What Is Alzheimer’s Disease? A Brief Overview

In General Information by Matthew Bell

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>.