There is treatment for Alzheimer’s disease.  Realistically, Alzheimer’s gives ample time to be proactive.  It is a slowly progressive neurological disease that unfolds over the course of several decades. Treatment involves being proactive rather than reactive.  These are the steps we all need to take beginning now.

Assessment.  We all have wellness plans that are managed through annual physicals with our physicians.  We need to include annual memory assessment by a memory expert as a part of this plan.  The assessment should, at the minimum, thoroughly assess short-term memory by means of a challenging, standardized memory test and be administered by a memory expert.

Treat short-term memory before it changes.  We seem to lose track of the fact that we took notes in school to manage short-term memory.  It never worked like a muscle.  It takes time, focus, and effort to remember.  Incorporate the One Minute Rule into your everyday life before it becomes the “two minute rule.”

Put legal directives in place.  Make sure you have wills, Living Wills, Durable Powers of Attorney, and trusts up to date.  You need to have these documents in place before you need them.  Make sure your representatives know where things are.

Create a family plan.  If you are concerned about your memory or have greater risk for future memory loss, have a family meeting and openly discuss your concerns, the details of assessments, your goals, and how to manage if you decline.  This plan should be created before you need it to protect everyone involved.  Plan for a good life as you age even if your memory fails.  Let  your family know your desires and needs.

Finances.  Make a plan about finances.  Have a system that includes sometime checking your abilities to manage estates, investments, and checkbooks.  Have a plan for transfer early if these skills decline.

Driving.  Make a plan to monitor your driving skills.  Consider having periodic on road assessments by certified driving evaluators.  Make a plan for stopping driving if you become unsafe and include a way to get around if you can’t drive.

Exercise.  The most protective activity that you can either maintain or add to your life is regular exercise.  There is increasing evidence that moderate exercise reduces some of the wear and tear on the brain that result from aging.  Aim for about 2 two and a half hour a week as a minimum.

Know the options for assistance if needed.  What are your options for assistance if you and your family need care in the future.  What are the services that come into the home?  Where are day care centers?  Where are the memory care facilities?  Consider participating in educational programs by agencies like the Alzheimer’ Support Network in Naples.  Know what your options are before you need them.

Stay engaged in your interests.  You need to have an active plan to keep socially and intellectually engaged.  So do those who care for you.  Make sure you calendar has activities that you love to do in addition to what you have to do.

 

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The AARP Bulletin ran an interesting title in April, “Am I losing my mind?”  This article is in response to the growing paranoia about memory fed by the news that the rate of Alzheimer’s is rising and that many more die of Alzheimer’s than are reported in official statistics.  It’s no wonder that if I have a senior moment, I briefly consider whether I am on the slippery path to dementia. 

 Dementia is a generic term that refers to more than just memory loss.  Dementia is a permanent, irreversible and, in some cases, progressive decline in brain skills that interferes with independent living – hence produces disability.  There are a multitude of possible causes of dementia.  Among sudden causes are stroke and head injury.  Slow onset progressive causes include Alzheimer’s disease, Lewy body disease, and Huntington’s chorea.

You can have brain pathology such as stroke, head injury, or Alzheimer’s disease and not be demented.  Dementia is a term that reflects the severe loss of ability to function well in the world.  Mild or temporary confusion or befuddlement is not dementia.

There are two steps in assessing memory loss and confusion.   A good assessment both considers the possible underlying medical causes and provides a description of cognitive strengths and weaknesses, functional skills.  Medical assessment for confusion involves more than just a routine physical.  There are several important considerations.  The following issues, which may respond to treatment, may either the source of the confusion or may make it worse.

Metabolic disorders.  For example diabetes, hypothyroidism, or hyperthyroidism are treatable conditions that often present as confusion.  Simple blood tests evaluate these systems and are routinely a part of annual physicals.

Brain pathology.  Conditions such as normal pressure hydrocephalus, head inuries, stroke (sometimes “silent”), tumors, or vascular malformations may be the source of the confusion.  These conditions are assessed by means of brain imaging studies such as an MRI.

Emotional disorders.  Severe depression, grief, posttraumatic stress disorder, or anxiety disorders may add to confusion and need to be evaluated as part of the assessment.

Vitamin deficiencies/excess.  For example, deficiencies in vitamin B12 produce pernicious anemia, which can be life threatening if left untreated.  A part of the work up for confusion should be an assessment of critical vitamins and nutrition.

Medications (including drugs and alcohol).   There are a multitude of drugs and medications that can produce confusion or memory loss but very few that improve memory.  Assessment needs to broadly consider current medications and make appropriate adjustments.

Neuropsychological assessment.  What are your cognitive strengths and weaknesses?  Which memory systems are the problem and which continue to work well?  How do you know if treatment is helping and how much?  How is reasoning and problem solving working?  Neuropsychological assessment helps you, as well as those who live with you, better understand how your brain is working and what practical steps to take in developing a treatment plan.

 

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 We are all subject to random bouts of forgetting.  Where did I park my car?  I forgot my grocery list.  Why am I in this room?  These complaints increase with age and are the source of both jokes about senior moments and serious fear of developing Alzheimer’s disease.  However, there is a huge difference between the increasing inefficiencies in memory resulting from aging and memory loss and dementia.

 The fears have produced a burgeoning business in brain training programs such as Lumosity.  Lumosity has about 50 million users and is the best known of these programs.  It promises to improve attention and the capacity to learn.  Strong promises if short-term memory begins to fail.  The Centers for Medicare Services is exploring whether to pay for memory fitness training, which would create a boom market for these services.

But does brain training work as promised?  There are actually several questions within this broader question that are quite different.  First, can interventions that challenge the brain really raise intelligence?  Second, can brain training help mitigate the normal cognitive changes that result from aging?  Third, does brain training stave off or slow down the trajectory of progressive decline such as Alzheimer’s disease?

Most of the actual research on brain training has addressed its effects in treating ADD or traumatic brain injury/stroke or healthy adults.  Older methods of training the brain were called mnemonics and consisted of strategies such as the method of loci.  For example, Mark Twain memorized talks by walking a route on his property and “hanging” parts of the talk on different landmarks that he could use by mentally take the walk as he gave the speech.  Alternatively one could learn a list of words by making a story of them.

There are numerous reviews of research addressing the issue of brain training in healthy adults and children.  For example, Monica Melby-Hume and Charles Hulme asked the question “Is working memory training effective…?” (Developmental Psychology, 2013, 49, 270-291). The reviews are consistent in concluding that while training improves the skills that are trained, there is no evidence that these gains transfer to other tasks or skills.  In other words you get better at he games but you still forget where you parked your car.

The question of whether brain training staves of memory loss such as Alzheimer’s disease has not been adequately addressed.  The bottom line is that the science isn’t up to the hype.  The marketing promises go beyond the data.  Cognitive stimulation and learning are good things.  But when it comes down to paying for these programs I have to ask are subscriptions really better than designing your own self selected methods of challenge?

 

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I was giving a talk last week and asked the question of whether Alzheimer’s disease can be diagnosed by means of an alpha-beta PET scan.  This refers to the use of a brain scan with amyloid markers in the detection of early Alzheimer’s disease before clinical symptoms appear.  A review by Steven Peterson (Journal of the American Medical Association Internal Medicine, 2014, 174, 133-134) concludes that it cannot. 

 I have already had a couple of clients who presented to me after they had obtained a PET scan with an amyloid marker and told, despite the fact that they had no symptoms or neuropsychological assessment, that they had early Alzheimer’s disease.  Of course, this was very alarming and they sought assessment and council.  After careful testing, these two clients had superb short-term memory, the loss of which is the hallmark and necessary symptom of Alzheimer’s disease.  I reassured them and suggested they track their memory over time similar to tracking blood sugars or cholesterol.

Dr. Peterson concludes that a positive PET scan is not diagnostic of Alzheimer’s disease.  Furthermore, a positive scan is not useful in predicting the conversion of Mild Cognitive Impairment to Alzheimer’s disease.  He adds that a negative PET scan is associated with a reduced risk that existent cognitive impairment is a result of Alzheimer’s disease. Current scans are not a diagnostic tool for Alzheimer’s disease.

The most recent statement from Medicare (CMS) also concludes that the evidence is not sufficient to use PET imaging studies as reasonable and necessary for either the diagnosis or the treatment of Alzheimer’s disease.  Therefore, Medicare will not cover amyloid imaging by PET scan in the diagnosis of Alzheimer’s disease.  Medicare will cover one PET scan to differentiate between Alzheimer’s disease and frontotemporal dementia in appropriate cases and clinical studies that address treatment and prevention under very restrictive prior approval.

There are four problems with the current evidence base for PET scans for Alzheimer’s disease.  1. There are too few studies available.  2. Currents studies do not address the benefits and harms of making a diagnosis based on imaging data.  What if the scan is positive and the client never develops a memory disorder?  3. Current studies have very restrictive selection criteria.  They do not address the full spectrum of typical clinical clients – they are not representative samples.  4. There is no evidence that a positive scan changes clinical management or provides any health benefits.

PET scans for Alzheimer’s disease are useful and intriguing research tools.  They are not clinical tools at this time.  Don’t forget to monitor your memory.  I have developed a focused, thorough short-term memory assessment that is brief and affordable.  Contact my office for details if you want to check out your memory.

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Although the clinically significant phase of Alzheimer’s disease is characterized as a disorder of memory, it is so much more.  There are a number of cognitive skills that become progressively compromised as it progresses.  For example, in addition to loss of memory there is a decline in attention, concentration, orientation, judgment, reasoning, visuospatial ability, executive function, and language. 

The language changes present a real challenge for caregiving as we function in the world by language abilities that we take for granted.  In the mild stages (Late Confusional to Early Dementia) there are often deficits in language such as anomia (cannot name common objects) and circumlocutions (provide functions of objects rather than names) in addition to the forgetfulness.  For example, a person may look at a clock and say it’s for telling time or point to the lights rather than saying light switch.

In the middle stages of Alzheimer’s disease there is not only greater short-term memory loss but also a progressive decline in language that is similar to those who have had a stroke that produces aphasia (difficulty putting thoughts into words).  This decline is both semantic and pragmatic.  Semantic errors manifest as paraphrasias (using the wrong word), empty speech (using ambiguous referents “that thing”), and a reduction in verbal fluency (for example when asked to name animals or grocery items quickly they cannot get many to come out).

Pragmatic errors include speaking too much, speaking at inappropriate times, talking too loudly, repetitiveness, and digressing from the topic of discussion.  Of course, these changes reflect not only language decline but also short-term memory loss, decreased concentration, and disinhibition.

Changes unfold over the course of ten years or more and need to be differentiated from Primary Progressive Aphasia, which is characterized by progressive language decline but often less memory loss in the early stages (about 25% of those diagnosed with Primary Progressive Aphasia have Alzheimer’s disease).  Of course, this distinction is more academic than practical as impaired expressive and receptive communication is the problem either way.

Even in early stages of language decline there is also an increasing loss of comprehension making it increasingly difficult to understand spoken and written language and, in later stages, increasingly difficult to make ones needs known.  This makes it difficult to explain things like why one must stop driving or why one cannot stay alone.  Furthermore, there is increased agitation, social withdrawal, loss of friendships, and passivity adding to the complexity and stress of caregiving.

Treatment involves understanding, patience, and compassion.  Activities often need to focus on doing rather than saying (e.g., art, music), past memories rather than new memories, being in smaller groups, being invited into simpler conversations, encouragement to talk even if repetitive or tangential, giving simple single step directions, and not over-explaining. The objective is to keep the language-impaired person engaged with others and interacting within their own limits.  A monumental task that best requires more than a single caregiver.

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The most common question that I am asked is  “What can I do to prevent Alzheimer’s disease?”    The honest answer is that nobody actually knows.  Much of what we read or hear on the news is overstated for emphasis.  Our current beliefs are mostly based on anecdotal reports, marketing, and epidemiological studies (looking backwards to see what someone says they did) with a few prospective studies (ongoing studies of people as they age) to add intrigue. 

There are few randomized control studies (the gold standard for scientific inferences of cause and effect) to guide us in answering this important question.  Epidemiological studies tell us what is correlated or associated with desired outcomes.  However, they cannot tell us root causes.

It seems intuitively sensible that what we eat is important for our health and may impact the course of neurodegenerative disorders.  Indeed there are epidemiological studies on a number of nutritional choices.  I found a recent review that was helpful: “Nutrition and the risk of Alzheimer’s disease” (Biomed Research International, 2013, 2013, article ID524820).

On a global level, there is an association of being overweight/obese with Alzheimer’s disease.  But the relationship is complicated.  It appears that being overweight in middle age increases (does not cause) the risk of Alzheimer’s disease in old age.  However, being overweight in late life reduces the risk.  This finding may stem from the typical weight loss in those who have Alzheimer’s disease in late life.

There are numerous nutrients that have been explored: vitamins A C, E, B, D; metals, copper, fatty acids, carbohydrates, fish consumption, fruits, vegetables, dairy, coffee, and tea.  There are very few randomized control studies in humans to guide us.  The findings are correlational and complex with little quality supportive evidence for any of these nutrients taken alone.  Mostly, the findings support the fact that deficiencies in nutrients such as vitamins and minerals cause problems in cognition and may be correlated with the risk of Alzheimer’s disease.

Another approach to the question of nutrients has been to study dietary strategies including the Western diet (red and processed meats, refined grains, sweets, ad desserts), Japanese diet (fish and plant foods), “Healthy diet,” DASH (Dietary Approaches To Stop Hypertension), and Mediterranean diet.  Again there are no randomized clinical trials to draw from but correlational findings support an eating strategy such as the Japanese, Mediterranean/DASH/Healthy diet.

In conclusion, there are no hard facts about the causal link between nutrition and Alzheimer’s disease. Participants in epidemiological studies may not be the same as the “average” resident in the United States.  They may be generally more health conscious beyond just nutrition.  There is no clear guidance about doses of supplements to take other than that too little is a problem as is too much.  We would obtain better guidance from randomized clinical trials but these are not generally feasible and who really wants to be in a placebo group for this type of study?  Furthermore, trials would need to extend over decades to provide meaningful guidance about Alzheimer’s disease as it takes decades to unfold.  Finally, prevention must start even before there are even subtle symptoms if it is to be effective.

We must decide on nutritional strategies based on mostly epidemiological studies and faith.   I am betting on the Japanese, Mediterranean/DASH/Healthy diet that makes fruits, vegetables, and fish as the best approach to nutrition.  There just doesn’t seem to be any good evidence that supplements are useful in people who are not deficient or malnourished.

 

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Caffeine appears to enhance memory consolidation according to a study published in Nature Neuroscience (“Post-study caffeine administration enhances memory consolidation in humans,” 2014, 17, 201-203).  But before you down an extra cup of coffee or an extra diet Coke, consider the details of the study. 

The subjects were 160 young adults who reported they consume little caffeine each week – < 500 mg, which is less than the equivalent 2-3 cups of coffee per week.  Furthermore, they consumed caffeine pills not coffee.  Participants studied 200 pictures, swallowed the caffeine pill, and returned the next day for a surprise memory test.  Those who had the caffeine were better able to discriminate items similar to those actually seen from different items – familiarity not memory as most of us think of it.

Let’s break down this result.  First, there were three doses of caffeine used, 100, 200, or 300 mg.  The benefit was only for the 200 mg dose.  100 mg was too little and 300 mg was too much –caused side effects such as nausea and headache.  Second, the same findings may not apply to moderate to heavy caffeine users.  Third, the drug had to be administered immediately after the learning experience and testing was the next day. This is called “post-trial facilitation” and also occurs with use of alcohol, benzodiazepines, and norepinephrine – similar to adrenalin.  Fourth, the study used caffeine not coffee, which has hundreds of chemicals in it.

Caffeine is the most used psychoactive drug in the world.  It is used to improve alertness and attention by about 80% of those in the United States (Beckwith, 2008, “A primer of psychopharmacology for clinicians,” Healthforumonline).  As I pursued background for this article, I ran across some interesting studies on coffee.  For example, community dwelling women volunteers aged 65 and older who drank at least three cups of coffee per day showed less decline (does not address the issue of Alzheimer’s) in memory over the course of 4 years than those who drank one cup or less.  There was no association between coffee consumption and memory in men (“the neuroprotective effects of caffeine: a prospective study, Neurology, 2007, 69, 536-545).

There was a special series of articles on caffeine in the Journal of Alzheimer’s Disease (2010, Supplement).  There have been numerous attempts to explore the effects of caffeine/coffee on memory.  The most confident conclusion from these studies is that caffeine has no effect on intentional memory.  Rather it appears to help working memory/multitasking as long as the dose is not too high.  There appears to be no effect on long-term memory and the action seems to result from increasing alertness and counteracting fatigue.

In short, caffeine does not appear to be a pure cognitive enhancer but rather helps improve mood and alertness at the right dose – some people are hypersensitive and too much caffeine impairs performance.  There are no randomized clinical trials from which to draw.  Three to five cups of coffee per day may have potential for slowing and/or treating Parkinson’s disease.  But the caveat is that caffeine may worsen anxiety, induce migraines, cause arrhythmias, interfere with sleep, worsen GERDS, and induce withdrawal.  As with all drugs you must consider the cost-benefit ratio for each individual.

The jury is still out for caffeine and other supplements.  Caffeine’s benefits are probably small rather than profound.  There is no magic bullet.

 

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As we age we need to constantly work toward managing healthy behaviors such as exercising, eating healthy, and being engaged in social/intellectual activities.  These are proven ways to mitigate the effects of aging on health, wellness, mood, and memory.  It is becoming increasingly clear that we need to start this lifestyle  earlier in life to maximize effectiveness.

A new study (“Alcohol consumption and cognitive decline in early old age,” Neurology 2014, , in press)  adds our drinking behaviors to the formula of proactive lifestyle.  Drinking too much alcohol from at least middle age onward may accelerate cognitive decline.  The study reports the findings from the Whitehall longitudinal study of 7153 British civil servants 67% of who were male.  The study began in 1985-87 with cognitive tests administered in 1997-8 and administered twice during the next ten years.  Participants were aged 44-69 to begin the study and 64-89 at  the end of the study.

The findings for men were clear.  Drinking more than 3-4 drinks per day was associated with cognitive decline in all areas tested – especially memory.  For women (who were under represented in this population) drinking was associated with decline in executive functions and it took less alcohol to produce the effect in women than in men.  Women abstainers were also subject to greater decline than abstaining drinkers (however, there were too few abstainers to adequately assess this effect and abstainers may have a past history of heavy use).

There are a number of biological effects of heavy drinking that may contribute to the deleterious effects of alcohol on the brain and memory as we age.  Drinking too much at one time or chronically may produce cardiomyopathy (stretching and drooping of the heart muscle), and irregular heartbeats that can produce high blood pressure and stroke.  Alcohol induces changes in liver function such as inducing a fatty liver, hepatitis, fibrosis,  and cirrhosis.  Alcohol may cause pancreatitis and compromises the immune system for up to 24 hours after as single episode of getting drunk.  There are also a number of cancers that may be induced or worsened by heavy drinking.  These cancers include mouth, esophagus, throat, liver, and breast cancer.

As we age the effects of alcohol are magnified by an increasing sensitivity.  The effects happen more quickly and with less alcohol.  Heavy drinking as we age increases the risk for diabetes, high blood pressure congestive heart failure, liver disease, osteoporosis, memory disorders, and  depression/anxiety.  Finally, drinking is associated with falling and motor vehicle accidents.

How much is too much alcohol to drink?  The National Institute of Health recommends no more than 7 measured drinks per week if you are 65 or older.  “Safe” drinking for those under 65 is judged to be 2-3 measured drinks for men and 1-2 measured drinks for women.  The issue here is not alcoholism but rather healthy life style as you age.

To quote Reinhold Niebuhr (1943):  “God, grant me the serenity to accept the things I cannot change, the courage to change the things I can, and wisdom to know the difference.”  Successful aging takes work and effort and must begin at least in middle age.

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Does taking a multivitamin/mineral supplement help prevent or delay cognitive decline?  In 2012, Mayo Clinic Health Letter (March 2012) reviewed well-conducted research concluding that many vitamins and minerals that we used to think prevented diseases may not help after all.  Furthermore, there are consistent findings that under some circumstances vitamins and supplements may cause harm – even use of a multivitamin in those who are well nourished may slightly increase the risk of premature death.

A recent editorial, “Enough is enough: stop wasting money on vitamin and mineral supplements,”  in the Annals of Internal Medicine (2013, 59: 851) pushed the issue even further.  The journal published three articles presenting data that indicate no benefits from a multivitamin/mineral supplement in well-nourished adults.

A review of primary prevention studies focused on community dwelling adults with no nutritional deficiencies.  There was no clear evidence that a multivitamin had any benefit on mortality, cardiovascular disease, or cancer.

Another study explored the effects of high dose multivitamin use in 1708 men and women who had prior myocardial infarctions.  After a nearly 5 year follow up there were no benefits of vitamin or mineral supplements when compared to a placebo.

More to the point for memory, a large (5947 male physicians over age 65) randomized trial was undertaken comparing use of a multivitamin/mineral supplement to a placebo.  Cognitive tests were performed four times during the course of 12 years.  There was no difference in test scores for those taking the supplements than for those taking the placebo.  The conclusion is that taking a multivitamin/supplement has no long-term benefit on cognition.  It does not prevent dementia.  This finding is consistent with 12 other “good” studies indicating no cognitive benefit from a multivitamin, vitamins B, C, E or omega-3-fatty acids in healthy, well-nourished adults.  The data for supplemental vitamin D is not yet clear.

As is the case for supplementation with vitamin E (high doses may provide benefits when administered to mildly to moderately demented individuals), I am sure that this is not the final word.  Understanding and knowledge are a process that unfold, evolve slowly and incrementally.  I  am also sure that there will be a strong backlash from those with strong faith in supplements as well as those who make money on supplements – it is a 28 billion dollar industry.   My only hope is that they provide substantial evidence for their claims rather than rely on anecdotal testimonial and case studies.

Don’t forget to monitor your memory.  I have developed a focused, thorough short-term memory assessment that is brief and affordable.  Contact my office for details if you want to check out your memory.

 

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In 2004 the best available research indicated that supplementation with vitamin E slowed Alzheimer’s disease.  A major clinical trial at the time indicated that taking 2000 IU of vitamin E per day delayed placement in care facilities by several months compared to placebo.  By the way, treatment with selegiline (a type of antidepressant) produced the same effect.  Another study at the time demonstrated that eating a diet high in vitamin E was correlated with higher mental function in men and women aged 65 – 100.  Hence, many were taking high doses of vitamin E and supplementation was the standard of care for Alzheimer’s disease.

However, there were concerns regarding such a high dose of vitamin E as it produced side effects such as potentiating the effects of anticoagulants such as aspirin and Coumadin and increasing bruising and risk of bleeding.  There was also evidence that doses above 1500 IU suppressed immune function as suggested by a study in the Netherlands showing slower resolution of upper respiratory infections in institutionalized elderly.  Other studies at the time (Annals of Internal Medicine, 2005, 142,37-46) indicated that supplementation with vitamin E did not reduce the risk of cancer or major cardiovascular events but did increase the risk of heart failure and mortality.   Finally, treatment did not alter the course on Mild Cognitive Impairment “converting” to Alzheimer’s disease.

Hence, the recommendation was that generally using more than 400 IU of vitamin E was not prudent because the risks were too high.

Fortunately research continued.  The most recent clinical trial of vitamin E showed that treatment of those with mild to moderate Alzheimer’s disease slowed functional decline in activities in daily living (“High-dose vitamin E slowed the decline of people with mild and moderate Alzheimer’s disease,  Journal of the American Medical Association, 2014, 11, 29-30, 33-44).

The study was conducted at 14 VA medical Centers on 613 mostly male participants.  Participants were randomly assigned to receive Vitamin E (20000 IU per day), Namenda, vitamin plus Namenda, or placebo treatments.  Nearly all (97%) were treated with either donepezil or galantamine before and during the study and diagnosed with mild to moderate Alzheimer’s disease.  Over the course of 2.3 years those treated with vitamin E had less functional decline.  Namenda had no effect and, surprisingly, the combination of Namenda and vitamin E had no effect.  There was no increase in mortality as a result of treatment with this high dose of vitamin E.

In short, treatment with high dose vitamin E was effective and did not appear to cause harm.  On the other hand, treatment with Namenda did not have an effect and treatment with Namenda and vitamin E cancelled the benefits. None of the treatments delayed cognitive decline.  Vitamin E or Namenda have no preventative action for those without memory symptoms or for those with Mild Cognitive Impairment.  Apparently the stage of Alzheimer’s disease is an important factor in treatment that is only beginning to be understood.

Don’t forget to monitor your memory.  I have developed a focused, thorough short-term memory assessment that is brief and affordable.  Contact my office for details if you want to check out your memory.

 

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