There are retirement stories both ways. Some have a long and rewarding retirement. Others seem to decline either physically or mentally shortly after retirement. The fear is that by retiring, one becomes disengaged and cognitive impairment sets in. After all, educational attainment, social engagement, exercise, challenging work, and bilingualism are “neuroprotective so they decrease the risk” of such problems as Alzheimer’s disease. Of course, the conundrum is that we cannot determine cause as there is no study that disentangles whether time of retirement is a result or the cause of cognitive decline. This is further complicated by the fact that Alzheimer’s disease unfolds over the course of decades with subtle onset.

But what does the research tell us? There are a few studies that indicate that there is a correlation, an association between retirement and the risk of developing dementia. The findings are often quoted as a delay in onset of Alzheimer’s disease for each year retirement is delayed. One study suggests a delay of 0.13 years for each year that retirement is put off. This begs several questions like are we talking delays after 65, 60? The most recent study was conducted in connection with the European Alzheimer’s imitative (“Retirement age and the age of onset of Alzheimer’s disease, PloS One, 2015, 10, e0115036, PMID 25714815).

The study was based on an epidemiological study in Europe of 815 patients with Alzheimer’s disease. The database included age at retirement (excluded anyone leaving work before age 50) and age of onset of Alzheimer’s disease. Both age of symptom onset and age of diagnoses were considered. Several possible confounding factors were considered in the analysis: gender, level of education, income, complexity of job, as well as medical variables like hypertension, diabetes, depression, and stroke. Average age of retirement in this study was about 61.

Overall, later retirement age was associated with both delays in age of onset of symptoms (average = 74.9) and age at diagnosis (average = 77.1). This association held even when considering only those who retired before age 65. However, there was no significant association for those who retired before age 65 and developed Alzheimer’s disease ten years or more after retirement indicting that some of those who retired early did so because of symptoms interfering with work performance. The results were not associated with gender, income, medical conditions, occupation, or education.

In conclusion, there is an association between age of retirement and the age of onset of Alzheimer’s disease. However, whether early retirement speeds up the onset of Alzheimer’s disease is unresolved. It is clear that developing cognitive impairment can speed up the age of retirement. I find these data a relief as I an in the early stages of retirement and, so far, seem to be cognitively able.


“Music is ubiquitous in our lives” (Turn off the music! Music impairs visual association memory performance in older adults, 2015, The Gerontologist). It’s present while we are driving, studying, working, shopping, and dining. I often feel that when I’m out and about, I am barraged by music and background TV. Further adding to my frustration is the fact that others are choosing what I have to hear as well as how loud it is.

What is the impact of this noise on cognition and memory? Does it facilitate conversations at diner? Does background music help concentration? Does it help or impair memory? Does it release stress? There is evidence that background music enhances performance on simple tasks like naming as many animals as you can in one minute – called fluency. Then there is the controversial “Mozart Effect.” In the original study listening to Mozart’s sonata for two pianos improved spatial reasoning in college students. It didn’t take long to extrapolate this finding to inferring that listening to Mozart, maybe all classical music, increased intelligence. Later research was unable to confirm this effect.

The study of interest to us assessed the effect of background music on associative memory. The task required learning to associate names with faces and later recognition of which name went with which face. Subjects were younger (aged 18-30) versus older (aged 60-75) healthy adults who had no signs of memory disorder. Each participant was also screened and found not to have significant hearing impairment.

There were three conditions for this study. One group had silence while learning and recalling the task, a control condition. A second heard “musical rain,” computer generated sounds that were not structured like music, anther control. The experimental group heard instrumental background music that was unfamiliar to them as lyrics would be clearly distracting.

The findings were clear. The younger participants were better at this memory task than the older subjects. More relevant to the question addressed, background music as well as “musical rain” similarly impaired memory in the older participants. Interestingly, all participants found the music distracting and preferred silence during learning and remembering. In short, background music as well as “musical rain” was distracting to all and detrimental to the old.

Of course, using familiar music may have produced different results as unfamiliar music draws attention and therefore would likely be more distracting – a question for future research. This becomes more of a problem as we age in that we have a more difficult time multitasking. This limits our ability to ignore irrelevant background when we are engaged in complex cognitive operations.

The implication seems clear to me. Turn off the background music and noise if you need to think or learn – especially if you are past middle age or have any sign of cognitive decline or hearing loss.


What is a neuropsychological evaluation, what good is it, and how is it best done? Let’s start by making a distinction between testing and evaluation. Tests are rigid, standardized, formal measuring tools to determine things like mastery of information, placement in school programs, and outcomes for clinical trials of drugs. The test administrator needs to be consistent, neutral, not help, and not give feedback that may influence the results. Many neuropsychologists administer “tests.”

On the other hand, an evaluation is more flexible. The interaction is less formal and can be modified to meet the needs and personalities of those needing evaluation. For example, memory evaluations start by observing whether the client is on time. Did he or she remember the paperwork? Can he or she find the office? Find their insurance cards? Know their birthdate? Remember a list of words? Evaluation can be more relaxed, friendly. The intention is to put the client at ease. After all, in forensic work the client may want to look as bad as possible. However, no one wants to look demented. Cheating and exaggeration are unlikely.

Neuropsychological evaluation is like blood work – but no one has ever fainted on me. The question addressed is that one has a set of brain skills that have served them well throughout life. The intent is to determine if those skills are holding or declining. Skills may include memory, thinking, problem solving, attention, judgment, using language, nonverbal problem solving. This is the stuff of independence and competence. When well done, the results describe strengths and weaknesses in a way that informs treatment of any deficiencies and takes advantages of strengths. The results inform caregivers of what they are managing and how to help compensate for weaknesses. The results scale the severity of the problem and serve as tracking devices to determine patterns over time and effects of treatments.

I feel strongly that family members should be part of the process. After all, if someone forgets that they forget they can’t tell you what you need to know. Indeed, not including family in the evaluation of memory is a formula for making mistakes that lead to incorrect treatment plans or incorrect assessment of severity of the problem. Furthermore, family members should sit in on the “testing.” That way they better see what they are dealing with. The assessment is part of the treatment and for memory disorders this is a family issue. Being there also enhances feedback, which should be in detail and understandable. Assessment is a teaching device for family members as well as clients with memory concerns.

Diagnosis is a minor part of the process. It informs physicians of treatment parameters. But neuropsychological assessment can be so much more. It is a human interaction. Clients and family deserve to understand not only the findings but also the implications as well as practical guidance of how to deal with often-difficult issues. Assessments should help understanding of how to have a good life despite memory loss as well as to inform decision-making.


It seems that there is a mass sense of awaiting the magic bullet – the medication or the supplement – which we can take to make neurological disease go away. I hear so often how disappointed my audience is when I honestly say there is no magic potion available nor is there one that I can see on the horizon. We have come to expect medicine to offer a cure for Alzheimer’s or Parkinson’s disease just as it can offer antibiotics for certain infections or analgesics that make a migraine go away.

However, if we actually understand how the brain functions, there are treatments right under our nose. I recently read Norman Doidge’s article in the Wall Street Journal (February 7/8, 2015) “Brain, Heal Thyself” with great interest. He points out how our evolving metaphors of the brain, despite having immense heuristic value, have constrained our thinking about treatment of brain diseases.

The French philosopher Rene Descartes proposed an early model. He proposed the brain functioned as a machine. His model was further refined by the added proposition based on the brain’s electrical nature that the brain consists of circuits that have specific roles. Of course, this evolved into the current metaphors of the brain as a computer. These models limit our thinking as the focus on “hardware” and “software” that make the brain inflexible and mechanical. It is something to manipulate from the outside via a chemical or a surgery.

But the brain is anything but static. The brain is a fluid, dynamic organ that defines and constantly redefines itself from birth. The brain creates and refines its skills, microcircuitry, from experiences. It learns. It elaborates skills and parts it uses and it weakens those not needed or used. Consider the miracle of language. We learn language by experience without effort in our early years when all languages are possible. The brain is not fixed but rather it is flexible and evolving. It elaborates itself by use and wastes away by underuse.

Mr. Doidge discusses some interesting implications of this understanding for treating neurological disease. For example, Alzheimer’s disease can be understood as a progressive loss of the brain’s plasticity. It has diminishing returns of benefits from experience. As Alzheimer’s disease unfolds over decades and only becomes disabling at the end of its course, it is treated by lifestyle interventions like found in a recent epidemiological study. The results indicated that the “risk of dementia” is reduced by healthy eating, maintaining normal weight, limited alcohol, not smoking, walking at least the equivalent of 2 miles a day. These interventions appear to mitigate some of the decline attributed to normal or abnormal aging.

Consider also the frustrations of those with Parkinson/s disease that Doidge describes as the “tightening noose.” Fast walking helps motor function in Parkinson/s disease. But the rub is that this becomes increasingly difficult as the disease progresses so those afflicted back off on walking fast further adds to the disability by “learned nonuse.” Also, there is a disengagement of rhythmicity of motor execution in Parkinson/s disease. This may explain why walking on treadmill or dancing to music helps as these activities aid rhythms and help increase speed.

All of this is encouraging. We can treat neurologic disease as well as balance changes from aging by taking advantage of the brain’s natural placidity. We need to better understand these treatments, quit waiting for the magic bullet, buying unproven computer games, and take advantage of the brain’s natural ability to manage itself.


It’s not just those who have memory disorders that want to remember better. In everyday life, at school, or at work we rely on memory to stay engaged, advance, and track information. Seems so simple. It is not. Ever try to remember which movies you have seen over the last 6 months? What books have you read (who wrote them? Details for discussion?)? What you have to do at 3:00? Here are some strategies that help.

1. Read physical books. Reading is reading, right? Apparently not. Turns out that reading a physical book leads to better memory than reading on an electronic reader. Also, taking written notes leads to better learning than transcribing notes on a computer or tablet. When I don’t care if I remember (like for reading just for fun novels), I read electronically. If I am reading to remember, I read hard copy as active notes seem to work better than highlighting functions on electronic readers.
2. Being married. Two memories are better than one. Additionally there can be division of memory labor. Pamela remembers some things better than I and I remember some things better than her. Together we construct a more complete memory of our past and present.
3. Write things down. The act of writing – especially elaborative writing – locks in memory better than single quick experiences or information that are not pondered. Even better, try to teach someone else what you want to remember. Being able to convey information beyond the self creates better understanding as well as better future recall.
4. Walk through the woods or on the beach. A recent study compared the recall of new learning between a group of participants that walked around in a forest to a group who walked around in an urban environment. The persons who walked in the forest did better on a later memory test.
5. Make associations. The best way to learn new information is to associate it with something you already know. Make a story. Draw a sketch. Associate the information with a song. Mark Twain used to walk a familiar route on his estate as he learned new speeches.
6. Review. Takes notes. Review notes often over increasing intervals. Quiz yourself.
7. Don’t ignore the One Minute Rule. This is the old science of mnemonics. The more time, effort, and thought you put into something, the better you understand and remember it.


There are multiple memory systems in the brain. Each has its own organization and structure as well as unique role in our adaptively managing the world about us. I most often discuss short-term and long-term memory as these are so critical for our understanding of senior moments as well as common memory disorders. Short-term memory is the systems that allow new learning and is like the save command in a computer. Long-term memory is autobiographical information, knowledge, habits, sense of self and is like the hard drive of a computer.

Working memory is the memory system that manages the complex inputs we are constantly bombarded with from within (thoughts, feelings) and without. It consists of awareness, near awareness, and rapid decision-making. It is constantly juggling multiple inputs and deciding what to attend to, what to process further, and what to ignore. It is the desktop on a computer, it is the processor on the computer, and it is your active involvement with deciding what to do with all of the possible information and tasks available to you on a computer.

Working memory is a limited capacity system. It is part like the sport light of attention, constantly screening out distraction and focusing on what is import in the moment and in the near future. It allows us to follow conversation. It allows us to hold a phone number long enough to dial it. It allows us to know what we have to do at 3:00. It’s the system that allows us to do mental arithmetic.

Working memory switches from one task to another rapidly and slows more with each demand placed on it. We cannot do two things as quickly as one. Furthermore, as with most skills it slows and becomes less efficient as we age. We are able to juggle fewer things less efficiently, which adds to senior moments.

Hence it becomes essential as we age to actively optimize working memory by spending our cognitive resources and energy more wisely, another manifestation of the One Minute Rule. Here are some suggestions that will help:
1. Reduce and manage stress. Being distressed and overwhelmed takes resources away from working memory. Practice relaxation as a skill, increase mindfulness.
2. Stay fit. A conditioned body optimizes brain function.
3. Become an “expert.” The more we practice a skill or a talent, the more elaborate the brain circuitry underlying the skill, the greater the associations, and the more automatic the execution and the less we need to use working memory. This applies to learning athletic skills, creating knowledge, doing crossword puzzles, playing Bridge, doing art, as well as playing a musical instrument.
4. Get enough rest. Working memory slows when we are tired. Do cognitively demanding work when you are alert and rested.
5. Realize that many drugs (e.g., alcohol) and medications (benzodiazepines, pain medications) compromise working memory.
6. Limit interference (turn off the ringer on the phone) and unnecessary multitasking as much as possible.


I was invited to participate in a panel discussion at Avow Hospice. The theme was “what are the three things that you want all of your clients to know.” This is an interesting challenge for two reasons. First, each panel member has only ten minutes to make their point, Second, as I have recently turned 70 and am rapidly approaching retirement, what do I need to know for myself as I am not immune to the complex cognitive and physical changes that accompany both normal, true senior moments, and abnormal aging, memory and physical loss.

1. We do not yet know what causes Alzheimer’s disease. A recent issue of the ARRP newsletter states that the problem is a lack of research funding. But the issue is more complex. Where do we put the money? Amyloid treatments are a bust despite the fact that amyloid theories have caused mass tunnel vision within the scientific and medical community. We need a paradigm shift. The good news is that Alzheimer’s disease gives advanced warning so we can make plans to have a good life in the face of future memory loss. Furthermore, not everyone with the pathology of Alzheimer’s disease becomes demented and not everyone with dementia has Alzheimer’s disease.
2. The key to treatment of Alzheimer’s disease is short-term memory. There are slowly progressing changes in the ability to learn new information or skills that unfold over the course of a decade before dementia (read as disability) sets in. There is adequate time to strategically plan both to compensate for memory changes and for a higher quality of life for those who are forgetful as well as those who live with them. Make your life plan before you forget that you forget.
3. Treating short-term memory loss requires planning how to remember – the One Minute Rule. Simply, anything given less than one minute of thought will fade from your memory. Moreover, the more minutes you spend the better you will remember something. Quit trying to remember. Plan on how you will remember. A well-placed Post-it note trumps a good intention. Write things down in an organized way. Live by your calendar that contains both what you love to do and what you have to do. Organize your memory tools. The time and effort pays off.

Plan to have a good life even if you don’t remember it.


The cholinesterase inhibitors like Aricept (i.e., donepezil, rivastigmine, and galantamine) have been available for treatment of dementias such as Alzheimer’s disease since the mid 1990s. These medications slow the progression of Alzheimer’s disease (in those who tolerate them) and discontinuing them after extended use may induce a rapid decline even in those so impaired that they are in skilled nursing facilities. Despite these facts, the cholinesterase inhibitors are often maligned, not used, or discontinued too soon because they do not produce dramatic effects and do not arrest or reverse decline.

Although Alzheimer’s and similar dementias are classified as memory disorders, they actually have an impact on many brains skills or domains. In addition to memory, Alzheimer’s disease may produce impairments in attention, language such as word finding, visuospatial skills like drawing/handiwork, personality, mood, and/or executive functions. All of these skills are affected by changes in acetylcholine, the neurotransmitter that is increased by use of cholinesterase inhibitors. If we were to understand the benefits of these medications as consumers, it would be helpful to know what specific domains of possible benefits to expect.

This was the question addressed by “Treatment effects in multiple cognitive domains in Alzheimer’s disease: a two-year cohort study (Alzheimer’s Research and Therapy, 2014, 6, 48-60, PMID 25484926). As pointed out by the authors, there have been 4 large clinical trials demonstrating the benefits of cholinesterase inhibitors on global cognitive functioning (such as changes in the total score on the MMSE) for at least two years when compared to untreated matched control cases. However, there has been very little study of the specific domains or brain skills that respond to this treatment. It is especially important to understand the effects on executive functions as they are strongly correlated with activities such as cooking, driving, shopping, and managing the checkbook.

The focus of the study was to determine the effects of cholinesterase inhibitors on treated and untreated persons with Alzheimer’s disease for up to two years. Both measures of global functioning (MMSE and Dementia Rating Scale (DRS) total scores) and domain specific (e.g., memory, executive function) scores were obtained. The two groups were well matched in terms of age, education, and beginning MMSE and DRS scores. Treatment produced benefits on total score on both the MMSE and the DRS. For example; the average MMSE score began at 24.2 and declined to 20.2 in the treated group but declined from 22.9 to 16.4 in the untreated group.

More importantly, the major effects of treatment were in the domains of attention, visuoconstructive skills, and executive function. Despite being thought of as memory enhancers, these medications had little benefit on memory. In short, cholinesterase inhibitors do not improve short-term memory. Rather they slow the rate of decline in critical skills such as word finding, engaging in the world, and thinking abstractly. They reduce the burden of care by keeping together routines and self care skills longer than in the absence of treatment. These are important benefits despite the progressive nature of these dementias; treatment with cholinesterase inhibitors buys time.


Alzheimer’s disease and other progressive dementias are not the only cause of cognitive impairment. It is commonly known that as the heart goes, so goes the brain. An estimated 5 million Americans suffer from heart failure and this number is expected to double over the next 40 years (“Heart failure and cognitive dysfunction,” International Journal of Cardiology, 2014, 178, 12-23, PMID 25464210). Cognitive impairment is common in those with heart failure with a prevalence ranging from 25% to 75% with greater degree of heart failure associated with higher levels of cognitive impairment. Those in heart failure with a left ventricular ejection fraction of less than 45% are especially prone to cognitive impairment that is at least mild.

Cognitive impairment may involve any one or all of several brain functions. These include attention, memory, executive function, language, speed of thinking, and/or constructive ability. Heart failure causes hypoperfusion (decreased blood flow) of the brain, which reduces oxygen and delivery of glucose to the brain. This in turn may lead to the destruction of neurons. The risk for cognitive impairment in heart failure is greatest for those with diabetes, systolic blood pressure of greater than 180, or diastolic blood pressure less than 65. There does not appear to be an association with low systolic or high diastolic blood pressure.

There are a multitude of secondary effects of heart failure that may contribute alone or together to increase cognitive impairment. Among these factors is depression, which may be severe or mild. Many medications that regulate blood pressure and heart function have anticholinergic side effects that are notorious for inducing confusion. Diabetes is known to induce cardiomyopathy, heart disease, and hypoglycemia. Inflammatory cytokines are released and are associated with cognitive impairment. Homocysteine, an amino acid, is elevated in heart failure and associated with cognitive impairment and decline. Finally, atrial fibrillation is strongly associated with cognitive and functional decline if left untreated.

Cognitive impairment associated with heart failure has a number of consequences. It compromises the skills necessary to manage a complicated treatment routine including managing medications, tracking follow up appointments, and managing heart healthy diet. It also may compromise the ability to recognize symptoms in oneself. On a practical level these changes may impair IADLs like driving, managing finances, paying bills, or preparing meals. In the extreme, cognitive impairment may lead to hospitalization and increased mortality in heart patients, mortality in heart failure with cognitive impairment is 18% at one year versus 3% in those with normal mentation.

The bottom line is that heart disease adds cognitive burden that affects treatment and outcome. The cognitive changes may be subtle or obvious, temporary or persisting. Assessment of cognitive function is an essential component in managing and treating heart disease.


Alzheimer’s disease does not develop suddenly. It emerges over the course of decades. There is a history of short-term memory loss that often dates back a decade before more obvious symptoms arise. Onset is subtle. How many of us have had senior moments? How do we know if they are benign or the hallmark of progressive cognitive decline? Changes are complex and differ across individuals depending on the region of the brain that is affected.

One way to make sense of these complicated pathways is to have a category that reflects significant changes in memory that fall short of a dementia. The solution has been to create a category – diagnosis if you like – for individuals who have memory changes but are not demented. This is Mild Cognitive Impairment (MCI) (“Mild cognitive impairment and mild dementia: a clinical perspective,” David Knopman and Ronald Peterson, Mayo Clinic Proceedings, 2014, 89, 1452-1459, PMID 25282431).

MCI (the amnestic type) is memory decline that is greater than the inefficiencies of normal aging. It is marked by cognitive impairment that falls short of a dementia. The afflicted person remains independent but there are concerns as well as performance on objective tests that are lower than expected from those with similar age and education. A person with MCI can still pay bills, shop, and prepare meals. MCI marks the risk of future decline that is greater than for those with normal memory.

How is MCI different from mild dementia? Those with mild dementia also have poorer memory than either those who age normally or those with MCI. Mild dementia is marked by substantial decline at work or at home in abilities such as paying bills, shopping, or taking medications. However, personal care like dressing, preparing snacks, and grooming are fine. Persons with mild dementia almost always decline over time whereas some with MCI do not.

How are these conditions diagnosed? Mostly by a careful history obtained from the person of concern and an informant such as a family member or close friend. Despite the advancements in imaging techniques, a good clinical interview and objective cognitive tests are the gold standard for diagnosing MCI and mild dementias. If these assessments suggest decline further medical evaluation is necessary to determine if the problems are a result of a medical disorder such as stroke, thyroid disorder, or diabetes.

What should you look for in everyday life to indicate that someone may be at risk for progressive decline? Mostly the early signs will show as functional changes. Look at abilities like paying bills, balancing the checkbook, getting taxes ready, managing affairs, organizing papers, being able to shop alone, preparing meals, tracking current events/interests, following movies/TV shows, taking medications, finding one’s way around. If any of these skills are of concern, seek assessment.

  • Managing Your Memory

    Practical Solutions for Forgetting

    Order Now
  • Shopping Cart

    Your cart is empty
    Visit The Shop
  • Upcoming Events

    Sorry, there aren’t any upcoming events right now. Check back soon!
  • Sign up for our mailing list.

  • Categories