Author: Matthew Bell

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Alzheimer’s-Proof Your Diet: Vitamin D and Other Nutrients

Alzheimer’s-Proof Your Diet: Vitamin D and Other Nutrients

The prospect that I might end up like my dad frankly terrifies me. I watched helplessly as he slowly lost his faculties – both mental and physical. It’s no exaggeration to say that Alzheimer’s Disease appeared to strip him of his humanity. If I thought that making changes to what I eat would – or even could – result in improved odds for avoiding dementia in my old age, then I would happily alter my diet.

In fact, some recent scientific research provides an indication – not to say a hope – that such dietary changes might be possible. Amazingly, such modifications are arguably easily implemented.

Vitamin D

Vitamin D is among the candidate nutrients that figure prominently in such a nutritional-reform project. To be a bit technical, the term “vitamin D” actually refers to a group of compounds rather than one single thing.[1] It also turns out that the stuff we call vitamin D is perhaps better described as a hormone that helps to maintain healthy cells as opposed to a “vitamin” in a traditional sense.

However scientists classify it, though, vitamin D interests me because of what it might be able to do for me. In this vein, there is an impressive list of things that vitamin D is believed to help.

According to Medical News Today[2] vitamin D plays an important supporting role in promoting:

  • favorable blood pressure readings
  • balanced blood sugar
  • strong bones
  • optimal brain and nervous-system operation
  • healthy breast tissue
  • excellent calcium absorption (among other metabolic processes)
  • robust immunity
  • vigorous lung and cardiovascular function
  • overall longevity
  • uncomplicated pregnancies and deliveries
  • normal vision and macular health

To this already extensive and impressive list, let me not forget (no pun!) to add vitamin D’s alleged capability of staving off dementia.

An article from the highly esteemed Mayo Clinic started my journey into finding more research on this possibility. The pertinent article concerned a study from 2014, which showed that people with vitamin-D deficiency were twice as likely to develop dementia in general, and Alzheimer’s in particular.

Predictably, the clinic’s doctors took a cautious stance. They said, circumspectly, that more research was needed before anything conclusive could be declared. For my part, I am not as interested in making causal claims – even true ones – as I am in stacking the deck in my favor, health-wise.

Since discovering the Mayo Clinic post, I have unearthed several other pieces of information outlining correlations between vitamin D and dementia. Sayer Ji’s website, GreenMedInfo, has been an outstanding resource in my investigations.

I have learned that one study, published in 2012 in the scientific journal Neurology, compared scores on a state exam and concluded that low cognitive abilities corresponded with low vitamin D levels. That same year, a study followed almost 500 women for seven years. Experimenters obtained similar findings. Women who were determined to be vitamin-D deficient as the program began, were adjudged more likely to develop Alzheimer’s.  A third study from 2012 professedly demonstrated that vitamin D helped to clear the sort of “amyloid plaques” that form in the brains of dementia patients.

Is vitamin D a panacea? When it comes to giving the proverbial “definitive answer,” we should probably agree with the Mayo Clinic’s physicians: more research is needed.

However, when it comes to deciding how to structure my diet, I cannot see much reason to neglect supplementing with vitamin D.

If you too are persuaded that vitamin D might be helpful for you or someone that you love, here are some ways to incorporate it into your life.

How to Get More Vitamin D

The most direct way of obtaining vitamin D is through exposure to sunlight. So, take a walk outside.

I hear you exclaiming: “But I heard that (excessive) sunlight was bad for you!”

First of all, bear in mind that there are 2 types of rays that penetrate the earth’s atmosphere: UVA and UVB. UVA is indisputably a harmful one. UVB, on the other hand, is our natural vitamin-D3 source. UVB rays are readily available during certain times of the year in different locations. Purportedly, the sun needs to be at 50 degrees at or above the horizon. It seems like the winter sun would not be as beneficial as the sun in spring through fall – not that you need a reason beside presumably frigid temperatures to stay inside.

For most of human history we worked and virtually lived our lives outside. You might say that we were, well …made to be in nature. So I am planning on spending lots of time outdoors.[3]

But for those who balk at the idea of getting more “rays,” or for those who are (for whatever reason) otherwise unable to do so, it should be said that vitamin D is also found in numerous foods. It’s available in caviar, egg yolks, fish (of various sorts, including mackerel, salmon, sardines, and tuna[4]), and milk (raw).

Still, even if you’re getting moderate sun exposure and eating fish, you might find it desirable to augment your diet with commercially available vitamin-D supplements.

From what I have read, you want to look for the word cholecaliferol on the label. This form of vitamin D – known as vitamin D3 – appears to be the “best” in terms of things like efficacy, potency, and absorption.[5]

My chosen brand in the past was NOW, which makes a whole assortment of vitamin D3 capsules.[6] One that I have purchased repeatedly is NOW’s 5,000IU offering. Recently, due to the slightly lower price, I have switched to Doctor’s Best, also in a 5,000IU amount.

How Much Should You Take?

I need to emphasize that I am neither a doctor nor a nutritionist. Presumably, the most accurate way to arrive at a dosage amount would be to have your levels of vitamin D tested, and then (on the assumption that you are not already where you need to be) to have a customized recommendation as to how to move that measured level into its ideal range. Obviously, I cannot administer such a test on anybody and I cannot make any sort of customized recommendation.

I can, however, report my research findings and disclose my own practices (which you may take or leave).

Let me begin with the former. Alternative medical “guru” Dr. Andrew Weil suggests that supplementing with 2,000 IU each day ought to suffice as a good supplementary starting point for most people.

For me, personally, 5,000 IU is my go-to amount during the winter months, when sunlight is on the decline and time outdoors is hard to come by. I am by no means a nutritionist, but I take 1 capsule daily as a maintenance dose. To put it another way, I take one 5,000 IU capsule every day in order to keep my vitamin D3 levels up. If I feel myself falling ill (for example, with a respiratory illness), I may double up the dosage or take a single dose more than once.

I do also keep other amounts of vitamin D3 on hand. Right now, I have 1,000IU and 400IU products from Finest Nutrition and Origin. My idea is to augment, when necessary, my vitamin D3 levels during times (perhaps during the summer), when I might feel under-the-weather or be otherwise stuck inside and unable to get my daily sun exposure.

Some sources indicate that vitamin D3 should be taken alongside vitamin K, in order to aid absorption. I have been a bit lax in terms of following this advice. But now that I am reminded of it, maybe it’s time to make a change.

Other Nutrients

Looking into supplements reported to help in preventing Alzheimer’s, you quickly find out that vitamin D is not the only substance to consider. Four other figure conspicuously in the pertinent literature.

Folic Acid is a water-soluble vitamin also known as Folate or B9. Folate occurs naturally in vegetables like asparagus, avocados, beans (dried), beets, broccoli, lentils, peas, and spinach. It also turns up in fruits – chiefly bananas – as well as in liver. Technically, folic acid is the synthetic form of folate, and it is contained in many fortified foods and available separately as a supplement.

Folic acid and folate aids in:

  • maintaining brain and nerve function
  • generating red blood cells
  • and generally helping your cells to reproduce and combine DNA appropriately

(This latter responsibility of the cells, if done incorrectly, could contribute to the growth of cancers because it can lead to damaged or mutated DNA.)

Vitamin B12 is also a water-soluble vitamin. Called Cobalamin, B12 is found in beef liver, sardines, Atlantic Mackerel, lamb, wild-caught salmon, nutritional yeast, feta cheese, grass-fed beef, cottage cheese and eggs.

Available in chewable tablets, regular tablets, and liquid, is important in:

  • making red blood cells
  • maintaining brain and nerve function
  • supporting energy levels
  • protecting the cardiovascular system
  • improving bone density and strength

A deficiency in B12 could block folate so that it can’t change into its active form. If folate can’t change into the active form, it can’t do the job of aiding the cell during DNA reproduction. This, in turn, can lead to DNA corruption.

Magnesium is a mineral that is found in spinach, chard, yogurt, almonds, cashews, pumpkin and sunflower seeds, avocados, bananas, black beans and dark chocolate.

Magnesium (in aspartate, carbonate, citrate, glycinate, L-threonate, orotate, oxide, malate, and taurate forms[7]) supports:

  • calcium and potassium absorption[8]
  • nerve and neurotransmitter function
  • blood-sugar control
  • blood-pressure regulation
  • maintenance of energy levels

Fish oil comes, funnily enough, from “oily” fish – such as wild-caught salmon, herring, tuna and sardines. Fish oil is a wonderful source of omega-3 fatty acids.

Studies have shown that fish oil, and omega-3 fats, yields positive benefits in these areas:

  • Alzheimer’s Disease
  • anxiety
  • arthritis
  • cancer
  • cardiovascular disease
  • diabetes
  • eye disorders
  • immune function

Additional Supplements to Consider

Although the jury is still out, the following might also be worth your time and attention:

Vitamin E is a fat-soluble vitamin found in almonds, asparagus, broccoli, butternut squash, chard, olive and palm oils, spinach, sunflower seeds, sweet potatoes, trout, and wheat germ. It is an antioxidant that prevents damage to specific and important fats in your body.

Vitamin E benefits us in virtue of its abilities to:

  • Assist our bodies’ regulation of cholesterol
  • Support the repair of skin damage
  • Promote balanced hormone levels and healthy muscles
  • Improve vision (at least, in conjunction with vitamin C, beta carotene and zinc)
  • Protect against heart disease
  • And, crucially for the present discussion, slow the progression of Alzheimer’s Disease

Ginkgo (ginkgo biloba[9]) is considered an herb. The stuff comes from an ancient tree whose benefits have been known in Chinese medicine for thousands of years. It may be consumed as a tea (for example, as a hot infusion) or in capsule form. In general, ginkgo has become quite well known among herbalists as an anti-inflammatory as well as a brain-function and nervous-system enhancer. Given this folk reputation, it is not difficult to see why it may be beneficial to dementia sufferers – and to those who wish to avoid that description.

Alleged benefits of gingko include:

  • Conservation of visual acuity (possibly along with beta carotene, eyebright, and lutein)
  • Improved cognitive function (especially increased memory capacity and heightened concentration)
  • Maintenance of energy levels
  • Promotion of positive mood (perhaps similarly to St. John’s Wort and “SAMe,” S-Adenosyl methionine)
  • And reduction of dementia risk

Turmeric is a powerhouse herbal whose potency – over a wide range of conditions – has been suggested to be superior to pharmaceutical-based medicine.[10] Turmeric shows up on too many lists to adequately summarize here. Suffice it to say that turmeric boasts benefits as a(n):

  • Anticoagulant
  • antidepressant
  • anti-inflammatory
  • cancer treatment
  • cholesterol regulator
  • pain reducer (particularly for arthritis)

It is also taken in supplement form. Black pepper (bioperine) should be added to assist the bioavailability of the curcumin – one of turmeric’s principal active ingredients. There are two option. One option is to get a turmeric-pepper combination product. The other is to acquire bioperine individually.

CoQ10 is an element that is naturally produced in our bodies. As we age, that production decreases. Fortunately, Coenzyme Q10 is found in many foods like grass-fed beef, cage-free eggs, free-range chickens, strawberries, herring, broccoli, cauliflower, beans, nuts, oranges and rainbow trout.

Many positive benefits are touted for CoQ10. It:

  • boosts energy levels
  • promotes healthy cardiovascular systems and lungs
  • reduces muscle diseases
  • stabilizes blood sugar
  • and, of course, may help cognitive disorders like Alzheimer’s

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Notes:

[1] Specifically, they are fat-soluble steroids.

[2] See, for example, here.

[3] There is some evidence that vitamin D production can be stimulated through light exposure to tanning lamps. For more information on that, in my view, back-up option, see here. Besides being pricey (see Sperti’s “Fiji Sun” model), artificial light just pales (okay, maybe that is a little pun) in comparison to the real McCoy.

[4] Of course, you should keep in mind the adage “all things in moderation.” Tuna, amongst other fish types, may contain disadvantageous things like mercury.

[5] Food that is labeled “fortified with vitamin D” often contains D2 (ergocalciferol), a form of D which your body cannot absorb as well as D3. This may be due, on part to the source of each form. Vitamin D2 is plant-based, while D3 is animal-based (fish usually). In any event, the superiority of D3 over D2 has led to some writers referring to D3 as the “real” form of vitamin D. I won’t take a position on that, here. I simply want readers to be aware of the terminology.

[6] Though, I have begun to consider giving preference to products with bases of pure safflower oil instead of soybean or coin oil. This is due to GMO worries – another can of worms entirely. Readers who share this concern might take a look at Bluebonnet, Nature’s Plus, and other companies that manufacture such safflower-based products.

[7] Oxide and carbonate are generally inexpensive, but are also (supposedly) poorly absorbed. I have been supplementing with citrate and malate forms – alternating in order to increase the bioavailability of each form. I have read good things about aspartate, orotate, and taurate in terms of heart health. However, for Alzheimer’s support – and possible prevention – my money is presently on glycinate, L-threonate, and malate, due to their association with cellular-energy and cognitive support.

[8] In fact, most magnesium is found in the bones.

[9] Note that “ginkgo” is alternately rendered “gingko.” While I disfavor this spelling for some perhaps veiled psychological reason, it does comport more closely with the way that I pronounce the word.

[10] Herbalists and naturopaths sometimes disparagingly refer to this sort of medicine as “allopathy.”

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What Is Alzheimer’s Disease? A Brief Overview

Alzheimer’s Disease: A Brief Overview

“Alzheimer’s Disease” and “dementia” are specific and general terms for loss of memory and degradation of cognitive skills that is serious enough to interrupt the sufferer’s everyday life. Alzheimer’s is a kind of dementia, ostensibly caused by degeneration of the brain, that is primarily characterized by sever memory deficits. These difficulties issue in marked and negative changes in intelligence and behavior.

Inevitable aging is among the many risk factors, as most people with Alzheimer’s are 65 and older. But, unfortunately, Alzheimer’s is not just a disease of old age. Purportedly, a 27-year-old has, heretofore, been the youngest person with a confirmed case of the disease.

Alzheimer’s is a progressive disease in which symptoms worsen over time. In initial phases, memory loss may be barely noticeable, but in later phases Alzheimer’s patients are unable to carry on their usual routines. Patients are rendered unable to interact with their environments – both physical and social.

Alzheimer’s presently has no cure, but various medications may be administered to help manage a sufferer’s care, as well as to alleviate his or her symptoms and potentially slow the rates of mental and physical decline. Researchers continue to investigate its root cause.

Alzheimer’s Devolution

Classically, the first indication of Alzheimer’s occurs when a person struggles to recall freshly learned information. This is because the disease usually begins with the destruction of brain cells that are concerned with preserving and retaining new information. 

Of course, Alzheimer’s patients display marked decline in brain function over a broad range. This decline is correlated with loss of neurons (and neuronal connections) seemingly beginning in the cerebral cortex. Areas chiefly affected include the hippocampus, as well as the frontal, parietal, and temporal lobes.[1] As the condition worsens, other brain structures, including the cerebellum, are implicated.

The Alzheimer’s patient experiences confusion, and this manifests in (increasingly pronounced) shifts in attitude and conduct. Afflicted individuals may misperceive events and lose the ability to track changes in places and times – things that normally functioning people take for granted. Daily activities become Herculean tasks, and interpersonal communication becomes muddled. Language ability dwindles to nothing. Some sufferers become dangers to themselves and to others and require around-the-clock care.

Tragically, as the memory losses escalate, the individual may become unfamiliar with even family members and close friends.

What Is the Cause? 

The ultimate cause is unknown. There is much speculation that Alzheimer’s may be the result of particular deficiencies (e.g., vitamin D). There is also some evidence that Alzheimer’s impacts the body on a cellular level. 

Although the research is still in early stages and conclusions are far from entirely clear, as brain destruction extends, brain cells actually appear to die. This triggers unalterable modifications in the brain.

Two unusual structures – termed “plaques” and “tangles” – are principal suspect culprits in this nerve-cell destruction. At this time, investigators have not yet discovered the exact role of these plaques and tangles in Alzheimer’s Disease. However, autopsy results from affected persons suggest that these structures are old-age related. In Alzheimer’s patients, the growth of these structures is often fast and inexplicable. Said growth usually begins in portions of the brain that are directly responsible for memory storage, before it spreads to other regions.

From what I have been able to ascertain, these plaques and tangles are responsible for blocking communication between nerve cells. Furthermore, they disrupt processes that are vital for the cellular survival. The memory failures and behavioral transformations are precursors to devastating physical incapacities like problems walking and, eventually, chewing and swallowing. Plausibly, these things are due to loss or death of nerve cells.

One prominent hypothesis has it that about Alzheimer’s says that the neural plaques tangles are due to the accretion of certain proteins (amyloid beta and tau). The hope is that if a way could be found to stop the protein accumulation, then the disease could be halted. 

Another hypothesis blames the reduction of the bioavailability of the neurotransmitter acetylcholine.

For my article on how Alzheimer’s Disease may be detected, see “How to Detect Alzheimer’s: 10 Tests of Varying Accuracy”

What About Genetics?

A major consideration in Alzheimer’s detection and research is the so-called Apolipoprotein E. This gene, referred to as APOE for short, is believed by numerous geneticists to be a prime indicator for a genetic risk Alzheimer’s dementia. The folks at MedicineNet expand, writing that: “People with one copy of the e4 allele have an increased risk of developing type 2 Alzheimer disease, a familial late-onset form of the disease. People who inherit two copies of the e4 allele have a still higher chance of developing type 2 Alzheimer disease. However, the relationship between APOE e4 and Alzheimer disease is not a simple direct one. APOE e4 is clearly neither necessary nor sufficient by itself to cause Alzheimer disease.”[2] This means that there are cases of Alzheimer’s in which the afflicted person does not have the APOE gene; and there are instances where a person has the APOE gene but does not manifest Alzheimer’s. (For information on genetic testing for Alzheimer’s, see HERE.)

What Are Some Alzheimer’s Statistics?

Alzheimer’s, the most common sort of dementia, is currently the number six cause of death in the United States. It kills more than breast cancer and prostate cancer combined. Over 5 million people are believed to be living with Alzheimer’s Disease in the United States right now. Some estimates have this number rise as high as 16 million by the year 2050. Almost every sixty-six seconds, someone in the US develops this fatal disease. 18.2 billion hours of care, valued almost over $230 billion, was delivered by Alzheimer’s and memory specialists in 2016.

What Is the Prognosis for Alzheimer’s?

There is presently no “cure” for Alzheimer’s and no way to reverse the neuronal damage that it causes. Survival after diagnosis can range from four to twenty years (depending partially upon the stage in which it is detected), but generally a sufferer lives an average of eight years once his or her symptoms become obvious. (Admittedly, this is difficult to quantify precisely. Some people’s conditions may go unnoticed for longer than others.)

What Is the Treatment for Alzheimer’s?

Compounds like cholinesterase and pharmaceuticals like Namenda (Mementine) are available which are believed (or hoped) to inhibit the breakdown of chemicals that are crucial for memory and thought. As mentioned previously, these drugs are administered to reduce symptoms and slow the progression of the Disease. For some people, this may be enough to allow them to continue certain daily tasks a little longer than they would without the medication.

Some drugs are also available that aim to dissolve the various “plaques” and “tangles” (as described previously) that form in the brains of Alzheimer’s patients.

Other than pharmacological interventions, various lifestyle measures might provide some damage control. One recommendation is to try to maintain normal, healthy lines of communication with one’s family and social circles. Preferably before, but certainly after disease diagnosis, it’s important to engage aging loved ones in activities and hobbies that gave them pleasure in their past. Provide a positive and friendly atmosphere in which Alzheimer’s patients may feel more involved with life and in control. Encouraging activities for Alzheimer’s patients help them engage with others emotionally. It also stimulates creativity and expressivity, as well as possibly minimizing the nervousness and irritation that Alzheimer’s sufferers may experience due to changes about which they feel powerless.

For more on these topics, see:

What Are the Stages of Alzheimer’s?

Depending upon the system that one is referencing, Alzheimer’s may be thought of as having two, three, or seven “stages.” There are no hard and fast rules for selecting a system, and the choice is largely one of expedience and utility. In two-stage lingo, we could describe Alzheimer’s sufferers and going from a pre-symptomatic first stage to a symptomatic second stage.

A simple three-stage schema can be generated by putting a “prodromal” intermediate stage between the pre-symptomatic and symptomatic stages. An alternative model assigns the adjectives early, middle, and late to each of three, loosely reckoned, stages. The actual transition between stages is difficult to track.

It’s a bit like the so-called “sorites paradoxes” that are well-known in philosophical circles. These puzzling cases, also called “little-by-little” paradoxes, can be illustrated by considering properties such as baldness. How many hairs does a person have to lose in order to count as “bald”? It is hard to say. We are far more comfortable with obvious cases. Obviously, Fabio is not bald and Patrick Stewart is. But just how one transitions between the two is tough to quantify. Similarly, just how much cognitive or memory loss qualifies a person as being in “late stage” Alzheimer’s as opposed to the “early” or “middle” stages? The question is difficult to answer. At some point, the patient just gets demonstrably and obviously worse.

Finally, Dr. Barry Reisberg, of New York University Medical School’s Alzheimer’s Disease Center for Cognitive Neurology, carved out a sevenfold taxonomy. On this picture, the stages are as follows: “Normal,” “Normal Aged Forgetfulness” (similar to V. A. Kral’s idea of “benign senescence”), “Mild Cognitive Impairment,” “Mild Alzheimer’s Disease,” “Moderate Alzheimer’s Disease,” “Moderately Severe Alzheimer’s Disease,” and “Severe Alzheimer’s Disease.”

Within this framework, everybody is assigned some “stage” on the Alzheimer’s spectrum. For most people with healthy cognitive function, presumably, this will be “Normal.” Even a baby will be at “stage 1” on Reisberg’s Alzheimer’s continuum. This may strike some people as an odd way of speaking. Indeed, one might intelligently press the point that, by his own admission, Reisberg’s stages don’t touch on actual Alzheimer’s Disease until stage 4. However, it may not be an argument worth having.

There is conflicting information online concerning the question of whether Alzheimer’s has three (3) or seven (7) stages. For my discussion of this question (and other, related questions), see: “Does Alzheimer’s Disease have Three Stages or Seven Stages?”

What Do the Terms Come From?

The word “dementia” hearkens back to two Latin words: the noun mens, meaning “mind” and the (ablative) preposition de, meaning “away from,” “down from,” or “out of.” Hence, de–mens denotes being out of your mind. In the nineteenth century, being “demented” carried the significance of being insane or “mad.” (For more, see HERE.) Likewise, “senility” stems from the “…Latin senilis[,] ‘of old age,’ …” Senile, in the sense of “weak or infirm from age” goes back to the mid-1800s.

“Alzheimer’s Disease” is of more recent vintage. It is a close cousin of two terms that predated it: dementia præcox and senium præcox. “Alzheimer’s” is actually an eponym. It derives from the 19th-20th-century German psychiatrist Aloysius “Alois” Alzheimer. The Online Etymology Dictionary reports: “The disease name was not common before 1970s; shortened form Alzheimer’s first recorded 1954.” (The same website adds that the “surname is from the place name Alzheim, literally ‘Old Hamlet.'” This is an interesting since the proper name “Hamlet” is associated with the Shakespearean drama in which a Danish prince feigns madness in order to investigate and avenge his father’s murder.)

[1] One school of thought has it that each brain area is believed to govern a particular brain function. For example, the frontal lobe is reputed to play a leading role in decision-making; the temporal lobe supposedly helps forms new memories; the parietal lobe deals with processing language and sensory information; and so on. Others maintain that the entire brain is involved in higher-level cognitive functions. I don’t know!
[2] N.n., “Medical Definition of Apolipoprotein E,” MedicineNet, reviewed Dec. 11, 2018, <https://www.medicinenet.com/script/main/art.asp?articlekey=13299>.

Further Resources

For more information, also see these printed or audio-video resources:

  • Linda Altman, Alzheimer’s Disease, San Diego, Calif.: Lucent Books, 2001.
  • Joseph Boudreaux and Randal Scott, Alzheimer’s Disease: Pieces of the Puzzle, DVD, re-released by Gayle Sumida and Kevin Siegert, Univ. of Arizona, Health Sciences Center, Tucson, Ariz.: Biomedical Communications, 2000.
  • Michael Davidson, ed., “Alzheimer’s Disease,” Psychiatric Clinics of North America, vol. 14, no. 2, 1991, pp. 461-482.
  • Phyllis Braudy Harris, The Person With Alzheimer’s Disease: Pathways to Understanding the Experience, Baltimore, Md.: Johns Hopkins Univ. Press, 2002.
  • John Hodges, Early-Onset Dementia: A Multidisciplinary Approach, Oxford: Oxford Univ. Press, 2001.
  • Julian Hughes, Alzheimer’s and Other Dementias, Oxford: Oxford Univ. Press, 2011.
  • Margaret Lock, The Alzheimer Conundrum: Entanglements of Dementia and Aging, Princeton: Princeton Univ. Press, 2013.
  • Steven Sabat, Alzheimer’s Disease and Dementia: What Everyone Needs to Know, Oxford: Oxford Univ. Press, 2018.
  • Glenn Smith and Mark Bondi, Mild Cognitive Impairment and Dementia: Definitions, Diagnosis, and Treatment, Oxford: Oxford Univ. Press, 2013.
  • Peter Whitehouse, Konrad Maurer, and Jesse Ballenger, eds. Concepts of Alzheimer Disease: Biological, Clinical, and Cultural Perspectives, Baltimore, Md.: Johns Hopkins Univ. Press, 1999.
  • Wolstenholme and Maeve O’Connor, Alzheimer’s Disease and Related Conditions, London: J. & A. Churchill, 1970.

Partial Bibliography

  1. “Alzheimer’s and dementia,” Alz.org, 2017, <https://www.alz.org/alzheimers_disease_what_is_alzheimers.asp>.
  2. “Alzheimer’s Disease and Related Dementias,” various articles from the National Institute on Aging, 20127, <https://www.nia.nih.gov/health/alzheimers>.
  3. Sabrina Bachai, “Alzheimer’s Kills More People Than Breast And Prostate Cancer Combined, So Why Is It So Underfunded?” Medical Daily, May 13, 2014, <http://www.medicaldaily.com/alzheimers-kills-more-people-breast-and-prostate-cancer-combined-so-why-it-so-underfunded-282090>.
  4. Neil Burgess, Dennis Chan, Laura Marie Gallaher, Kuven Moodley, Ludovico Minati, and Tom Hartley, “The 4 Mountains Test: A Short Test of Spatial Memory with High Sensitivity for the Diagnosis of Pre-dementia Alzheimer’s Disease,” Journal of Visual Experiments, no. 116, 2016, <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5092189/>.
  5. Robert Egge, “Alzheimer’s Caregivers Feel Cost of Care in Multiple Ways,” The Hill, July 13, 2017, <http://thehill.com/blogs/congress-blog/healthcare/341673-alzheimers-caregivers-feel-cost-of-care-in-multiple-ways>.