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Alzheimer's Disease

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Original Editors - Students from Bellarmine University's Pathophysiology of Complex Patient Problems project. Top Contributors - Josie Little, Stephanie Schwebler, Laura Ritchie, Admin, Lucinda hampton, Elaine Lonnemann, Chioma Clara Okeakpu, Kim Jackson, Hayaa Yousri, Emily Pollom, Dave Pariser, Vidya Acharya, Kirenga Bamurange Liliane, Alexandra Stead, Nikhil Benhur Abburi, Lauren Lopez, Ahmed M Diab, 127.0.0.1, Shaimaa Eldib, Joseph Ayotunde Aderonmu, Evan Thomas, WikiSysop, Tolulope Adeniji, Naomi O'Reilly, Safiya Naz, Ewa Jaraczewska, Peace Samuel and Wendy Walker  

Introduction

AD cause brain shrinkage

Alzheimer's Disease (AD), a neurodegenerative disorder, is the most prevalent form of dementia among the elderly globally.[1] It is the most frequent type of amyloidosis in humans and results from the extracellular accumulation of amyloid-β (Aβ)1–42 peptides and intracellular neurofibrillary tangles (NFTs) comprising Aβ oligomers and phosphorylated tau proteins.[1] The symptoms of AD include emotional fluctuation, sleep disorders, behaviour changes, and cognitive decline.

In the advanced stages, it can cause severe complications such as malnutrition, functional impairment, behavioural changes and increased susceptibility to infections such as pneumonia, which are common causes of death in advanced AD.[2] Some researchers have proposed the term 'type 3 diabetes' to describe the brain insulin resistance seen in AD, although this remains a research hypothesis rather than an accepted clinical classification.[3] There is currently no cure for the disease, but treatments are available to slow down the progression.[4]

Epidemiology

There is estimated to be roughly 416 million people across the AD continuum globally, effecting an estimated 22% of people aged 50 and over.[5] For those with Aβ-positive AD, this figure is at 32 million worldwide.[6] This prevalence increases with age and typically increases in the female population.[4][6]

According to the World Alzheimer Report 2018, a new case of dementia develops every 3 seconds around the globe with 66% of these people living in low‐ and middle‐income countries.[7]

Aetiology

After years of research into the causes of AD, AD is now understood to be multifactorial, with genetic, age-related and vascular contributions; despite considerable research progress, a single unifying cause has not been identified.[8][9] Genetics is a factor in some cases of early and late-onset AD.

[10]

Several risk factors (see also Dementia: Risk Factors) have been associated with AD including:[11]

  • Advancing age, >85 y/o risk increases by nearly 50%[12]
  • Direct family member with the disease (mother, father, brother or sister)
  • Apolipoprotein E-e4 (APOE4) carries the strongest risk of developing Alzheimer’s Disease (a genetic mutation of APOE)[8]
  • Traumatic brain injury
  • Deterministic genes have a direct cause of early-onset AD, however, they only account for less than 5% of cases: amyloid precursor protein (APP), presenilin-1 (PS-1), presenilin-2 (PS-2) [13]
  • Trisomy 21
  • Cardiovascular risk factors: mid-life obesity, mid-life hypertension, hyperlipidaemia, diabetes mellitus[14]

As well as the genetic and environmental factors above, the age when clinical signs show is affected by socioeconomic factors, such as:[4]

  • Formal education
  • Income
  • Occupational status
  • Social network and family support

People with higher function/supports prior to diagnosis are able to compensate for early disease changes more effectively and present later. When these people present, they tend to have more marked morphological changes on imaging.[4]

Pathology

AD is known as a complex neurodegenerative disease with various pathological mechanisms of which the first pathological sign of AD in the human cortex presents as the gradual accumulation of β-amyloid plaques, followed by the appearance of gliosis, misfolded tau, and neurodegeneration.[15] [16] A number of promising therapeutic strategies have been evaluated yet haven't been able to address AD effectively due to its complex pathology. Previous failures indicate that targeting on a single factor alone may not work well on a disease caused by multiple factors therefore more extensive and intensive fundamental studies are still needed.[15]

The various pathological factors involved in AD include:[15]

  • Synaptic Dysfunctions in Alzheimer’s Disease
  • Neurotransmission in Alzheimer’s Disease
  • Amyloid Cascade Hypothesis in Alzheimer’s Disease
  • Tau Toxicity Cascade in Alzheimer’s Disease

Cerebral amyloid-β deposits occur predominantly in:

  • Entorhinal cortex in the hippocampus (important in spatial memory and navigation, and helps turn short-term memory into long-term memory)[17][18]
  • Association areas of the neocortex
  • Limbic cortex

The fundamental reason for the accumulation of neuritic plaques and neurofibrillary tangles is not as yet understood. Evidence partially points to chronic inflammation having a role. This inflammatory state leads to prolonged activation of microglial cells (phagocytose and remove foreign or damaged material, cells) which causes inflammatory mediators to be released resulting in neuronal damage and amyloid-induced neurodegeneration.[4]

Clinical Presentation

Icon: for amnesia or dementia

The typical patient with AD will present initially with decreased ability to form/retain new memories. With time (often years), cognitive deficits progresses, with eventual problems with attentional and executive processes, semantic memory, and visuoperceptual abilities. Mental health problems affect almost all patients eventually, including apathy, depression, anxiety, aggression/agitation, and psychosis (delusions and hallucinations).[4]

Stages of Alzheimer's Disease

AD may progress through the following stages as follows:[19][20]

Mild Alzheimer’s Disease (Early Stage)

May Function Independently: may drive, work or maybe apart of social activities. Memory Lapses: familiar words, location of objects, names of new people, recently read material. Difficulties noticed by family, friends and doctors: challenges performing activities at home or work, difficulty planning. Lack of spontaneity. Subtle personality changes. Disorientation to time and date

Moderate Alzheimer’s Disease (Middle Stage)

Longest stage may last for years. Personality changes: moody or withdrawn, suspicious, delusions, compulsive, repetitive behaviour. Increased memory loss: forgetfulness regarding personal history, unable to recall address, phone number, or high school they graduated from. Decreased independence: trouble controlling bowel and bladder, increased risk of wandering or becoming lost, dependence with choosing appropriate clothes for event or season, increased Confusion. Impaired cognition and abstract thinking. Restlessness and agitation. Wandering, "sundown syndrome". Inability to carry out activities of daily living.

Severe Alzheimer’s Disease (Late Stage)

Decreased response to the environment: decreased ability to communicate and may speak in small phrases, decreased awareness of experiences & surroundings. Dependence on caregiver: decreased physical functioning: walking, sitting & swallowing; increased vulnerability to infections, incontinence. Emaciation, indifference to food

Diagnosis

It is vital to recognise the early signs and symptom which mostly presents as a minor change or decline in cognition and behaviour and understand how to use the most appropriate assessment tools designed to detect the early clinical effects of the disease.[21] The neuropathologic hallmarks of AD (Aβ plaques and NFTs) can be detected decades prior to the onset of symptoms as biomarkers reflecting this underlying pathology represent an important opportunity for early identification of patients at greatest risk of developing AD.

Biomarker information can be gathered from imaging modalities such as magnetic resonance imaging (MRI) and positive emission tomography (PET) which visualises early structural and molecular changes in the brain, respectively. Fluid biomarker testing, such as cerebrospinal fluid (CSF) are also used; CSF biomarkers directly reflect the presence of Aβ and aggregated tau within the brain and this can contribute important information diagnostically in the early stages of AD. Research to expand the current range of tests that can be used by clinicians as part of the multistage diagnostic process are ongoing and this could create the option of blood-based biomarkers to identify patients at risk of developing AD and for monitoring disease progression once approved.[21]

Other tests include:

  • EEG shows a slowing with no focal features, again non-specific.
  • neuropsychological testing. including a psychiatric evaluation (looking for mental health conditions).
  • Genetic Testing: Inheriting a single copy of the ApoE gene, encoding for apolipoprotein E, increases the chances of developing Alzheimer disease three times, whilst inheriting both copies increases one's risk eightfold.[4]

Screening

AD screening is an important issue with various studies indicating that the first detectable cognitive changes related to AD development 10 years prior to clinical diagnosis. A measurement of AD from its preclinical phase through its progression to mild dementia is needed for identification of AD early, with no reliable tool yet existing.[7]

Objective tools have been validated in order to screen for AD such as the Mini-Cog, Mini-Mental State Exam (MMSE), Clock-Drawing, & Neurobehavioral Cognitive Status Exam.[22]

Systemic Involvement

The most noticeable symptoms initially are the cognitive and memory-related symptoms. However, AD can affect other parts of the body causing symptoms other than those affecting memory and cognition. Often abnormal motor signs can be apparent depending on the area of the brain affected by the disease. The presence of tremors can be associated with increased risk for cognitive decline, the presence of bradykinesia with increased risk for functional decline, and the presence of postural-gait impairments with increased risk of institutionalisation and death. Additionally, patients may develop disorders of sleeping, eating, and sexual behaviour.[23]

Medical Management

There is currently no cure for AD, so medical management is focused on maintaining the quality of life, maximising function, enhancing cognition, fostering a safe environment and promoting self engagement.[24] Maximising dementia functioning involves monitoring the patient's health and cognition, patient and family education, initiation of pharmacological and non-pharmacological treatments.

Cognitive symptom treatment

Although the disease progression cannot be altered, it may be slowed by the pharmacological medication listed in the medications section.

Behavioural and psychological symptom treatment

  • Agitation, aggression, depression, and psychosis are the primary cause of assisted living or nursing home placement.
  • Assessment of behaviours occurring suddenly is important to increase patient comfort, security, and ease of mind.

Monitoring Alzheimer’s disease

  • Patients should return on a regular basis in order for the physician to monitor the course of Alzheimer’s disease (behavioural and cognitive changes).
  • Regular follow-up appointments allow for the adaptation of treatment styles to fit the needs of the patient.
  • Non medical/social Issues the patients need to address:
    • Need for ongoing support & information
    • A living will or power of attorney
    • Review of finances/planning for future and end of life care

Alternative Treatment

  • There are concerns regarding alternative treatments in addition to physician-prescribed medicine. If any concerns or questions arise, the physician should be notified.
  • The idea that aerobic and strengthening exercise might slow cognitive impairment in dementia has gained widespread popularity. Many studies describe plausible mechanisms using mammalian models, but there are fewer studies using human participants.[25]
  • Some researchers consider exercise replacement for drugs to decrease the negative effect of dementia on cognitive function as memory, executive and physical function as strength, balance and endurance.[26]
  • Effect on dementia have conflicted one review observed exercise has a positive effect on physical status not cognitive, while another review concluded aerobic exercise affects physical and cognitive functions.[25]
  • Positive effects of exercise are increase of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-type I (IGF-1), vascular endothelial growth factor (VEGF), and homocysteine [15–23] that is enhance memory and executive function.[25]
  • Music therapy treatment may enhance both psychological and physical by lowering stress levels, and reduction of plasma cortisol levels. some researcher measured salivary cortisol samples with moderate or severe dementia. limited number of studies explained effect of music therapy on dementia.[27]

Importance of Caregiver

  • Many caregivers seek to meet the needs of the physician and the patient which increases rates of stress and depression. Physicians should continue to monitor the status of the caregivers watching out for burnout and providing them with resources as well.

Medications

Below is a list of some commonly used medications use in the treatments of the symptoms of Alzheimer's. There is also the use of other treatments such as antioxidants, anti-inflammatory agents, and oestrogen replacement therapy in women to prevent or delay the onset of the disease.[23][28]

  • Cholinesterase inhibitors e.g. donepezil
  • Partial NMDA receptor antagonists
  • Medications for behavioural symptoms
  • Antidepressants
  • Anxiolytics
  • Antiparkinsonian (movement symptoms)
  • Anticonvulsants/sedatives (behavioural)
  • Recently Aduhelm (aducanumab) has been approved by the FDA, professed to reduce amyloid-beta plaque in people, however its efficacy and long-term benefits remain controversial.[4]

Physiotherapy Management

In the early and middle stages of AD, physical therapists can assist people stay mobile. This helps them maintain a degree of independence, and continue to perform their roles in the family and in the community.

Later as AD progresses physical therapists assist in keeping them able to perform daily activities for as long as possible, reducing the load on family members and caregivers. Physical therapists can perform a home assessment to ensure help the home is a safe environment and possibly delay the need for facility-based care.

Physical Activity

Physical activity is important to incorporate in a patient’s with Alzheimer’s disease life. Problems with balance and gait can often be lessened by regular physical therapy sessions, thereby reducing the risk of falls, fractures, and other injuries.[29][30]

Resistance Training

Studies show that resistance exercise has the highest probability of being the optimal exercise type for slowing cognitive decline in patients with cognitive dysfunction, especially in patients with dementia while compound exercise tends to be most effective in protecting global cognition and executive function.[31] See Preventing Dementia and Cognitive Decline

Managing Gait and Cognitive Impairments

Gait is not just a motor task but rather an activity that involves executive function, attention, and the environment. Older people with cognitive impairment (CI) are twice more likely to fall and be injured compared to those without CI and therefore caution should be taken into their management due to their probability of high risks of falls.[32] Also, mental processing which includes executive function, focus, and visuospatial perception are all influenced by cognitive impairments in older adults with AD therefore changes in even one either executive function, focus, or visuospatial perception will result in falls. A research study suggests that poor visual acuity resulted in poorer executive function, which further caused more inadequate balance control, thus demonstrating the importance of assessing executive functions besides vision and balance in older individuals living with Alzheimer's dementia.[33] See Falls and Dementia

This 4 minute video outlines the role of Physiotherapy may play in AD.

[34]

Dietary Management

It has been found that maintaining a healthy diet may help to prevent or slow the progression of Alzheimer's. It is suggested that the diet be low in fat, high in omega-3 oils, and high in dark vegetables and fruits, also adding vitamin C to the diet along with coenzyme Q10, and folate may work to lower the risk of Alzheimer's. There does not seem to be one single aspect of diet that provides neuroprotection, rather than the items work together to decrease the risk of AD.[23] There is also some interest in the use of antioxidants such as vitamin E and ginkgo, along with anti-inflammatory agents, and oestrogen replacement therapy for women.[28] 

Differential Diagnosis

Low Resource Health Settings

More than half of all people with dementia are from low and middle-income countries. Alzheimer’s disease, other dementias, and non-communicable diseases are expected to continue to be a burden on health systems throughout sub-Saharan Africa, as country populations age and communicable disease mortality and morbidity go down.[35] The number of people with Alzheimer's disease and dementia in general is estimated to increase far more rapidly in the upper middle, lower middle and low-income countries (LMICs) than in the high-income countries.[36] There is a general lack of awareness of the disease among the population, therefore patients don't seek for medical care and do not get the treatment they need. Hence, it is under-recognised, under-disclosed, undertreated, and undermanaged, particularly in LMICs.[37] The living environment also often poses little cognitive challenge because families may not understand their relative’s behaviour.[38] Many of the cognitive and functional assessment tools used in LMICs were originally developed and validated in High Income Countries. There is a need to adapt it to be used more effectively in LMICs.[39]

Summary

Alzheimer's Disease is the leading cause of dementia worldwide, and although there is still no cure, ongoing advances in diagnosis and treatment continue to improve outcomes and quality of life. Physiotherapy plays a valuable role throughout the disease course, helping to preserve mobility, function, and independence, reduce fall risk, and ease caregiver burden through targeted exercise and individualised, interprofessional care. As the evidence base continues to evolve, physiotherapists should stay up to date with current best practice to ensure care remains safe, effective, and person-centred.

Resources

See also Category:Dementia

References

  1. ↑ 1.0 1.1 Singh MK, Shin Y, Ju S, Han S, Kim SS, Kang I. Comprehensive overview of alzheimer’s disease: Etiological insights and degradation strategies. International Journal of Molecular Sciences. 2024 Jun 24;25(13):6901.
  2. ↑ Clifford K, Moreno M, Kloske CM. Navigating late‐stage dementia: a perspective from the Alzheimer's Association. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring. 2024 Jan;16(1):e12530.
  3. ↑ Meng X, Zhang H, Zhao Z, Li S, Zhang X, Guo R, Liu H, Yuan Y, Li W, Song Q, Liu J. Type 3 diabetes and metabolic reprogramming of brain neurons: causes and therapeutic strategies. Molecular Medicine. 2025 Feb 18;31(1):61.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Radiopedia Alzheimer disease Available:https://radiopaedia.org/articles/alzheimer-disease-1?lang=gb (accessed 16.1.2023)
  5. ↑ Gustavsson A, Norton N, Fast T, Frölich L, Georges J, Holzapfel D, Kirabali T, Krolak‐Salmon P, Rossini PM, Ferretti MT, Lanman L. Global estimates on the number of persons across the Alzheimer's disease continuum. Alzheimer's & Dementia. 2023 Feb;19(2):658-70.
  6. ↑ 6.0 6.1 Gustavsson A, Norton N, Fast T, Frölich L, Georges J, Holzapfel D, Kirabali T, Krolak‐Salmon P, Rossini PM, Ferretti MT, Lanman L. Global estimates on the number of persons across the Alzheimer's disease continuum. Alzheimer's & Dementia. 2023 Feb;19(2):658-70.
  7. ↑ 7.0 7.1 Zhou X, Ashford JW. Advances in screening instruments for Alzheimer's disease. Aging Medicine. 2019 Jun;2(2):88-93. Available:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6880670/ (accessed 16.1.2023)
  8. ↑ 8.0 8.1 Scheltens P, De Strooper B, Kivipelto M, Holstege H, Chételat G, Teunissen CE, Cummings J, van der Flier WM. Alzheimer's disease. The Lancet. 2021 Apr 24;397(10284):1577-90.
  9. ↑ Pluta R. A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model. Current Alzheimer Research. 2024 Mar;21(3):166-82.
  10. ↑ Dementia - Causes, Symptoms and Treatment Options [Internet]. YouTube. YouTube; 2014 [cited ‏/06‏/2014]. Available from: [https://www.youtube.com/watch?v=nLdLfmFzLSo/ref https://www.youtube.com/watch?v=nLdLfmFzLSo
  11. ↑ Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, Brayne C, Burns A, Cohen-Mansfield J, Cooper C, Costafreda SG. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The lancet. 2020 Aug 8;396(10248):413-46.
  12. ↑ Alzheimer's & Dementia Testing Advances | Research Center [Internet]. Alzheimer's Association. [cited 2017Apr2]. Available from: http://www.alz.org/research/science/earlier_alzheimers_diagnosis.asp
  13. ↑ Alzheimer's and Dementia Causes, Risk Factors | Research Center [Internet]. Alzheimer's Association. [cited 2017Apr1]. Available from: http://www.alz.org/research/science/alzheimers_disease_causes.asp#apoe
  14. ↑ Latest Alzheimer's Facts and Figures [Internet]. Latest Facts; Figures Report | Alzheimer's Association. 2016 [cited 2017Apr1]. Available from: http://www.alz.org/facts/
  15. ↑ 15.0 15.1 15.2 Ju Y, Tam KY. Pathological mechanisms and therapeutic strategies for Alzheimer’s disease. Neural regeneration research. 2022 Mar 1;17(3):543-9.
  16. ↑ Gazestani V, Kamath T, Nadaf NM, Dougalis A, Burris SJ, Rooney B, Junkkari A, Vanderburg C, Pelkonen A, Gomez-Budia M, Välimäki NN. Early Alzheimer’s disease pathology in human cortex involves transient cell states. Cell. 2023 Sep 28;186(20):4438-53.
  17. ↑ Kumar A, Sidhu J, Goyal A, Tsao JW. Alzheimer disease. Available:https://www.ncbi.nlm.nih.gov/books/NBK499922/ (accessed 16.1.2023)
  18. ↑ Kiddle Hippocampus Available from:https://kids.kiddle.co/Hippocampus (accessed 17.1.2023)
  19. ↑ Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
  20. ↑ Stages of Alzheimer's Symptoms [Internet]. Alzheimer's Association. [cited 2017Apr1]. Available from: http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
  21. ↑ 21.0 21.1 Porsteinsson AP, Isaacson RS, Knox S, Sabbagh MN, Rubino I. Diagnosis of early Alzheimer's disease: clinical practice in 2021. The journal of prevention of Alzheimer's disease. 2021 Mar 1;8(3):371-86.
  22. ↑ Cedervall Y, Stenberg AM, Åhman HB, Giedraitis V, Tinmark F, Berglund L, Halvorsen K, Ingelsson M, Rosendahl E, Åberg AC. Timed Up-and-Go Dual-Task Testing in the Assessment of Cognitive Function: A Mixed Methods Observational Study for Development of the UDDGait Protocol. International journal of environmental research and public health. 2020 Jan;17(5):1715.
  23. ↑ 23.0 23.1 23.2 Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
  24. ↑ Medical Management and Patient Care [Internet]. Alzheimer's Association. [cited 2017Apr1]. Available from: http://www.alz.org/health-care-professionals/medical-management-patient-care.asp
  25. ↑ 25.0 25.1 25.2 Lamb SE, Sheehan B, Atherton N, Nichols V, Collins H, Mistry D, Dosanjh S, Slowther AM, Khan I, Petrou S, Lall R. Dementia And Physical Activity (DAPA) trial of moderate to high intensity exercise training for people with dementia: randomised controlled trial. bmj. 2018 May 16;361.
  26. ↑ Sanders LM, Hortobágyi T, Karssemeijer EG, Van der Zee EA, Scherder EJ, Van Heuvelen MJ. Effects of low-and high-intensity physical exercise on physical and cognitive function in older persons with dementia: a randomized controlled trial. Alzheimer's research & therapy. 2020 Dec;12:1-5.
  27. ↑ Lam HL, Li WT, Laher I, Wong RY. Effects of music therapy on patients with dementia—A systematic review. Geriatrics. 2020 Sep 25;5(4):62.
  28. ↑ 28.0 28.1 Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
  29. ↑ Mahalakshmi B, Maurya N, Lee SD, Bharath Kumar V. Possible neuroprotective mechanisms of physical exercise in neurodegeneration. International journal of molecular sciences. 2020 Aug 16;21(16):5895.
  30. ↑ Mercerón-Martínez D, Ibaceta-González C, Salazar C, Almaguer-Melian W, Bergado-Rosado JA, Palacios AG. Alzheimer’s disease, neural plasticity, and functional recovery. Journal of Alzheimer’s Disease. 2021 Jun 22;82(s1):S37-50.
  31. ↑ Huang X, Zhao X, Li B, Cai Y, Zhang S, Wan Q, Yu F. Comparative efficacy of various exercise interventions on cognitive function in patients with mild cognitive impairment or dementia: a systematic review and network meta-analysis. Journal of sport and health science. 2022 Mar 1;11(2):212-23.
  32. ↑ Adzhar MA, Manlapaz D, Singh DK, Mesbah N. Exercise to improve postural stability in older adults with Alzheimer’s disease: A systematic review of randomized control trials. International Journal of Environmental Research and Public Health. 2022 Aug 19;19(16):10350.
  33. ↑ Hunter SW, Divine A, Madou E, Omana H, Hill KD, Johnson AM, Holmes JD, Wittich W. Executive function as a mediating factor between visual acuity and postural stability in cognitively healthy adults and adults with Alzheimer’s dementia. Archives of Gerontology and Geriatrics. 2020 Apr 19:104078.
  34. ↑ Pollom E, Little J. PT Management of Alzheimer's Disease [Internet]. YouTube. YouTube; 2017 [cited 2017Apr2]. Available from: https://www.youtube.com/watch?v=rW3rQ73rQFE&t=8s
  35. ↑ Mubangizi V, Maling S, Obua C, Tsai AC. Prevalence and correlates of Alzheimer’s disease and related dementias in rural Uganda: cross-sectional, population-based study. BMC geriatrics. 2020 Dec;20(1):1-7.
  36. ↑ Global Prevalence. Available from:https://www.dementiastatistics.org/statistics/global-prevalence/( Accessed, 20/09/2021).
  37. ↑ Ferri CP, Jacob KS. Dementia in low-income and middle-income countries: different realities mandate tailored solutions. PLoS medicine. 2017 Mar 28;14(3):e1002271.
  38. ↑ George-Carey R, Adeloye D, Chan KY, Paul A, Kolčić I, Campbell H, Rudan I. An estimate of the prevalence of dementia in Africa: a systematic analysis. Journal of global health. 2012 Dec;2(2).
  39. ↑ Sexton C, Snyder HM, Chandrasekaran L, Worley S, Carrillo MC. Expanding Representation of Low and Middle Income Countries in Global Dementia Research: Commentary From the Alzheimer's Association. Frontiers in Neurology. 2021 Mar 15;12:271.
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