzheimer's final stage. They do not stop the
progression of Alzheimer's disease.
Q. What's the difference between Alzheimer's and
dementia ?
A. Alzheimer's is a form of dementia. There are many
other causes of dementia.
Q. What are the studies with stem cells and
Alzheimer's?
A. I have not kept abreast of stem cell research and
Alzheimer's.
Q. My mom has symptoms of Alzheimer's disease, is a flu shot okay to give?
A. I don't see why not.