





































Special Edition: Junior Clinical Research (2022), Vol. 2 No. S2 
 https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  86 2022, Vol. 2 No. S2 86-92 
   

 

COMMENTARY 

What are the Risk Factors for Alzheimer's 

Disease? 

Brittney Benedetti1,2, Shiv Singh1,3, Darlene Vargas1,2, Leith El-Zaim1,4, Ashely Pruneda1,2, Mia 

Padron1,2, Nadia Ramirez1,5  

 
12nd Annual Junior Clinical Research Internship, South Texas Academy for Education & Training in Research, DHR Health 

Institute for Research & Development 
2PSJA Memorial High School, Alamo, TX 
3Langley High School, Great Falls, VA 
4South Texas ISH Science Academy, Mercedes, TX 
5McAllen High School, McAllen, TX  

 

All correspondence should be addressed to Program Director, 2nd Annual Junior Clinical Research Internship Program, DHR 

Health Institute for Research & Development, 5323 S McColl Road, Edinburg Texas, 78539 

 

Received 07/01/2022 

Accepted for publication 08/05/2022 

Published 08/05/2022 

 

Keywords: Alzheimer’s disease; dementia; Texas 

  

Introduction 

 

Every 68 seconds a person in America is 

diagnosed with Alzheimer’s disease. Today, 6 million 

Americans 65 years and older have been affected by 

Alzheimer’s disease; this number is expected to 

double in the next 30 years (1). Alzheimer's disease is 

now the most common form of neurodegenerative 

dementia in the United States with a disproportionate 

disease burden in minority populations. Alzheimer’s 

disease was first discovered by Alois Alzheimer’s in 

1901 when he was treating one of his patients (2). 

Alzheimer's disease is a type of dementia that refers to 

a particular onset and course of cognitive and 

functional decline associated with age together with a 

particular neuropathology. Alzheimer's disease is a 

disorder that causes degeneration of the cells in the 

brain, and it is the main cause of dementia, which is 

characterized by a decline in thinking and 

independence in personal daily activities.  AD is 

considered a multifactorial disease (3). Alzheimer's 

disease care requires timely diagnosis and 

multidisciplinary management. Evaluation involves 

structured patient and caregiver history and symptom-

function reviews, examination, and testing to delineate 

impairment level, determine the cognitive-behavioral 

syndrome, and diagnose cause. Additionally, several 

risk factors such as increasing age, genetic factors, 

head injuries, vascular diseases, infections, and 

environmental factors play a role in the disease (4). 

Early reviews identified over 20 risk factors associated 

with Alzheimer's disease including age, familial 

inheritance, exposure to aluminum, traumatic brain 

injury and associated co-morbidities such as vascular 

disease and infection. 

 

Stages of Alzheimer’s  

 

Alzheimer’s tends to set in during peoples 

mid-60’s and proceeds to slowly worsen, affecting the 

memory, processing skills, and overall problem-

solving skills of the subject. There isn't a set timeline 

for Alzheimer’s and everyone's experience with the 

disease is different. Alzheimer’s usually progresses in 



Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  87 2022, Vol. 2 No. S2 86-92 
   

5 distinct stages. Stage one is preclinical Alzheimer's 

disease. Alzheimer's manifests itself long before any 

symptoms begin to show and during this stage it is 

practically impossible to know whether a subject has 

Alzheimer's or not (5). 

 

Stage 2 would be mild cognitive impairment 

caused by Alzheimer’s. This means that someone at 

this stage would suffer mild changes in memory and 

thinking ability. However, it should be noted that mild 

cognitive impairment (MCI) is a byproduct of 

Alzheimer's; not everyone who has Alzheimer’s will 

experience it and not everyone who suffers from it has 

Alzheimer’s (5). 

 

The third stage of the disease is mild 

dementia. This is the stage where Alzheimer's is 

usually diagnosed, because at this stage it becomes 

fully apparent that the patient is suffering from the 

symptoms of Alzheimer's. Some symptoms that 

people may encounter are changes in personality, 

memory loss of recent events, difficulty with problem 

solving, and frequent loss of items of personal value 

(5). 

  

The fourth stage is a progression of the 

previous stage, with amplified symptoms and a few 

new ones introduced. During this stage, people 

experience even more severe personality changes, 

increased memory loss, and in some cases, even lose 

the ability to perform everyday tasks without 

assistance (5). 

 

The fifth and final stage of Alzheimer's is 

severe dementia. At this stage, the disease severely 

affects the mental function of the patient and harshly 

affects the physical abilities of the patient. Once it has 

progressed this far, the disease renders the patient 

incapable of doing anything without extensive 

assistance. The patient would require help with even 

the most menial of tasks. Bathing, clothing, eating, 

defecating, and in some extreme cases even walking 

would be beyond the patient's abilities. Additionally, 

the patient also becomes more vulnerable to 

infections, loses bowel control, bladder control and 

may even lose the ability to comprehend their 

surroundings (6). 

 

Genetics 

 
There are genetic risk factors that contribute 

to why Alzheimer’s Disease affects many individuals 

worldwide. According to researchers, approximately 

70% of the risk of developing AD can be attributed to 

genetics (7).  As one of the most severe 

neurodegenerative diseases, Alzheimer's disease (AD) 

is a terrible condition (8).  

 

The strongest genetic risk factor for sporadic 

Alzheimer's disease is still the APOE 4 allele. 

However, there are currently no APOE-specific 

treatments available (9). The most important genetic 

risk factor for late-onset AD is the APOE 4 allele, but 

its specific function in the condition is yet unknown. 

Apolipoprotein E (ApoE) is abundantly expressed in 

the brain and is produced by the APOE gene. There 

are three different isoforms; the two that affect AD risk 

are apoE2, which increases risk and apoE3, which is 

the most common allele in the population. It is 

strongly contested how ApoE affects the development 

and progression of disease because it has a variety of 

roles that affect both neuronal and non-neuronal cells 

(10).  Presenilin 1 (PSEN1) was discovered to be an 

EOAD gene with unidentified functions using genetic 

mapping, gene cloning, and mutation screening of 

candidate genes.  

 

A second presenilin protein, known as 

presenilin 2, was found in the area connected to AD in 

a group of families known as Volga-German 

descendants. It was discovered based on protein 

homology (PSEN2) (11). As per the Alzheimer’s and 

Dementia textbook issue 12 volume 6, researchers 

have found that Early Onset Alzheimer Disease 

(EOAD) has a heritability of between 92 and 100 

percent and is nearly entirely genetically based. 

Between 35 and 60 percent of EOAD patients have at 

least one first-degree family who is afflicted, and in 10 

to 15 percent of these familial EOAD patients, 

autosomal dominant transmission is the mode of 

heredity (11).  

 

The three EOAD genes, which code for the presenilin 

1 and 2 (PSEN1 and PSEN2) and the amyloid 

precursor protein (APP), were shown to have high-

penetrant mutations by genetic analysis of unusually 

large and informative monogenic pedigrees (11). 

 

Adults with Down syndrome develop the 

neuropathological hallmarks of Alzheimer's disease 

and are at very high risk of developing early-onset 

dementia, which is now the leading cause of death in 

this population (12). Diagnosing dementia in patients 

who have Down syndrome is a lot harder than others 

who do not have the genetic disorder. Fluid and 

imaging biomarkers in those who have Down 

syndrome have shown great diagnostic performances 

and a strikingly similar being of changes with respect 

to sporadic and autosomal dominant Alzheimer's 

disease (13).  

https://doi.org/10.1186/s12929-019-0524-y


Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  88 2022, Vol. 2 No. S2 86-92 
   

External and Environmental Factors  

 
It is commonly established and proven that 

exposure to pollution, intentionally and 

unintentionally, can cause harmful effects to various 

parts of the human body. However, some of these 

negative effects go beyond just lung damage and heart 

diseases. According to a study in England, 39% of a 

large number of adults aged 50 to 79 were diagnosed 

with dementia, 29% with Alzheimer’s disease, and 

32% with vascular dementia (14). All affected patients 

were living in an area that contained the highest annual 

concentration of pollution (14). Compared to the other 

study participants who lived in an area of lower 

concentration, they were 1.4 times more likely to be 

diagnosed with those 3 cognitive diseases (14). 

 

A prevalent (and intentional) source of bodily 

harm from toxic pollutants is smoking, which causes a 

risk of Alzheimer's disease and other forms of 

dementia. A blog from Alzheimer’s Research UK 

explains and establishes how the excessive inhalation 

of tobacco smoke can possibly cause oxidative stress, 

an imbalance of antioxidants which the body uses to 

remove toxic molecules. This imbalance damages 

cells in the brain, resulting in an increased risk of 

cognitive diseases (15). 

 

Our dietary lifestyle has major effects on our overall 

physical and even mental health. A lack of regulation 

and moderation of the intake of certain foods can cause 

long-term damaging effects on various parts of the 

body. According to a USC News article, a diet 

consisting of foods that are high in fat, sugars, and 

cholesterol may affect people who carry the ApoE4 

gene by causing a greater risk of Alzheimer’s disease. 

To prove this statement, researchers from the USC 

Davis School of Gerontology presented the results of 

their experiment involving an unhealthy diet, genes, 

and their effect on mice. According to the researchers, 

the mice that carried the Alzheimer's related gene were 

fed an unhealthy diet and were later found to have 

more signs of brain inflammation, however those with 

a variant of the gene showed no such signs. This 

concludes that genetics carry heavy influence over 

outcome, however, a consistent healthy diet can 

potentially lower the risk factor for such brain diseases 

in the future (16). 

 

Although negative emotions such as stress, 

anger, and anxiety are often considered to be mere 

states of mind, they can potentially influence the risk 

of dementia and related diseases. It has been found that 

people with Alzheimer’s commonly have raised levels 

of the stress level cortisol, which potentially plays a 

role in neurodegeneration. Patients with Alzheimer’s 

that have consistently high levels of stress are found to 

have less success when it comes to coping with the 

pathological changes that are brought on by 

Alzheimer’s disease. It can be established that the best 

way to reduce this risk factor is to find healthy ways 

to reduce stress in everyday life. An environment that 

constantly induces negative emotions can inflict long 

term negative issues on the brain. A healthy and calm 

kept mind seems to be the best way to prevent any 

potential risks or influences of dementia or particularly 

Alzheimer’s disease (17). 

 

Family History 

 
Many people affected by dementia are 

concerned that they may inherit or pass on dementia. 

People with first-degree family history of Alzheimer's 

disease are at an increased risk of developing dementia 

by 30% (18). Subjective memory impairment among 

individuals with no measurable cognitive deficits may 

also indicate elevated dementia risk. The researchers 

say that it remains unclear whether nondemented 

people with a positive family history of Alzheimer's 

disease are more likely to experience cognitive deficits 

and whether such an association reflects underlying 

neuropathology. They investigated subjective memory 

impairment in 40 healthy adults and 35 patients with 

amnestic. (18). This suggests that subjective memory 

impairment could reflect preclinical stage 

neurodegeneration among individuals with the family 

history risk factors (18). The majority of dementia is 

not inherited by children and grandchildren. In rarer 

types of dementia, there may be a strong genetic link, 

but these are only a tiny proportion of overall cases of 

dementia. According to researchers, a child whose 

biological mother or father carries a genetic mutation 

for one of these three genes has a 50/50 chance of 

inheriting that mutation (19). They say if the mutation 

is in fact inherited, the child has a very strong 

probability of developing early-onset Alzheimer's 

disease (19). The researchers suggest that if 

Alzheimer's runs in the family, patients should keep 

the brain sharp and engage in new learning throughout 

their lifetime. Other ways to prevent getting 

Alzheimer's is eating a brain-healthy diet, preventing 

head injury, and getting screenings.  

 

The researchers say the Self-Administered 

Gerocognitive Exam, known as SAGE, is a brief pen 

and paper cognitive assessment tool designed to detect 

the early signs of cognitive, memory or thinking 

impairment. The test evaluates your thinking abilities. 



Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  89 2022, Vol. 2 No. S2 86-92 
   

This can help your doctor understand how well your 

brain is functioning (20).  

 

Obesity & Diabetes 

 
According to researchers, factors such as 

cerebrovascular diseases (loss of blood flow to the part 

of the brain, which causes damage to the brain tissue), 

diabetes (a class of conditions where there is an excess 

of blood sugar; high blood glucose), & obesity 

(Complex interactions between genetic, 

socioeconomic, and cultural factors lead to obesity.) 

increase the risk of Alzheimer’s disease development. 

Diabetes and obesity are among the modifiable risk 

factors for Alzheimer's disease. It's interesting to note 

that new epidemiological studies show that diabetes 

considerably raises the likelihood of getting 

Alzheimer’s Disease, indicating that diabetes may be 

a causal factor in the pathogenesis of Alzheimer's 

Disease. (21). A study observed that Obesity is a 

chronic, multifaceted disorder that affects many 

different organs and tissues abnormally and has a 

severe impact on human health. Amyloid plaques and 

neurofibrillary tangles in the brain are connected with 

Alzheimer's disease, a neurodegenerative condition 

that progresses and cannot be reversed. Although there 

is a link between obesity and Alzheimer's disease, the 

chemicals and molecular mechanisms behind this 

connection have not yet been fully understood. (22). 

Oxidative stress, mitochondrial dysfunction, and 

inflammation have all been found to contribute to the 

neurodegenerative processes seen in these illnesses. 

Researchers discovered critical links between diabetes 

and Alzheimer's disease that are provided by the 

advanced glycation end products produced by chronic 

hyperglycemia (posing risk to a variety of cell types 

and are strongly correlated with the myriad of DM-

Related complications, causing long-term 

complications if untreated). Despite being an immune-

privileged organ, the brain has been shown to interact 

with peripheral and central inflammation. Aging-

related damage to the blood brain barrier can cause 

immune cells to infiltrate the brain, aggravating the 

central inflammatory response. A key contributing 

factor to cognitive impairment, neuroinflammation 

may be the main mechanism behind illnesses linked to 

aging (23). Further research could help evaluate 

whether early interventions and lifestyle modifications 

could lower dementia risk, for obesity and diabetes 

continue to be serious public health problems in the 

U.S today.  

 

 

How TBI’S can affect with Alzheimer's 

Disease  

 
As reported in the Alzheimer's Association 

traumatic brain injury and Alzheimer's disease are 

both disastrous neurological disorders, whose 

complex is not yet understood. Cerebrovascular 

pathology, a key element in both conditions, could 

represent a mechanistic link between AB/tau 

deposition after TBI and the development of 

Alzheimer's disease. (24) 

 

More research is needed to fully understand the 

relationship between traumatic brain injury and 

Alzheimer’s and to understand why moderate, severe 

and repeated mild traumatic brain injuries are at an 

increased risk. Current research on how traumatic 

brain injuries changes brain chemistry indicates a 

relationship between traumatic brain injury hallmark 

protein abnormalities linked to Alzheimer’s. Within 

hours after injury, severe traumatic brain injury is seen 

to increase levels of beta amyloid, one hallmark 

protein (25). 

  

Traumatic brain injuries affect over 1.7 

million people every year and are often followed by 

changes in brain structure and function and by 

cognitive problems such as memory deficits, impaired 

social function, and difficulty with decision making. 

Although mild TBI’s are known as concussion, it is 

also a risk for Alzheimer's disease. Using MRI’S is a 

way to tell the similarities between Alzheimer and 

TBI’S in how the brain's gray and white matter 

degrade after injury. In multiple brain areas of both 

TBI and Alzheimer’s participants, the researchers 

found reduced cortical thickness when compared to 

the healthy controls. Cortical thickness is roughly 

correlated with brain age and its thinning is often 

associated with reductions in attention, memory and 

verbal fluency, as well as with decreased ability to 

make decisions, integrate new information and adapt 

one’s behavior to new situations, among other deficits. 

(26) 

 

Treatment 

 
   As of 2022, the number of people living with 

Alzheimer’s in Texas is about 400,000. With no cure 

or true method of treatment, by the year of 2050, 

Americans 65 and up with this disease are predicted to 

be as many as 12.7 million people (27). While there is 

no known cure at this time, there are several ways to 

manage the disease with more currently in the research 

phase. 



Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  90 2022, Vol. 2 No. S2 86-92 
   

The current treatment that we have today is 

not a cure but options to manage the disease slow its 

progression. Over the years, there has been a lot of 

progression in the understanding of pathophysiology, 

methods to diagnose the disease, and treatments. There 

are two categories of pharmacological therapy that are 

available to patients. They include the cholinesterase 

inhibitors, a group of medicines that block the normal 

breakdown of acetylcholine. Donepezil, rivastigmine, 

and galantamine are the recommended therapies for 

people with mild, moderate, or severe Alzheimer’s 

Disease Dementia (28).  These methods are able to 

show beneficial effects on awareness, activities of 

daily living, behavior, and overall clinical rating (28).  

In the past ten years, the omega-3 fatty acid 

supplements including fish oil have gained a lot of 

attention owing to their cardiovascular benefits (28).  

“Two recent randomized, controlled, double-blinded 

studies showed improvement in thinking and memory 

in patients with MCI who took fish oil supplements, 

though these studies were limited by small sample 

size.” (28) There are also many other hands-on 

activities that patients can take part of to improve 

neuropsychiatric symptoms and their quality of life. 

Several case studies show that art therapy has 

improved one's attention, provides pleasure, social 

behavior skills, and self-esteem (29).  

Our future holds a lot of opportunities for 

new ways to help these patients who are developing 

Alzheimer’s or have already been diagnosed with AD. 

The research into further treatments of Alzheimer’s 

disease will include targeting of the neurofibrillary 

tangles and senile plaques. (28) All around there are 

debates on which anomaly mark to slow down 

neurologic decline and how soon the treatment should 

be initiated. Spreading the information of clinical trials 

and including family members will bring in patients at 

the opportune time. By doing that, we will be able to 

slow these early stages of Alzheimer’s. The Clinical 

Trials in AD Committee in 2016 studied many of these 

trials to strive to identify the most effectful measures 

of patient recruitment and retention, infrastructure 

development, and patient evaluation including 

biomarkers and objective testing for the clinical end 

result. (2) When having to push through with trying to 

find the correct solution you will run into different 

encounters in learning which medicines will help, and 

which will not. With a collaborative attempt between 

researchers, exclusive and public funding, and 

screening of at-risk populations, a better predictor of 

successful clinical trials can be created. (28) 

 

 

Conclusion 

 
Alzheimer’s is one of the world’s most 

common diseases that we are facing today. The risk 

factors that come along with this disease are 

influencing our communities, families, and friends. 

Our healthcare communities are coming together, 

researching, and learning new information every day 

that will eventually slow down the rise of cases. 

Someday in the future Alzheimer’s may be eradicated 

and no one will ever have to deal with the fear of this 

disease. 

 

Acknowledgments 

 
Dr. Monica Betancourt-Garcia, MD, Scientific 

Director; Melissa Eddie, MS, Program Manager; 

Xochitl Lopez, BS, Program Coordinator 

 

Funding 

 
Funded by DHR Health Institute for Research & 

Development; DHR Health; Region One ESC 

GEARUP College Ready, Career Set! Region One 

ESC GEARUP College Now, Career Connected and 
Region One ESC PATHS 

 

References 

1. Alzheimer's Disease Facts and Statistics. 

(2022). Fisher Center for Alzheimer's 

Research Foundation. Retrieved June 30, 

2022, from 

https://www.alzinfo.org/understand-

alzheimers/alzheimers-disease-facts-and-

statistics/ 

2. Soria Lopez JA, González HM, Léger GC. 

Alzheimer's disease. Handb Clin Neurol. 

2019;167:231-255. doi: 10.1016/B978-0-12-

804766-8.00013-3. PMID: 31753135.  

3. Breijyeh Z, Karaman R. Comprehensive 

Review on Alzheimer's Disease: Causes and 

Treatment. Molecules. 2020 Dec 

8;25(24):5789. doi: 

10.3390/molecules25245789. PMID: 

33302541; PMCID: PMC7764106. 

4.  A. Armstrong R. Risk factors for 

Alzheimer's disease. Folia Neuropathol. 

2019;57(2):87-105. doi: 

10.5114/fn.2019.85929. PMID: 31556570.  

Mayo Clinic. (2021, April 29). Alzheimer's 

stages: How the disease progresses. Mayo 

Clinic.https://www.mayoclinic.org/diseases-

https://www.alzinfo.org/understand-alzheimers/alzheimers-disease-facts-and-statistics/
https://www.alzinfo.org/understand-alzheimers/alzheimers-disease-facts-and-statistics/
https://www.alzinfo.org/understand-alzheimers/alzheimers-disease-facts-and-statistics/
https://www.mayoclinic.org/diseases-%0cconditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=


Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  91 2022, Vol. 2 No. S2 86-92 
   

conditions/alzheimers-disease/in-

depth/alzheimers-stages/art-

20048448#:~:text=There%20are%20five%2

0stages%20associated,dementia%20due%20

to%20Alzheimer's%20disease.  

6. Alzheimer's Association. (n.d.). Alzheimer's 

Stages - Early, Middle, Late Dementia 

Symptoms | alz.org. Alzheimer's Association. 

Retrieved June 29, 2022, from 

https://www.alz.org/alzheimers-

dementia/stages 

7. Silva, M.V.F., Loures, C.d.M.G., Alves, 

L.C.V. et al. Alzheimer’s disease: risk factors 

and potentially protective measures. J 

Biomed Sci 26, 33 (2019). 

https://doi.org/10.1186/s12929-019-0524-y 

8. Muñoz, S.S., Garner, B. & Ooi, L. 

Understanding the Role of ApoE Fragments 

in Alzheimer’s Disease. Neurochem Res 44, 

1297–1305 (2019). 

https://doi.org/10.1007/s11064-018-2629- 

9. Serrano-Pozo, A. (2021, January 01). 

ScienceDirect. 20(1), 68-80. 

https://doi.org/10.1016/S1474-

4422(20)30412-9 

10. Munoz, S. (2018, September 17). 

https://doi.org/10.1007/s11064-018-2629-1 

11. Cacace, R. (2016). Alzheimer's and 

Dementia, 12(6), 733-738. 

https://doi.org/10.1016/j.jalz.2016.01.012 

12. Fortea, J., Zaman, S. H., Hartley, S., Rafii, M. 

S., Head, E., & Carmona-Iragui, M. (2021). 

Alzheimer's disease associated with Down 

syndrome: a genetic form of dementia. The 

Lancet. Neurology, 20(11), 930–942. 

https://doi.org/10.1016/S1474-

4422(21)00245-3   

13. Budson, A. E. (2020, July 3). Does air 

pollution cause Alzheimer’s disease? 

https://www.health.harvard.edu/blog/does-

air-pollution-cause-alzheimers-disease-

2020072320627  

14. Puckering, K. (2020, January 13). All you 

need to know about smoking and dementia. 

https://www.alzheimersresearchuk.org/blog/

all-you-need-to-know-about-smoking-and-

dementia/#:~:text=A%202019%20Lancet%

20Commission%20on,likely%20to%20deve

lop%20Alzheimer's%20disease. 

15. Gersema, E. (2017, June 12). Poor diet, plus 

Alzheimer’s gene, may fuel the disease. 

https://news.usc.edu/122919/poor-diet-plus-

alzheimers-gene-may-fuel-the-

disease/#:~:text=A%20diet%20high%20in%

20cholesterol,a%20new%20USC%20study

%20indicates. 

16. Pratt, E. (2021, June 28). How Chronic Stress 

May Increase the Likelihood of Developing 

Alzheimer’s Disease. 

https://www.healthline.com/health-

news/how-chronic-stress-may-increase-the-

likelihood-of-developing-alzheimers-

disease#The-role-stress-may-play 

17. Haussmann, R., Ganske, S., Gruschwitz, A., 

Werner, A., Osterrath, A., Lange, J., Buthut, 

M., Donix, K. L., Linn, J., & Donix, M. 

(2018). Family History of Alzheimer's 

Disease and Subjective Memory 

Performance. American journal of 

Alzheimer's disease and other dementias, 

33(7), 458–

462.https://pubmed.ncbi.nlm.nih.gov/29734

820/   

18. National Institute Aging. (2019, December 

24). Alzheimer's Disease Genetics Fact Sheet 

| National Institute on Aging. National 

Institute on Aging. Retrieved June 30, 2022, 

from 

https://www.nia.nih.gov/health/alzheimers-

disease-genetics-fact-sheet  

19. Kean, B., & Sinha, S. (2020, June 3). At-

Home SAGE Test for Alzheimer's and 

Dementia Detection. Everyday Health. 

Retrieved June 30, 2022, from 

https://www.everydayhealth.com/alzheimers

-disease/all-about-the-sage-test-for-

alzheimers-and-dementia-detection/  

20. Baglietto-Vargas, D., Shi, J., Yaeger, D. M., 

Ager, R., & LaFerla, F. M. (2016). Diabetes 

and Alzheimer’s disease crosstalk. 

Neuroscience and Biobehavioral Reviews, 

64(Complete), 272–287. 

https://doi.org/10.1016/j.neubiorev.2016.03.

005 

21. Picone, P., Di Carlo, M., & Nuzzo, D. (2020). 

Obesity and Alzheimer's disease: Molecular 

bases. The European journal of neuroscience, 

52(8), 3944–3950. 

https://doi.org/10.1111/ejn.14758  

22. Pugazhenthi, S., Qin, L., & Reddy, P. H. 

(2017). Common neurodegenerative 

pathways in obesity, diabetes, and 

Alzheimer's disease. Biochimica et 

biophysica acta. Molecular basis of disease, 

1863(5), 1037–1045. 

https://doi.org/10.1016/j.bbadis.2016.04.017 

23. Ramos-Cejudo, J., Wisniewski, T., Marmar, 

C., Zetterberg, H., Blennow, K., de Leon, M. 

J., & Fossati, S. (2018). Traumatic Brain 

https://www.mayoclinic.org/diseases-%0cconditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=
https://www.mayoclinic.org/diseases-%0cconditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=
https://www.mayoclinic.org/diseases-%0cconditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=
https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=There%20are%20five%20stages%20associated,dementia%20due%20to%20Alzheimer's%20disease
https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=There%20are%20five%20stages%20associated,dementia%20due%20to%20Alzheimer's%20disease
https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=There%20are%20five%20stages%20associated,dementia%20due%20to%20Alzheimer's%20disease
https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448#:~:text=There%20are%20five%20stages%20associated,dementia%20due%20to%20Alzheimer's%20disease
https://www.alz.org/alzheimers-dementia/stages
https://www.alz.org/alzheimers-dementia/stages
https://doi.org/10.1186/s12929-019-0524-y
https://doi.org/10.1007/s11064-018-2629-
https://doi.org/10.1016/S1474-4422(20)30412-9
https://doi.org/10.1016/S1474-4422(20)30412-9
https://doi.org/10.1007/s11064-018-2629-1
https://doi.org/10.1016/S1474-4422(21)00245-3
https://doi.org/10.1016/S1474-4422(21)00245-3
https://www.health.harvard.edu/blog/does-air-pollution-cause-alzheimers-disease-2020072320627
https://www.health.harvard.edu/blog/does-air-pollution-cause-alzheimers-disease-2020072320627
https://www.health.harvard.edu/blog/does-air-pollution-cause-alzheimers-disease-2020072320627
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://www.alzheimersresearchuk.org/blog/all-you-need-to-know-about-smoking-and-dementia/#:~:text=A%202019%20Lancet%20Commission%20on,likely%20to%20develop%20Alzheimer's%20disease.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://news.usc.edu/122919/poor-diet-plus-alzheimers-gene-may-fuel-the-disease/#:~:text=A%20diet%20high%20in%20cholesterol,a%20new%20USC%20study%20indicates.
https://www.healthline.com/health-news/how-chronic-stress-may-increase-the-likelihood-of-developing-alzheimers-disease#The-role-stress-may-play
https://www.healthline.com/health-news/how-chronic-stress-may-increase-the-likelihood-of-developing-alzheimers-disease#The-role-stress-may-play
https://www.healthline.com/health-news/how-chronic-stress-may-increase-the-likelihood-of-developing-alzheimers-disease#The-role-stress-may-play
https://www.healthline.com/health-news/how-chronic-stress-may-increase-the-likelihood-of-developing-alzheimers-disease#The-role-stress-may-play
https://pubmed.ncbi.nlm.nih.gov/29734820/
https://pubmed.ncbi.nlm.nih.gov/29734820/
https://www.nia.nih.gov/health/alzheimers-disease-genetics-fact-sheet
https://www.nia.nih.gov/health/alzheimers-disease-genetics-fact-sheet
https://www.everydayhealth.com/alzheimers-disease/all-about-the-sage-test-for-alzheimers-and-dementia-detection/
https://www.everydayhealth.com/alzheimers-disease/all-about-the-sage-test-for-alzheimers-and-dementia-detection/
https://www.everydayhealth.com/alzheimers-disease/all-about-the-sage-test-for-alzheimers-and-dementia-detection/
https://doi.org/10.1111/ejn.14758
https://doi.org/10.1016/j.bbadis.2016.04.017
https://doi.org/10.1016/j.bbadis.2016.04.017
https://doi.org/10.1016/j.bbadis.2016.04.017


Benedetti, et al. Alzheimer´s Disease 

https://doi.org/10.47488/dhrp.v2iS2.60 

 

 

 
 
 DHR Proceedings ǀ http://dhrproceedings.org  92 2022, Vol. 2 No. S2 86-92 
   

Injury and Alzheimer's Disease: The 

Cerebrovascular Link. EBioMedicine, 28, 

21–

30.https://doi.org/10.1016/j.ebiom.2018.01.0

21 

24. Alzheimer's association. (n.d.). Traumatic 

Brain Injury. Alzheimer's Association. 

Retrieved 06 30, 2022, from 

https://www.alz.org/alzheimers-

dementia/what-is-

dementia/related_conditions/traumatic-

brain-

injury#:~:text=Within%20hours%20after%2

0injury%2C%20severe,tau%20protein%2C

%20another%20Alzheimer%27s%20hallmar

k 

25. Miller, j. (2021). Brain changes following 

traumatic brain injury share similarities with 

Alzheimer’s disease. Jesse Miller. 

https://news.usc.edu/185354/traumatic-

brain-injury-tbi-alzheimers-disease-usc-

research 

26. Alzheimer's Disease Statistics. (2022, June 

3). Texas Department of State Health 

Services. Retrieved June 30, 2022, from 

https://www.dshs.texas.gov/alzheimers/statis

tics.shtm  

27. Weller, J., & Budson, A. (2018). Current 

understanding of Alzheimer's disease 

diagnosis and treatment. F1000Research, 7, 

F1000 Faculty Rev-1161. 

https://doi.org/10.12688/f1000research.1450

6.1  

28. Chancellor, B., Duncan, A., & Chatterjee, A. 

(2014). Art therapy for Alzheimer's disease 

and other dementias. Journal of Alzheimer's 

disease: JAD, 39(1), 1–11. 

https://doi.org/10.3233/JAD-131295  

 

 

https://doi.org/10.1016/j.ebiom.2018.01.021
https://doi.org/10.1016/j.ebiom.2018.01.021
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/traumatic-brain-injury#:~:text=Within%20hours%20after%20injury%2C%20severe,tau%20protein%2C%20another%20Alzheimer%27s%20hallmark
https://news.usc.edu/185354/traumatic-brain-injury-tbi-alzheimers-disease-usc-research/
https://news.usc.edu/185354/traumatic-brain-injury-tbi-alzheimers-disease-usc-research/
https://news.usc.edu/185354/traumatic-brain-injury-tbi-alzheimers-disease-usc-research/
https://www.dshs.texas.gov/alzheimers/statistics.shtm
https://www.dshs.texas.gov/alzheimers/statistics.shtm
https://doi.org/10.12688/f1000research.14506.1
https://doi.org/10.12688/f1000research.14506.1
https://doi.org/10.3233/JAD-131295

	Brittney Benedetti1,2, Shiv Singh1,3, Darlene Vargas1,2, Leith El-Zaim1,4, Ashely Pruneda1,2, Mia Padron1,2, Nadia Ramirez1,5
	Genetics
	There are genetic risk factors that contribute to why Alzheimer’s Disease affects many individuals worldwide. According to researchers, approximately 70% of the risk of developing AD can be attributed to genetics (7).  As one of the most severe neurod...
	The strongest genetic risk factor for sporadic Alzheimer's disease is still the APOE 4 allele. However, there are currently no APOE-specific treatments available (9). The most important genetic risk factor for late-onset AD is the APOE 4 allele, but i...
	A second presenilin protein, known as presenilin 2, was found in the area connected to AD in a group of families known as Volga-German descendants. It was discovered based on protein homology (PSEN2) (11). As per the Alzheimer’s and Dementia textbook ...
	The three EOAD genes, which code for the presenilin 1 and 2 (PSEN1 and PSEN2) and the amyloid precursor protein (APP), were shown to have high-penetrant mutations by genetic analysis of unusually large and informative monogenic pedigrees (11).

