Running head: ALZHEIMER’S DISEASE 1

Alzheimer’s Disease: A Biological and Neurological Analysis

Victoria Schlie

Physiological Psychology

Dr. Elliot
ALZHEIMER’S DISEASE 2

Alzheimer’s Disease: A Biological and Neurological Analysis

Dementia is a broad category of organic brain deterioration that results in an impairment

of intellectual abilities, especially memory (Carlson & Birkett, 2017, p. 510). This deterioration

can be the result of stroke, blood vessel complications, gene mutation, or Lewy bodies (abnormal

protein clumps in the brain), but the cause of most dementia is unknown (Mayo Clinic, 2017,

“Dementia”). This paper will focus on the effects of, neurological causes for, and biological

treatments for Alzheimer’s Disease, the most common form of dementia. It will also discuss the

disease’s effects and treatment methods through a Christian lens, taking into consideration the

disease’s spiritual and relational impact as well as Christian ethics and stipulations in treatment.

Effects of Alzheimer’s Disease

According to one study done on Alzheimer’s patients in Japan, those with the disease

consistently scored lower in recall and memory than normal individuals (Mori et al., 1999, p.

219). When analyzing the volume of specific brain structures compared to this inability to

remember, researchers found a significant correlation between amygdalar volume and emotional

memory recall (p. 220). Not only is functional memory and recall impacted, but the disease also

impacts centers in the brain tied to emotions and emotional responses. Although emotional

memory deficit is specifically linked to the deterioration of the amygdala, all areas of the brain

experience progressive atrophy during the course of Alzheimer’s (p. 220), inhibiting or distorting

the functions connected to each part of the brain effected. This total brain atrophy produces

numerous impaired functions and an overall shrinkage of the brain.

According to the ​Diagnostic and Statistical Manual of Mental Health Disorders: fifth

edition​ (DSM-5), the diagnostic criteria for Alzheimer’s disease include serious impairment in
ALZHEIMER’S DISEASE 3

learning and memory as well as in one or more neurocognitive domains; such as complex

attention (“sustained attention, divided attention, selective attention, processing speed”),

language, or perceptual-motor abilities (2013, p. 593-595, 611). Alzheimer’s can be diagnosed

with or without the feature of “behavioral disturbance” (p. 611). These abnormal behaviors can

include “​verbal or physical aggression, urinary incontinence, and excessive wandering”

(Muller-Spahn, 2003, p. 49). Mϋller-Spahn, MD, commented that one study found “Patients with

AD [Alzheimer’s Disease] were more likely to have delusions and less likely to have

depression,” although some links to depression have been found (p. 49). Therefore, the disease

distorts memory, perception, and responsiveness in addition to impairing them.

Christian Perspective of the Disease

Because the biological and behavioral effects of the disease are highly observable and

measurable, a Christian perspective would most likely agree on all symptomatology. However,

the next concern after identifying these symptoms is their effect on the spiritual state of the

patient. If Christian doctrine holds that humans are responsible for their actions and attitudes

toward God and others (Matthew 12:36-37 & 1 Corinthians 4:5, English Standard Version

(ESV)), then the disease’s effect on both of these would seem to also impact the spiritual state of

the patient. In Jesus’ parable of the servant keeping watch for his master in Luke 12, he says,

“…to whom much was given, of him much will be required” (Luke 12:48b, ESV). The inverse

of this statement is that to whom less was given (in terms of physical, emotional, and intellectual

control and capacity), less will be required. Although Scripture does not speak directly to the

subject of the state of a diseased person’s soul, Scripture constantly shows God as a just one and

proclaims, “a bruised reed he will not break” (Isaiah 42:3, ESV). A Christian perspective also
ALZHEIMER’S DISEASE 4

interprets the relational deficiencies that occur with the progression of Alzheimer’s with more

hope and positivity than determinism and materialism can; in the latter models, the family and

friends of the patient must accept that someone they knew emotionally, intellectually, and

relationally has deteriorated into a different, and often more hostile, person permanently. A

Christian viewpoint proclaims the sure hope of seeing that loved one renewed again in heaven

and restored relationship with them. These two viewpoints significantly affect how friends and

family members of the patient react to the situation, their depression levels, and how they treat

the patient.

Associated Neurological Damage

The hallmark characteristic of brain damage in Alzheimer’s is the over-production of a

defective long version of Amyloid β protein, which collects in plaques around the brain (Carlson

& Birkett, 2017, p. 511). The short version of the protein makes up 90% to 95% of the total

Amyloid β​ ​presence in a healthy brain, whereas the long version (which is normally destroyed by

microglia) can reach up to 40% of the total Amyloid β presence in a brain affected by

Alzheimer’s (p. 511). The natural role of Amyloid β is debated, as some studies have suggested

that its absence in the brain hinders axon guidance during neurogenesis (Rajapaksha, 2011, p. 5)

while other studies have shown that its chronic deficiency in mice does not result in any adverse

physiological or behavioral effects (Luo et al., 2003, pp. 86-7).

Another trademark in the neurology of Alzheimer’s is the presence of neurofibrillary

tangles (Carlson & Birkett, 2017, p. 510). Abnormal amounts of phosphate bind to tau protein, a

component of the brain’s microtubule transport system, and alters its form; this alteration

“disrupts transport of substances within the cell,” leaving localized networks of dying neurons
ALZHEIMER’S DISEASE 5

(p. 510). Increased instances of these tangles increase the rate and quantity of neuronal death in

different areas of the brain, leading to overall brain shrinkage (p. 510) and disrupting behavior

and mental processing.

Hypothesized Causes of Damage

Alzheimer’s is considered to have a genetic component, as one of the DSM-5 criteria for

probable Alzheimer’s diagnosis (as opposed to possible Alzheimer’s) is a family history of

Alzheimer’s or a gene mutation revealed by genetic testing (DSM-5, 2013, p. 611). “Because the

brains of people with Down syndrome (caused by an extra twenty-first chromosome) also

contain deposits of A β, some investigators hypothesized that the twenty-first chromosome may

be involved with the production of this protein” (Carlson & Birkett, 2017, p. 512). The strong

positive correlation between age and the presence of Alzheimer’s (p. 510) could mean that an Aβ

producing chromosome reaches a point of denaturation or malfunction from the ages of 65 to 85

in some people.

Health, lifestyle, and environmental factors also play a role in the development of the

disease, although the specific implications are unknown. Research regarding “​the ​relationship

between cognitive decline and vascular conditions​ such as ​heart disease​, ​stroke​, and ​high blood

pressure​, as well as metabolic conditions such as ​diabetes​ and obesity” is currently being

conducted (“What causes Alzheimer’s disease?”, 2017, para. 19). It has been a well-established

fact that a healthier lifestyle and overall positive health contributes to longevity and the

prevention of disease; however, these factors remain vague when analyzing Alzheimer’s

development (para. 20)

ALZHEIMER’S DISEASE 6

Biological Treatment Methods

Because studies have failed to demonstrate any significant negative effects associated

with the deficiency of Amyloid β, one proposed treatment of Alzheimer’s Disease is the forced

cessation of its production by debilitating the enzyme that cleaves amyloid precursor protein for

its creation (Luo et al., 2003, p. 81). This cessation would prevent further plaques from forming

in the brain; however, the possible side effects on the nervous system and organs are still

unknown.

Similarly, because plaques are the main neurological issue in Alzheimer’s disease,

finding a way to clear these plaques may reduce the symptoms of the disease or reverse them

(Bard et al., 2000, p. 916). Research with administering antibodies into the abdominal skin has

proven successful. The antibodies made their way into the central nervous system, easily

crossing the blood-brain barrier, and “reduced plaque burden by [up to] 93%” in the brains of

mice genetically modified to overproduce defective Aβ (p. 916). Micrographs of midbrain

sections revealed that most of the diffuse and large plaques were gone in mice that received

certain types of antibodies weekly for six months (p. 916). Not only did the antibodies stop the

continued production of the plaques, but they also cleared the ones present.

Christian Perspective on Treatment

Within the diverse views contained in Christianity, treatment of any physiological disease

is more controversial than the affirmation of the disease itself. Although no orthodox Christian

denomination explicitly denies the use of modern medicine and medical techniques, many

Christians are skeptical of medicine (and the products of science in general) as counter to firm

faith in God’s healing power (Guzder, 2009, para. 5). Verses such as James 5:14-16 seem to
ALZHEIMER’S DISEASE 7

suggest this stance: “​Is anyone among you sick? Let him call for the elders of the church, and let

them pray over him, anointing him with oil in the name of the Lord. And the prayer of faith will

save the one who is sick” (ESV).​ Some Christians also view medical treatment as a movement

against God’s sovereign will in allowing the disease to progress. However, the same James who

says prayer and faith brings healing also admonishes Christians to take care of the sick by

treating their physical needs when he says, “If a brother or sister is poorly clothed and lacking in

daily food, and one of you says to them, ‘Go in peace, be warmed and filled,’ without ​giving

them the things needed for the body​, what good is that?” (James 2:15-16, ESV, emphasis added).

The Bible affirms prayer and faith as conduits of healing for the sick, but does not make

exclusive statements declaring it the only conduit of healing. Luke, the author of the gospel of

Luke and Acts, was himself a physician and supported by the Apostle Paul (Colossians 4:14,

ESV). If medical techniques are available, affordable, and proven to aid in the physical

well-being of a diseased and deteriorating person, it seems to be more against Christian teachings

on compassion and provision to withhold this treatment than it is to embrace medical

intervention.

Cognitive Reserve as AD Prevention

According to a study that assessed the cognitive performance of Alzheimer’s patients

with varying years of previous education, those “AD patients with more education have better

ability than the patients with less education to compensate for the effects of atrophy” (Liu et al.,

2012, p. 934). This compensation is known as cognitive reserve, which “refers to the ability of

the brain to compensate for brain damage by using preexisting cognitive processing approaches

or recruiting compensatory approaches” (p. 934). Interestingly, those with more education (and
ALZHEIMER’S DISEASE 8

resulting thicker cortical regions) progress through brain atrophy and deterioration faster than

those with less education, yielding thinner cortical regions than less educated AD patients (p.

934). Yet, even with thinner cortices, these patients functioned cognitively at the same level or

better as those AD patients with thicker cortices and less education. The neurological

development and cortical thickening that occurs in learning over long time periods may build

cognitive reserve, which will allow those who develop Alzheimer’s disease to better cope with

the cognitive deficits (p. 937).

ALZHEIMER’S DISEASE 9

References

American Psychiatric Association: Diagnostic and statistical manual of mental disorders, fifth

edition​. (2013). Arlington, VA: American Psychiatric Association.

Bard, F., Cannon, C., Barbour, R., Burke, R., Games, D, Grajeda, H, … Yednock, T. (August

2000). Peripherally administered antibodies against amyloid β-peptide enter the central

nervous system and reduce pathology in a mouse model of Alzheimer disease. ​Nature

Medicine​, 6(8), 916-919.

Carlson, N. R. and Birkett, M. A. (2017). ​Physiology of behavior​ (12th ed.). Pearson Education.

Guzder, D. (February, 2009). When parents call God instead of the doctor. ​Time.​ Retrieved from

http://content.time.com/time/nation/article/0,8599,1877352,00.html

Liu, Y., Julkunen, V., Paajanen, T., Westman, E., Wahlund, L., Aitken, A., … Soininen, H.

(2012).

Education increases reserve against Alzheimer’s disease—evidence from structural MRI

analysis. ​Diagnostic Neuroradiology,​ 54, 929–938. doi:10.1007/s00234-012-1005-0

Luo, Y., Bolon, B., Damore, M. A., Fitzpatrick, D., Liu, H., Zhang, J., &… Citron, M. (2003).

BACE1 (​B​-secretase) knockout mice do not aquire compensatory gene expression

changes or develop neural lesion over time. ​Neurobiology of Disease,​ 14(1), 81.

doi:10.1016/S0969-9961(03)00104-9

Mayo Clinic. (2017). Dementia: Symptoms and causes. Retrieved from http://www.mayoclinic.

org/diseases-conditions/dementia/symptoms-causes/dxc-20198504

Mori, E., Ikeda, M., Hirono, N., Kitagaki, H., Imamura, T., & Shimomura, T. (1999). Amygdalar

volume and emotional memory in Alzheimer’s disease. ​The American Journal of

ALZHEIMER’S DISEASE 10

Psychiatry,​ 156(2), 216-222.

Muller-Spahn, F. (2003). Behavioral disturbances in dementia. ​Dialogues Clin Neurosci,​ 5(1),

49-59.

Rajapaksha, T. W., Eimer, W. A., Bozza, T. C., & Vassar, R. (2011). The alzheimer's beta-

secretase enzyme BACE1 is required for accurate axon guidance of olfactory sensory

neurons and normal glomerulus formation in the olfactory bulb.​ Molecular

Neurodegeneration, 6:​ 88. doi:http://dx.doi.org/10.1186/1750-1326-6-88

What causes Alzheimer’s disease? (2017). ​National Institute on Aging.​ Retrieved from

https://www.nia.nih.gov/health/what-causes-alzheimers-disease