There is increasing empirical evidence that a life style that includes at least moderate, consistent exercise improves cognitive and health outcomes as we age.   It seems logical that exercise would be helpful to improve outcomes of those with neurodegenerative diseases such as Parkinson’s disease where there is progressive loss of neuromuscular abilities.  Fortunately there is an encouraging review that serves as the basis for this article: “An evidence based exercise regimen for patients with mild to moderate Parkinson’s disease” (Brain Sciences, 2013, 3, 87-100

Parkinson’s disease is, by some accounts, the second most common neurodegenerative disorder and affects 4-5 million of those over 50.  The primary symptoms involve motor control: resting tremor, slow response initiation (called bradykinesia), muscular rigidity, and postural instability.  It is now clear that exercise improves physical function, self-reported quality of life, strength, and gait speed as well as prolongs life in Parkinson’s disease.

Prospective studies have demonstrated neuroprotective effects of exercise in Parkinson’s disease.  Moderate to strenuous but not light exercise reduces the incidence of Parkinson’s disease in population studies.  The exercises that were beneficial included swimming, running, tennis, basketball, and cycling.   It appears that exercising patterns of those between 35-39 are especially helpful in the long run.

Three general types of exercises should be included: cardiovascular/aerobic training, balance training, and strength training.  Increasing amounts/intensity of cardiovascular exercise produces better results.  High intensity treadmill or cycling improved gait, balance, and quality of life more than conventional therapy in mild to moderate Parkinson’s disease.  Intense cardiovascular exercise also improved brain plasticity, language, and cognitive functioning in Parkinson’s disease.

Balance training is also an essential component of exercise in Parkinson’s disease.  Dopamine replacement medications are insufficient to control postural instability and balance.  Balance and strength training improve gait, ambulation, and equilibrium.  Motor controlled video games may also be helpful.  Finally, there is clear evidence that Tai Chi is more effective in preventing falls than conventional physical therapy for balance in mild to moderate Parkinson’s disease.

The third component of exercise is strength training.   Parkinson’s disease not only induces motor dysfunction but also affects strength.  Indeed, the benefits of resistance  training include improved strength, endurance, and response initiation.  It is also clear that there are greater gains from three sets of each exercise when compared to only one set.

In summary, the prescription for exercise in mild to moderate Parkinson’s disease should include:

  1. Cardiovascular exercise such as treadmill, cycling, running, tennis at high intensity for up to 30 minutes three times per week.
  2. Strength training with 3 sets of each exercise with high load 2-3 times per week.
  3. Balance training such as Tai Chi for an hour 1-2 times each week.


There are two types of risk factors that are associated with the development of dementing conditions as we age.  First, there are factors that we cannot control.  The strongest risk factor for becoming demented is not directly controllable, age.  If you live to be in your mid-80s or older, the risk is near 50%.  There are other associated risk factors that are correlated with cognitive decline with aging such as apolipoprotein gene carrier status (Apoe4 has the greatest risk whereas Apoe2 has the least), Mild Cognitive Impairment, cancer (there is an inverse association between cancer and cognitive decline), and sex (women are at greater risk than men).

Second, there are also factors over which you have at least some degree of control.  These include history of head injury (hence the desire to wear seatbelts and helmets), blood pressure at midlife and beyond, type II diabetes mellitus, stroke, exercise), smoking, drug and alcohol use. 

Many believe, despite no good empirical evidence that dietary supplements such as vitamins may be neuroprotective.   The latter is interesting as health problems are associated with either deficiency or excess concentrations, which is not a problem for most of us.  A case in point is Vitamin D,  there has been a recent surge in interest in vitamin D to promote brain health.  Two recent findings from the Atherosclerosis Risk in Communities Study suggest that it is premature to take vitamin D to promote brain health.

First, the cognition study was published in the European Journal of Neurology in May 2014 based on analysis of 1650 participants.  There was no association between lower levels of vitamin D and cognitive testing.  Second, the MRI study was published in JAMA Neurology in May 2014 involving 1622 participants.  Levels of vitamin D were not associated with white matter disease and did not prevent “subclinical” strokes.

It appears from past studies that there is an association of between low levels of vitamin D and hypertension, diabetes, heart attack, and stroke but this may just be a marker for poor health.  It’s too early to recommend supplementation with vitamin D for those with normal blood levels as a “neuroprotective” strategy.

The relative risk of hypertension and cognitive decline is complex.  An article in Neurology (2014, 82, 2187-2195) reports findings from the Age, Gene/Environment Susceptibility Reykjavik Study suggested that cognitive impairment in late life are dependent upon having a history of hypertension in midlife.  Those with normal blood pressure in midlife had increased risk of white matter lesions and cerebral microbleeds if they experienced hypertension in late life.  On the other hand, those with midlife hypertension had more brain atrophy and lower memory scores if they had lower late life diastolic blood pressure.

Finally, there is another recent study (Neurology, 2014) showing an inverse association between cancer and cognitive decline.   There is no clear explanation of possible mechanism behind such a correlation.

The relationships between medical/life style factors and cognitive decline appear to be quit complex.  The most proactive things we can do are to stay in shape, eat healthy, seek experiences, maintain health/wellness, and keep monitoring our short-term memory.



The “amyloid hypothesis” of Alzheimer’s disease postulates that Alzheimer’s is caused by the accumulation of a protein named beta-amyloid that produces the “gunky” deposits called plaques in the brain.  Despite the evidence that this is not the root cause (may be an effect of the brain changes in Alzheimer’s rather than a cause), the theory has become scientific orthodoxy, dogma and accepted on faith rather than evidence.  It has dominated research aimed at slowing or reversing Alzheimer’s disease leaving little funding for other approaches.

 But there is a kink in the armor.  There is accumulating evidence that treating amyloids is not the solution.  For example, six new drugs that decrease beta-amyloid reached phase II and III clinical trials in 2012.  Three of the studies were discontinued because concerns about safety or lack of efficacy.    Furthermore, we know that the brains of those who will develop Alzheimer’s disease is different from the brains of those who don’t.  However, it is also clear that having amyloid deposits does not guarantee that one will develop symptoms.  Even autopsy studies, heretofore the “definitive” proof, demonstrate that we can die with the pathology of Alzheimer’s disease but without clinically relevant symptoms.

To date the clinical trials of amyloid drugs have been conducted on those who already clearly have Alzheimer’s disease.  The assumption is that intervention is too late; the pathology has advanced too far to reverse or slow.  The next strategy in pursuit of the amyloid hypothesis is to intervene earlier, before the brain is so severely damaged.

Hence the ambitious attempt to recruit seniors who are willing to have their brains scanned for amyloids well before any memory symptoms and are willing to enter a clinical trial of an anti-amyloid drug, the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Study (“Study tests healthy seniors for silent signs of Alzheimer’s disease,” June 10, 2014, Naples Daily News).  The question is “can intervening early make a difference for those who do [develop Alzheimer’s disease]?  We won’t know the results for several years but this is the clearest test of the amyloid hypothesis to date. 

In the meantime, Alzheimer’s is a complex disease that has no simple neurobiology.  There is current research that focuses on biological processes other than amyloids.  For example, we need to pursue more rigorously the other major pathology, Tau proteins that form tangles in the brain of those with Alzheimer’s disease.  We need to pursue research into the hypothesis that Alzheimer’s disease is related to “Type III diabetes.”  We need to pursue the “mitochondria hypothesis” (Laura Spinney, “Genetic risk for Alzheimer’s Ignored for decades,” 2014, Scientific American). We need to broaden our gaze if we are to find better treatments than we have now.



Notwithstanding many technological advances, there is still no fool-proof method for diagnosing Alzheimer’s disease, (avoiding the fact that the brain changes occur decades before symptoms).  There is no blood test or imaging technique that is definitive.  Even autopsy diagnosis has its problems.  Diagnosis of Alzheimer’s disease remains a clinical diagnosis based on history, symptoms, patterns, and clinical judgment.

 The criteria for a diagnosis of possible Alzheimer’s disease:

  • The afflicted individual must be demented – disabled by the decline.
  • Symptoms appear gradually over months to years
  • There is progressive worsening of cognition
  • The initial and cardinal deficit is short-term memory (i.e., new learning)
  • Less commonly language deficits (e.g., word-finding) appear early
  • There are deficits in other skills such as planning, reasoning, judgment, sequencing

The diagnosis of possible Alzheimer’s disease:

  • There is sudden onset of symptoms
  • Progression is not gradual
  • There is concomitant cerebrovascular disease
  • Clinical features of Lewy body disease
  • There are other medical (e.g., thyroid disease, cancer) or neurologic diseases (e.g., head injury, stroke) present that may impair mental functions
  • There are medications or drugs present that may impair cognition

Mild Cognitive Impairment is diagnosed when:

  • Cognitive decline noted by self or informant or clinician
  • Objective evidence of cognitive decline – most typically in short-term memory
  •  Independence is not compromised


  • CT or MRI based images are prudent to rule out pathology such as cerebrovascular disease or tumors that would modify clinical management
  • Amyloid tests in isolation cannot reliably diagnose Alzheimer’s disease or Mild Cognitive Impairment
  • Measuring CSF and/or blood levels of amyloid or tau proteins are not clinically useful at this time.

Persons with rapid onset (onset within one year) cognitive decline should be referred to specialists who have experience and diagnostic capabilities to evaluate and manage these conditions.

Pharmacological treatment:

  • Cholinesterase inhibitors (CHIs) include Aricept (donepezil), Exelon (rivastigmine), and Razadyne (galantamine)
  • CHIs are recommended for treatment of Alzheimer’s disease or Alzheimer’s disease with a cerebrovascular component
  • CHIs are recommended for treatment of dementia associated with Parkinson’s or Lewy body disease
  • The findings for effectiveness of CHIs for treating vascular dementia is inconsistent
  • Evidence of effectiveness of CHIs indicate that they are comparable and selection should be made based on clinical criteria such as tolerability and ease of use
  • The combination of CHIs and Namenda (memantine), although rational and safe, lacks empirical support for increased efficacy
  • CHI use may increase risk of gastrointestinal bleeding, tachycardia, or heart block; worsen asthma or other pulmonary disease; cause urinary obstruction; increase risk of seizures, or prolong actions of muscle relaxants
  • There is no clear evidence for efficacy of CHIs in neuropsychiatric disease
  • Discontinuation of CHIs should be based on side effects, drug costs, or dementia progressing to end stage (stage 7).



The most frequent question I am asked is “What can I do to improve my memory?”  The answer depends upon which type of memory you want to improve.  Practice, repetition, study, modeling, and imitation can all improve long-term memory.  Long-term memory involves reinforcing what is already stored in the brain.  It works like a muscle and strengthens and endures from use.

Short-term memory is a different issue.  Short-term memory is the process of storing new information.  It requires learning and is demonstrated by memory or skills that will be demonstrated at some future time.  This memory system does not work like a muscle.  It usually takes time and effort to learn new things.  You remember best those things when you slow down, attend to, think about something.  Hence anything given less than  one minute of thought will fade from your memory – the One Minute Rule.  Quit trying to remember.  Plan how you will remember.

Memory training has been referred to as mnemonics or study skills, which require effort and strategy.  These techniques allow deeper processing of information or skills and improve retention over time.   Many of these techniques are simple and effective if used consistently.

Good organization improves memory.  Clutter and disorganization interferes with memory.   For example, have one place for notes.  Having notes on random sheets of paper and in multiple locations increases the likelihood of forgetting.  How many Post-it notes do you need to have before they fight each other?  Create a memory notebook as the organized place to keep important notes and update it often.

A recent study (“The pen is mightier than the keyboard,” Psychological Science, 2014, Pam Mueller and David Oppenheimer) indicates that how you take notes will also determine how well you remember.  They had students watch TED talks and take notes.  Half took hand-written notes whereas the other half took notes by laptop computers.  Students were asked both factual and conceptual questions about the material learned 30 minutes and one week later.  Students who took hand-notes had better recall than those who took notes on their laptop.  This advantage remained after one week even though both groups had studied from their notes.

Hand-notes appear to engage us more with the information.  Many type faster than they write and therefore transcribe rather than make decisions about what to think about as they take notes.  Just transcribing, verbatim notes, is not enough.  This is a clear example of the One Minute Rule in Action.

Another example comes from an online article in The Philosopher’s Mail, “Why you should stop taking pictures on your phone and learn to draw.”  The conclusion  was based on the thoughts of John Ruskin, an English art critic.  In essence, we are so busy taking pictures that we forget to look at the world whose beauty and interest prompted the picture.  If you want to remember interesting things better, take the time to draw them irrespective of your talent for doing so.  Drawing teaches us to see and notice properly rather than to gaze absentmindedly.  It takes 10 minutes to sketch a beautiful tree but only a minute to gaze at the same tree.

The bottom line: spend the time and effort to improve your memory.  Don’t forget the One Minute Rule.”




How does caregiving unfold over time?  Diseases such as Alzheimer’s disease evolve over time – usually decades.  The person who is forgetful can manage early changes in memory.  But as the disease progresses, there is an increasing need for external guidance, prompts, and caregiving as the problems extend beyond just forgetfulness.  There are seven general stages of memory loss per the global deterioration scale.  The following presents general needs for care at each stage.

Stage one – normal.  This is the stage that we all hope to stay.  There are the typical “senior moments.”  No caregiving is needed.

Stage two – forgetfulness.  In this stage there is minor consistent forgetfulness and the person in this stage is typically aware that there are changes.  There may be an incident or pattern that raises minor concerns.  There is no need for caregiving but this is the stage when memory assessment to obtain a baseline and proactive family planning in case of future progression is quite fruitful.   Take advantage of educational programs such as those provided by the Alzheimer’s Support Network in Naples.

Stage three – early confusional state.   Forgetting is noticeable by those who are close.  There is slow execution of complex tasks such as doing  checkbook, organization, or managing finances.  Independence is still the rule but there is minor confusion.  Caregiving at this stage involves support, patience, and help to put in place external memory supports such as a consistent calendar habit.  Ability to do complex tasks (e.g., checkbook, finances, driving, cooking) should be assessed and monitored.  Family planning in case of progression is essential but caregiving is minimal.

Stage four –late confusional stage.  Forgetting is extensive.  The person is befuddled.  Higher order cognitive skills (e.g., balancing a checkbook, preparing a meal, finding new places, financial decision making, judgment, reasoning) often are riddled with mistakes.  Caregiving may involve such things as taking over the checkbook, bill paying, helping with meal preparation, or overseeing medications.  During this stage the treatment often shifts from the person with the memory loss to the caregiver as they have to increasingly take over family tasks and serve as the external memory.  Husbands, wives, and children make a gradual transition to a parenteral role as there is forgetting that you forget.  There may be little appreciation of what you are doing and resentment for being “treated like a child.”

Stage five – early dementia.  Forgetting is very extensive, insight is lacking,  and independence is no longer possible.  Caregiving is demanding, stressful, and constant.  The caregiver needs a plan in case they cannot provide care.  What is the plan if the caregiver is out of commission for two hours, two days, two weeks, or longer?  The hope is that you never need to implement the plan but you have to have the plan in place before you need it.

Stage six – middle dementia.  Personal care and communication are breaking down.  There are dangers such as wandering.  Care at home by a single caregiver is at best difficult as the demands are usually overwhelming.  The forgetful person cannot safely stay alone.  24 hour care/supervision is necessary. Either in home care or placement is necessary for safety.

Stage seven – late dementia.  The disease has progressed to the point where walking, talking, and feeding oneself is no longer possible.  Consider hospice services.


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.



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.



 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?



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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