With the pervasiveness of memory problems in conditions such as dementia, Alzheimer’s disease (AD), mild cognitive impairment (MCI), traumatic brain injury (TBI), and others, it is clear that there needs to be innovation in the field of neuropsychology to meet the healthcare demands that these conditions present. Often these types of problems arise in a subtle fashion that goes undiagnosed and untreated. In order to begin to address these issues, we have developed MemTrax—an online memory game that is designed to measure and track memory performance. It is our assertion that MemTrax has applications as a tool to assist in preventing cognitive decline in aging populations, and to help identify AD and other cognitive impairments.

Neuropsychological and cognitive assessments are both methods of understanding the capacity at which an individual is mentally performing. People that are familiar with cognitive and neuropsychological assessments are likely to have experiences with the Mini Mental Status Exam (MMSE). For those who have not had the opportunity to familiarize themselves with it, the MMSE is an assessment of the memory and cognitive performance in an individual. The MMSE is conducted by an interviewer who asks an individual a series of questions, including current date, time and location, along with others, while the individual gives verbal answers to the questions. The individual is also instructed to simultaneously keep a specific phrase in their memory, which they are asked to recall later in the test. The answers to the questions are marked down by the interviewer using a pen and paper. At the end of the interview, the answers to the test question are scored, and the test score is intended to reflect the individual’s mental status. Today, the MMSE and various other versions of pen-and-paper type tests continue to commonly be implemented to establish the level of performance of an individual’s memory and other cognitive abilities.

What is clear is that pen-and-paper assessments are not able to match the efficiency that software based tests offer. There is a growing need for efficiency in medicine, and electronic assessments also provide the added benefit of preventing the necessity of an interviewer, such as a doctor, for test administration. This frees up valuable time for medical professionals while allowing for anyone that is concerned or curious about their memory performance a quick and accurate assessment of their cognitive abilities.

The MMSE is conducted by an interviewer who asks an individual a series of questions, including current date, time and location, along with others, while the individual gives verbal answers to the questions. The individual is also instructed to simultaneously keep a specific phrase in their memory, which they are asked to recall later in the test. The answers to the questions are marked down by the interviewer using a pen and paper. At the end of the interview, the answers to the test question are scored, and the test score is intended to reflect the individual’s mental status. Today, the MMSE and various other versions of pen-and-paper type tests continue to commonly be implemented to establish the level of performance of an individual’s memory and other cognitive abilities.

The creation of new technologies—specifically, computers and the internet—allows for innovation to occur within the field of neuropsychological assessment. However, much of neuropsychological assessment is still done today using outdated pen-and-paper tests. This is where MemTrax.net provides an advantage over the current standard for assessing memory performance in the field of psychology.

The MemTrax test offers superiority to the MMSE in the following ways:

1. Higher precision in the measurement of memory performance
2. Added measurement of reaction speed within the nearest millisecond
3. Less time is taken for test administration
4. The need for an interviewer is eliminated
5. Provides interesting and stimulating assessment content
6. There is electronic storage of all prior test results
7. Results are easily accessed and understood
8. Can be administered at the user’s discretion

However, there are certain advantages that come with using the MMSE as well. First, it does not require a computer to administer. Another consideration is that it offers a more diverse assessment of cognitive functioning. Lastly, there a large advantage is that the MMSE score has been well researched to correlate with specific dysfunctions. This last advantage of the MMSE is a potential ability of the MemTrax.net assessment, but this requires further research and validation.

What is clear is that pen-and-paper assessments are not able to match the efficiency that software based tests offer. There is a growing need for efficiency in medicine, and electronic assessments also provide the added benefit of preventing the necessity of an interviewer, such as a doctor, for test administration. This frees up valuable time for medical professionals while allowing for anyone that is concerned or curious about their memory performance a quick and accurate assessment of their cognitive abilities.

1) Online screening can lead to earlier identification of cognitive impairments.

Traditionally, individuals do not suspect they have any form of cognitive impairment until they experience occasions where their memory or other cognitive faculties fail them, or someone close to them observes and voices concern about that individual’s cognitive performance. Having a test that is online, non-invasive, and easy-to-use empowers individuals to take care into their own hands, and identify problems at earlier stages of impairment.

2) Early identification of cognitive impairments will reduce monetary costs to individuals and society.

If cognitive problems are caught early, then individuals will be aware of their impairments and be able to take action to avoid potentially dangerous situations. For example, up to 60% of individuals with dementia are at risk for wandering away from their residence without notice [1]. Individuals that wander away place themselves in potentially dangerous situations, and put tremendous psychological strain on the ones that care for them. Furthermore, individuals that suffer from cognitive impairment are at an increased risk for being involved in serious accidents. However, if precaution is taken when there is identification of cognitive impairments, then the risk factors for these individuals can be greatly reduced through treatment and changes to their environment.

3) Screening will lead to better care.

Recognizing cognitive problems early gives patients a wider array of treatment options. Current pharmaceuticals that can help treat the cognitive symptoms of include cholinesterase inhibitors and memantine, which have been demonstrated to be effective in moderate to severe stages of dementia [2]. However, in earlier stages of cognitive impairment the supplement Gingko biloba has been shown to have favorable effects on cognitive performance and social functioning [3]. Furthermore, patients that recognize mild impairments can take measures to improve their cognitive functioning through beneficial activities, such as partaking in stimulating mental activities, physical exercise and other nonpharmacological interventions [4].

4) More time efficient and cost effective compared to traditional methods.

One traditional option that individuals may choose to gauge their cognitive performance is to be screened for memory problems at National Memory Screening Day, which is November 15th of this year [5]. However, this only presents a very limited window of opportunity for an individual to examine their cognitive performance. Another option is to see a doctor, who may administer a cognitive performance test or refer the individual to a specialist. With an online tool, an individual can skip the preliminary steps of going to a location and taking a test and instead be able to screen for problems from the comfort of their own home, thus saving time. This method can also reduce costs associated with doctors administering preliminary neuropsychological tests that measure cognitive performance.

5) Better overall health outcomes.

Ultimately, with the aforementioned benefits of screening for cognitive impairments using online tools, there is the possibility for better overall health outcomes for individuals. If an individual is fearful that they may be facing some form of cognitive impairment, then an online screening test may either indicate to them that there is nothing to worry about, or that they need to seek further help. In either case, the burden of fear is taken off the shoulders of that individual when they are able to quickly determine whether their fears are justifiable. Furthermore, when an individual is able to use an online tool to make data-driven decisions, they feel that their health outcomes are placed in their own hands. This has powerful implications in terms of the way that individuals conceptualize the overall course of treatment and how motivated they are to follow through with treatment plans.

References

[1] Wandering: Who is at Risk? <http://www.alz.org/national/documents/card_wanderingwhoisatrisk.pdf>

[2] Delrieu J, Piau A, Caillaud C, Voisin T, Vellas B. Managing cognitive dysfunction through the continuum of Alzheimer’s disease: role of pharmacotherapy. CNS Drugs. 2011 Mar 1;25(3):213-26. doi: 10.2165/11539810-000000000-00000. Review. PubMed PMID: 21323393

[3] Le Bars PL, Velasco FM, Ferguson JM, Dessain EC, Kieser M, Hoerr R: Influence of the Severity of Cognitive Impairment on the Effect of the Ginkgo biloba Extract EGb 761 in Alzheimer’s Disease. Neuropsychobiology 2002;45:19-26

[4] Emery VO. Alzheimer disease: are we intervening too late? J Neural Transm. 2011 Jun 7. [Epub ahead of print] PubMed PMID: 21647682

[5] National Memory Screening Day <http://www.nationalmemoryscreening.org/>

For now, I think we need to focus on improving our ability to measure memory. I don’t think that CSF values or fancier brain scans or more complex brain scan analyses are going to be useful at the individual clinical practitioner level yet. My argument in my talk was that we need to keep the costs down and the basic support up until we can develop real benefits for early diagnosis, which means preventive interventions.

J. Wesson Ashford 101 Sanders-own Building, University of Kentucky, College of Medicine, University of Kentucky, Lexington, KY 40536-0230, USA

Journal of Alzheimer’s Disease 4 (2002) 141–143 141 _______________________________________________________________________________________________________________________________ Is ApoE 2/3 good or is ApoE 4 evil? It is well established that ApoE genotype is highly associated with the risk of developing Alzheimer’s disease. The establishment of this association has led to an intense search for the role that ApoE plays in ain function, particularly in functions such as neuroplasticity that are most involved with the Alzheimer neuropathological process. In the course of this search, results have tended to show either that the ApoE e-3 protein has some beneficial effect, or the e-4 protein has some harmful effect. The issue in this debate hinges around this point, which perspective is most sound? Whether the e-3 protein helps to protect the ain from Alzheimer pathology (e-3 good) or the e-4 protein directly instigates the pathological process (e-4 evil)? The debate on the goodness of ApoE e3 or the badness of ApoE e4, in Cincinnati in July, 2001, and in the written summaries both reflect the dichotomous positions of the roles attributed to the different ApoE alleles. The disparity of the two sides and the importance of this issue were most clearly framed at the beginning of the summary statement by Rebeck et al., in relating the issue to treatment decisions:

– if ApoE 2/3 is good, the treatment would be directed to inducing ApoE expression and developing ApoE agonists (assuming there is only a relation with the quantitative action of these proteins that is relevant). – If ApoE 4 is bad, treatments would aim to inhibit or antagonize ApoE function. Consequently, this debate addresses an issue whose solution is required prior to developing specific therapies for AD. Both sides make strong cases, one clearly outlining the harmful effects of ApoE 4, the other presenting the benefits of ApoE 2/3. Thus, a oader perspective needs to be taken to recommend a concluding opinion. To consider “good” and “evil”, things must be placed at two ends of a continuum, and a midpoint of the continuum becomes the balance-point between the two sides. As the arguments are made in this debate, ApoE e2/e3 represent “good” and ApoE e4 is “bad”. However, neither side considers the position that both points could be correct. Rather, the issue is framed as whether ApoE e4 is good and ApoE e2/e3 are better, or the alternative view, that AooE e2/3 are not good, and ApoE e4 is very bad. Accordingly, do ApoE e2/e3 just represent an extreme of benefit, or does ApoE e4 represent the extreme of detriment. A related question to resolve is whether the differences between the various allelic proteins are only quantitative, or whether there is a clear qualitative difference in their actions. The critical perspective that is not discussed by either side is the evolutionary context. It is the back-drop of evolution that sheds light on biological function. That light is needed to resolve which debate position is stronger. In evolution, for a protein to survive, it needs ISSN 1387-2877/02/$8.00  2002 – IOS Press. All rights reserved 142 J.W. Ashford / ApoE4: Is it the absence of good or the presence of bad? to make a contribution in the ecological setting of the animal that is producing it.

Over time, a new protein may replace an old protein, either because it confers a new advantage in a stable ecological setting, or the ecological setting has changed and the new protein confers an advantage in the context of the next setting, which it may not have had in the original setting. ApoE ε4 is not a new detrimental allele. ApoE ε4, which exists in a similar form throughout mammals, presumably confers some general advantage. The ApoE ε3 allele appeared in humans about 300,000 years ago, and the ApoE ε2 allele appeared about 200,000 years ago. The question then is whether the advantage of ApoE ε4 became a disadvantage as humans enlarged their ains and extended their life-spans, with APOE ε2/ε3 conferring a reduced level of toxicity. The alternative question is whether APOE e4 is a beneficial protein, which was improved in humans to APOE e2/e3 as humans entered a niche with different stressors and different dietary resources, which required or provided increased cereal complexity and extended longevity. The team of Teter, Raber, Nathan, and Crutcher develops the concept that ApoE e4 is more toxic than ApoE e3. They divide their arguments into 6 categories, including the following:

1) Neurite sprouting: ApoE e4 protein is inhibitory, has no effect, or is weakly stimulatory, less than ApoE e3. This negative effect of ApoE e4 is dominant over that of ApoE e3. The difficulty with this argument is that it is not clear whether an inhibitory effect on sprouting is good or bad. Blockade of sprouting may be necessary, even protective, in some contexts. 2) Cognition: ApoE ε4 is said to be associated with impaired cognition in humans, relative to other ApoE genotypes. ApoE ε4 in mice is said to be detrimental relative to ApoE -/- mice. The issue in humans is a relative statement that does not address the question of absolute benefit or detriment. The mouse studies appear to address this issue and show that ApoE ε4 is bad for mouse memory, at least relative to APOE -/-, but there is no reason to think that a protein carefully adapted to the human would have anything but a negative effect in another species. 3) Tau metabolism: ApoE e4 seems to disrupt the neuronal cytoskeleton and predispose to the formation of neurofiillary tangles. First, it is possible that some disruption of neural cytoskeleton is important for ain function. For every anch and synapse created, another must be destroyed. As humans have grown larger ains with more connections thatmust endure for a longer life-span, there is presumably a natural tendency for NFTs to form. NFTs may indeed be considered pathological, but a legitimate counter perspective is that ApoE e4 just is not as efficient at degrading the hyperphosphorylated tau as the more modern ApoE e2/e3.

The team of Rebeck, Kindy, and LaDu takes the position that ApoE performs neuroprotective and neurotrophic functions that are normal ain mechanisms, and the ApoE ε2/ε3 alleles produce proteins that perform these functions more efficiently than the proteins produced by the ApoE ε4 allele. This team reviews the functions of ApoE, including lipid transport and a role in neuroplasticity, as well as possible activities in the metabolism of beta-amyloid and tau. Other possible properties, including anti-oxidant and anti-inflammatory actions, are described. In each case, ApoE ε2/ε3 are shown to be beneficial and more so than ApoE ε4. One particularly interesting issue that has arisen recently is the role of ApoE in beta-amyloid production, specifically in relationship to neuroplasticity. The Rebeck et al. team reviews some of the literature relating to this concept. There is evidence that the macroglia produce ApoE during times of neuroplastic acitivity. The ApoE then transports cholesterol to the dendrite memanes to form lipid rafts. The entire metabolism of the amyloid-pre-protein (APP) is thought to occur on these rafts. Presumably the APP molecule is transformed by the alpha-secretase into a “nexin” which will promote the formation of new synaptic contacts. Alternatively, the APP molecule may be cleaved sequentially by the beta-secretase to produce a secondary large protein, then by the gamma-secretase to produce beta-amyloid. The proteins produced by the second pathway, which include the apparently neurotoxic betaamyloid, may be responsible for destroying synapses that are destined to be removed. Both pathways may be essential for neuroplasticity, one for constructing new connections, and the other for destroying contacts that are no longer required or are under-utilized.

The ApoE e4 protein may transport cholesterol to produce lipid rafts which are not as efficient as those produced by ApoE e2/e3 transport, thus allowing accumulation of beta-amyloid, which has longer-term deleterious effects. This concept puts the ApoE allele at the center of the function of neuroplasticity, which is the core function attacked by the Alzheimer process. The role of ApoE would thus be J.W. Ashford / ApoE4: Is it the absence of good or the presence of bad? 143 seen as crucial for learning, but the ApoE ε2/ε3 alleles would clearly represent an advance over the ApoE ε4 allele, since they are less associated with Alzheimer’s disease, and might even be associated with greater levels of education.

The association between ApoE and cholesterol has become more central recently due to epidemiological findings, now widely confirmed [2,3], that the cholesterol reducing “statin” drugs are associated with a decreased incidence of Alzheimer’s disease. Specifically, the statin drugs appear to reduce plasma concentrations of ain derived 24S-hydroxycholesterol, indicating that the drugs actually reduce cholesterol turnover in the ain [1]. This data seem to indicate that the role of ApoE in cholesterol modulation could be a critical and modifiable modality for the prevention of Alzheimer’s disease. Given the considerations about ApoE, evolution, and diet, the concern about diet, particularly the role of cholesterol, needs to be clarified. One perspective is that the appearance of the ApoE ε2/ε3 alleles occurred as an “anti-dote” to diets rich in cholesterol that were associated with the eating of animal parts and products. However, an alternative view is that these alleles allowed early humans to live longer lives with less risk of heart disease and neurodegeneration, and this greater success allowed humans to include animal resources in their diet. At this time, there is not sufficient information to recommend a specific diet to prevent Alzheimer’s disease. However, there is some data suggesting that reduction of animal fat in the diet is associated with less Alzheimer’s disease (for discussion, see Debate 3, this volume). Consequently, a prudent recommendation for the present is to follow the generally recommended guidelines to keep the amount of cholesterol in your diet low. However, in the future, more studies are needed to define the optimal diet for preventing Alzheimer’s disease (see www.medafile.com, Top 10 Prevention Suggestions), and this recommendation might also be made with respect to the specific ApoE genotype of the individual. In sum, the Rebeck team makes strong arguments for several beneficial roles of ApoE, and such positive activities would be expected from the evolutionary perspective that a protein that is widely conserved across many species should have predominantly advantageous effects. The ApoE e4 protein does seem to have a major association with Alzheimer’s disease, and the points of the Teter et al., team are well taken. However, the Teter et al. team does not produce a large picture of ApoE e4 serving the role of harmful protein. The issue in life is to combat the stresses associated with time, and it appears after this debate that the ApoE e2/e3 is a good protein that is helping humans to age with less cognitive dysfunction than has the now less common ApoE e4, which was the only allele possessed by our ancestors.

References

[1] S. Locatelli, D. Lutjohann, H.H.-J. Schmidt, C. Otto, U. Beisiegel and K. von Bergmann, Reduction of plasma 24Shydroxycholesterol (cereosterol) levels using high-dosage simvastatin in patients with hypercholesterolemia: Evidence that simvastatin affects cholesterol metabolism in the human ain, Arch Neurol 59 (2002), 213–221.

[2] K. Rockwood, S. Kirkland, D.B. Hogan, C. MacKnight, H. Merry, R. Verreault, C. Wolfson and I. McDowe, Use of lipidlowering agents, indication bias, and the risk of dementia in community-dwelling elderly people, Arch Neurol 59 (2002), 223–227.

[3] K. Yaffe, E. Barrett-Connor, F. Lin and D. Grady, Serum lipoprotein levels, statin use, and cognitive function in older women, Arch Neurol 59 (2002), 378–384.

1. Take your blood pressure regularly; be sure that the systolic pressure is always less than 130.

2. Watch your cholesterol; if your cholesterol is elevated (above 200), talk to your clinician about appropriate treatment. Consider “statin” medications and be sure your cholesterol is fully controlled. Increase your dietary intake of omega-3-fatty acids (eat deep-sea finned fish at least 3 times per week) and nuts (especially almonds).

3. Exercise your body, mind, and spirit regularly. Physical exercise best 10-30 mins after each meal for 10-30 minutes, 3 times per day. Do aerobic and strengthening exercises. Maximize your education. If you have spare time, do mental puzzles (like crossword puzzles). Stay active with your friends and in your community.

4. Physically protect your brain. Wear your car seat-belt. Wear a helmet when you are riding a bicycle or participating in any activity where you might hit your head. Work to decrease your fall risk through physical exercise, making your environment safe.

5. Keep your BMI (Body Mass Index) in the optimal range (19-25):
——– BMI = 703 * weight (pounds) / height (inches) squared ——–
*To optimize your BMI, control your food intake and exercise. Decrease your risk of type II diabetes. Monitor your fasting blood sugar yearly. If you have diabetes, make sure that your blood sugar is optimally controlled.

6. Consult your clinician about your joint and muscle pains (treat arthritis with ibuprofen, sulindac, or indomethacin).

7. Take your vitamins daily (folate – 400mcg, B12 – 25mcg, C – 250 mg, and E – 200iu’s). Check with your clinician yearly to be sure your homocysteine levels are not high and you have no signs of or risk factors for B12 deficiency (ask your doctor to make sure your B12 level is above 400. If diet doesn’t help, take oral supplement. If oral supplement doesn’t work, get monthly B12 shots additionally. Maximize your vegetables.

8. Keep your hormones stable. Check with you clinician about your thyroid hormone. Discuss sex-hormone replacement therapy with your clinician (such therapy is not currently recommended for Alzheimer prevention, but may help memory and mood).

9. If you have difficulty getting to sleep, consider trying 3 – 6 milligrams of melatonin at bedtime. If you snore, consult your clinician about sleep apnea.

10. Monitor your memory regularly; have your memory screened yearly. Be sure the people around you are not concerned about your memory. If you think that you have significant difficulty with your memory, talk to your clinician about further evaluation. Consider therapy with cholinesterase inhibitors and memantine.

SCREENING RECOMMENDATIONS

See your clinician at ages 30, 40, 50, 55, 60, and 65. Get a check on blood pressure, cholesterol, fasting blood sugar, B12, and your BMI. Review your health habits, diet, sleep, and family history of diseases including dementia.

Beginning at age 65, see your clinician annually and have each of these areas checked.

VITAMIN SUPPLEMENT RECOMMENDATIONNS
for discussion, see: Willet WC, Stampfer MJ, What vitamins should I be taking, Doctor, NEJM, 345, 1819 (2001)

Take at the morning meals:
Vitamin E 200 iu’s
Vitamin C 250 mg
Multi-vitamin (with folate 400 mcg and no iron)
Keep your B12 level above 400.

If approved by your clinician: 1 enteric coated baby aspirin each day.

DIETARY RECOMMENDATIONS

OPTIMIZE:
Fruits – citrus, blue berries
Vegetables – green, leafy
Fish – deep sea, finned, oily, at least 3x/week
Nuts – especially almonds, chocolate

MINIMIZE:
Animal products – Red meat (more than once per week), Dairy.

At age 55–60 years: follow-up assessments
Review of systems, vital signs
Brief cognitive evaluation using longitudinal measures!!
CBC, B12, cholesterol

At age 65 years and older: begin annual assessments
Review of systems, vital signs
Brief cognitive evaluation watching longitudinal changes
CBC, B12, cholesterol

Take the screening test just CLICK HERE

Theoretical Study
Dr. Michael Addicott
Cognitive Labs

http://cognitivelabs.com

It has been speculated that dedicated gamers may have faster reaction times than ordinary average individuals, a hypothesis which has been supported by research in 2010. We conducted a study in 2005 to identify this research question and assist in the formulation of the hypothesis. In order to attract a suitable research study group, a LAN party was used as the venue. Twenty two gamers aged between 22 and 35 were conducted to a secure facility and immediately entered into competition using Halo2 as a stimulus. After appoximately 90 minutes of competition, the play was suspended and the player rankings were logged. At the same workstations, user experience was immediately toggled over to the Cognitive Labs working memory and recall games featuring speed of processing measures. The top quartile scored at or above the 99.9th percentile compared to ‘norms’ for all users. The second quartile scored above the 97th percentile, The third above 95th and the fourth above 93. Data from four
respondents who became distracted was not included. The results suggest that gamers are indeed faster. Other studies imply an age-adjusted differential of up to 100 milliseconds in response time. The data shows that intense workouts can improve cognitive speed at any age, which is a measure that links very closely to life expectancy in several independent studies, notably those of Ian Drury which examine IQ, reaction time, and life expectancy. The conclusion includes the finding that there is a substantive link between cognitive speed and and life expectancy, with the unknown variable being causality. Although the practice effect may account for some improvement up through a certain number of sessions (seven, for example) maintaining and enhancing cognitive speed and creating cognitive reserve appear to protect against the early onset of cognitive decline along with other diet and exercise approaches.

THE TOP TEN RECOMMENDATIONS A DEVELOPING PLAN TO PREVENT DEMENTIA AND ALZHEIMER’S DISEASE J. Wesson Ashford, M.D., Ph.D. Stanford / VA Aging Clinical Research Center 2/23/08

1. Maximize and continue your education and mental exercise:
   • Learn about your brain and how to care for it.
   • Develop habits to maintain your brain.
   • Take classes in subjects that interest you; education is associated with decreased Alzheimer’s risk, learning a new language may be very good.
   • Do mentally stimulating activities, including puzzles (like crossword puzzles, sudoku, but also learn new things).
2. Maximize and continue your physical exercise:
   • Have a regular exercise program.
   • Physical exercise is best 10-30 minutes after each meal for 10-30 minutes, 3 times per day.
   • Do both aerobic and strengthening exercises.
   • Stretching improves flexibility.
3. Maximize your social network and spiritual interactions:
   • Stay active with your friends and in your community.
4. Continually monitor and improve your diet:
   • Take your vitamins daily.
   • Take at the morning meals: Vitamin E 200 iu; Vitamin C 250 mg; Multi-vitamin (with folate 400 mcg and no iron). For discussion, see: Willet WC, Stampfer MJ, “What vitamins should I be taking, Doctor?” New England Journal of Medicine, 345, 1819 (2001)
   • Check with your clinician yearly to be sure your homocysteine levels are not high and you have no signs of or risk factors for B12 deficiency.
   • Ask your doctor to make sure your B12 level is above 400. If diet doesn’t help, take oral supplement. If oral supplement doesn’t work, get monthly B12 shots additionally.
   • Maximize your vegetables.
   • Increase your dietary intake of omega-3-fatty acids.
   • OPTIMIZE Plant products and fish: Fruits – citrus, blue berries; Vegetables – green, leafy; Fish – deep sea, finned, oily, at least 3x/week; Nuts – especially almonds, and also dark chocolate
   • MINIMIZE other animal products: Red meat (no more than once per week); Dairy (limit to low-fat); Poultry (limit eggs to 7 or fewer per week)
5. Keep your Body Mass Index (BMI) in the optimal range (19-25):
   • To optimize your BMI, control your food intake and exercise.
6. Physically protect your brain:
   • Wear your car seat belt.
   • Wear a helmet when you are riding a bicycle or participating in any activity where you might hit your head.
   • Decrease your fall risk through physical exercise; improve your balance.
   • Make your environment safe.
7. Visit your clinician on a regular basis. Know your body and your health risks:
   • Decrease your risk of type II diabetes. Monitor your fasting blood sugar yearly. If you have diabetes, make sure that your blood sugar is optimally controlled.
   • Consult your clinician about your joint and muscle pains (treat arthritis with ibuprofen or indomethacin).
   • Keep your hormones stable. Check with your clinician about your thyroid hormone. Discuss sex-hormone replacement therapy with your clinician (such therapy is not currently recommended for Alzheimer prevention, but may help memory and mood).
8. Optimize your cardiovascular health:
   • Take your blood pressure regularly; be sure that the systolic pressure is always less than 130, diastolic blood pressure is less than 85.
   • Watch your cholesterol; if your cholesterol is elevated (above 200), talk to your clinician about appropriate treatment. Consider “statin” medications and be sure your cholesterol is fully controlled.
   • If approved by your clinician: 1 enteric coated baby aspirin each day.
9. Optimize your mental health:
   • If you have difficulty getting to sleep, consider trying 3 – 6 milligrams of melatonin at bedtime (consider different brands if not helpful at first).
   • If you snore, consult your clinician about sleep apnea.
   • Get treatment for depression if needed.
   • Keep your stress level under control. Severe stress is bad for health; some stress is needed to maintain motivation.
   • Avoid excess alcohol use.
10. Optimize your cognitive health:
    • Monitor your memory regularly.
    • Have your memory screened yearly after 60 year of age.
    • Be sure the people around you are not concerned about your memory.
    • If you think that you have significant difficulty with your memory, talk to your clinician about further evaluation and therapy.
    • Attend book clubs, local museums and/or art show

HealthDay (6/30) reported that, according to a study published June 30 in Neurology, “the combination of a memory test and a brain scan may best predict the likelihood that an individual with mild cognitive” impairment (MCI) “will go on to develop Alzheimer’s disease.”

“Researchers from the University of California-Berkeley found that word-recollection memory testing combined with PET scans of the brain was best able to predict who would develop Alzheimer’s disease,” WebMD (6/30, Boyles) reported. “Study participants whose PET scans and memory tests were abnormal were nearly 12 times more likely to develop Alzheimer’s disease than people whose scores on both tests were normal.” The study population consisted of “85 mostly elderly people with mild cognitive impairment, a medical term used to describe a state of memory loss or other cognitive decline that is greater than would be expected with normal aging but has not yet progressed to dementia.”

Alzheimer’s Research Has Reached Point Of Significant Potential, Experts Say. HealthDay (6/30, Thompson) reported, “Research into Alzheimer’s disease has reached a point of significant potential.” Scientists “are identifying substances that bind with amyloid deposits and make them visible to imaging scans,” as well as “identifying genetic and biological markers that could indicate…increased risk for developing Alzheimer’s.” But, some experts “question the direction of research — worrying that efforts have been too tightly focused on eliminating amyloid from the brain.” Some also question the lack of funding for Alzheimer’s studies. For example, “The US National Institutes of Health expects to spend $527 million on Alzheimer’s disease research in the current fiscal year, compared with $6.1 billion on cancer research, $3 billion on HIV/AIDS, and $1.9 billion on heart disease research, according to spending data released Feb. 1.”