Definition/Description
Alzheimer’s disease (AD) is the most common cause of dementia worldwide [1] (dementia is an umbrella term for memory loss and other cognitive abilities required for activities of daily living) [2]. It is a neurodegenerative disease. The main known risk factor for the disease is aging But AD is not a normal part of aging. Alzheimer’s disease is progressive, so symptoms get worse over time. There is currently no cure for the disease, but treatments are available to slow its progression [3]. The mechanisms that manifest AD are complex. this The understanding of the pathophysiology of this condition is evolving [4].
Alzheimer’s Disease Brain Comparison
Alzheimer’s disease is characterized by cortical atrophy and neuronal loss, especially in the parietal and temporal lobes. As brain mass decreases, the ventricles enlarge as well [5]. Changes in brain tissue can slowly cause cognitive changes in a person.
Senile plaques, composed of extracellular amyloid, are found in higher concentrations in Alzheimer’s patients compared to normal aging brains [6]. Neurofibrillary tangles in the neocortex, amygdala, hippocampus, and ganglia basal of Meynert may also occur [7]. in normal operation Brain B amyloid dissolves and the brain reabsorbs it. When it is not reabsorbed, amyloid B can fold itself. The proteins then connect to each other and form plaques. These plaques cause an inflammatory response that results in more damage to neural tissue [8][9]. maybe Involvement of the blue-green paramedian reticular area of the dorsal thalamic tegmental area and the lateral nucleus of the hypothalamus [7].
Degenerative changes in these regions are caused by decreased choline acetyltransferase activity in the cerebral cortex and hippocampus and loss of cholinergic neurons in the hippocampal cholinergic projection pathway [7].
This link will take you on a tour of the brain and further explain how Alzheimer’s affects the brain.
Alzheimer’s Disease Brain Tour
Prevalence
By 2021, an estimated 6.2 million Americans age 65 and older will live with Alzheimer’s disease, 75 percent of whom will be age 75 and older. [10] Approximately 8 million people are affected worldwide [11]. This number is expected to nearly triple by 2050 115.4 million. The known prevalence is 6% in people over 65 years old, 20% in people over 80 years old, and over 95% in people over 95 years old. Alzheimer’s disease is the sixth leading cause of death in adults [12]. The time from onset to death is usually seven to eleven years.
Deaths from the other top 10 diseases declined from 2000 to 2014, while Alzheimer’s disease increased by 89 percent as the leading cause of death. A retrospective cohort study [13] found cardiovascular disease (CVD) to be an important cause of death in older adults with dementia Survival of about 4 years after a dementia diagnosis is relatively short.
Early-onset AD appears between the ages of 30 and 60. This occurs in 1-6% of all cases [10]. Late-onset AD appears after age 60 and accounts for about 90 percent of cases. Two-thirds of Americans with Alzheimer’s are women [10]. Older African-Americans and Hispanics Compared with older whites, they are more likely to develop Alzheimer’s disease or dementia [10].
Clinical Presentation
The progression of Alzheimer’s disease is continuous and usually does not fluctuate or improve. Often, early symptoms may be missed or ignored as they may be misinterpreted as signs of the natural aging process [14]. There are some key risk factors to consider and Alzheimer’s disease.
Primary Risk Factors
- Age >85 years increased risk by nearly 50% [15]
- An immediate family member (mother, father, brother, or sister) with the disease Risk genes that increase the likelihood of developing the disease
- Apolipoprotein E-e4 (APOE4) has the greatest risk of Alzheimer’s disease, and it is the genetic mutation of APOE [16]
- The risk is thought to increase if carriers of the gene also have a traumatic brain injury
- Definitive genes are the direct cause of early-onset AD, but they account for less than 5% of cases: Amyloid precursor protein (APP) Presenilin-1 (PS-1) Presenilin (PS-2) [17]
- Trisomy 21
- Cardiovascular risk factors: middle-aged obesity, middle-aged hypertension, hyperlipidemia, diabetes[18]
Possible Risk Factors
- Head trauma—Older adults had a 2.3-fold increased risk of moderate traumatic brain injury (TBI), and a 4.3-fold increased risk of AD with severe TBI. Believed to increase risk by increasing beta-amyloid and tau proteins. eg falls MVA sports injuries [19]
- History of depression
- Progression of Parkinson-like symptoms in the elderly
- Hyperhomocysteinemia
- Folate deficiency
- Hyperinsulinemia[20]
- Lower educational attainment
- Sleep disturbances
- High blood pressure in midlife
- Hyper/hypothyroidism [21]
Dementia Risk Factors
[22]
There are also factors that can help prevent people from developing Alzheimer’s disease.
The Possible Protective Factors
The following factors have been suggested to reduce the risk of Alzheimer’s disease:[23]
- Apolipoprotein E2 gene
- Regular fish consumption
- Consume omega-3 fatty acids regularly
- Years of higher education
- Regular exercise has cardiovascular benefits, increasing oxygen and blood to the brain
- Diets low in sugar and saturated fats
- Prevention of head trauma & falls
- NSAID therapy
- Moderate Alcohol intake
- Get enough vitamins CE B6 and B12 and folic acid.
10 Warning Signs of Early Alzheimer’s Diagnosis
Here are ten signs that may indicate early Alzheimer’s disease:[24]
1. Memory changes that disrupt daily life.
- One of the most common symptoms of Alzheimer’s
- Forgetting recently learned information
- Important dates or events
- Repeating questions or information
- Relying on memory aids or family members
- Typical forgetfulness: sometimes forgets names or appointments, but remembers later.
2. The challenge of planning or solving a problem.
- Changes in ability to make and follow plans or crunch numbers; such as following familiar recipes or keeping track of bills
- Difficulty concentrating on activities or taking longer to complete
- Typical problem with planning: Occasional mistakes when balancing checkbooks.
3. Difficulty performing familiar tasks at home at work or at leisure.
- Difficulty completing daily tasks
- Trouble driving to a familiar place
- Managing a budget
- Remembering rules to a favorite game
- Typical Problems: Occasionally need help using the microwave’s settings or recording a TV show.
4. Confusion with time or place.
- Forget the date, season or passage of time
- can’t understand what’s happening right now
- May forget how they got somewhere
- Typical trouble: getting confused about the day of the week, only to figure it out later.
5. Difficulty understanding visual images and spatial relationships.
- Reading
- Judging distances
- Determining color or contrast
- Altered perception: if you don’t recognize yourself in a mirror
- Typical: Changes in vision associated with cataracts.
6. New oral or written word problems.
- Unable to follow or join conversations.
- May stop in the middle of a conversation, not knowing how to continue or may repeat themselves.
- May have difficulty using vocabulary or finding the right word or (for example, referring to a “watch” as a “hand clock” for people with Alzheimer’s) May have difficulty following or joining conversations. They may stop in the middle of a conversation, not know how to proceed or they may repeat yourself. They may have trouble with vocabulary, finding the right words or calling things by the wrong names (for example, calling a watch a hand clock). What is typical? Sometimes the right words can’t be found.
7. Misplace things and lose the ability to return the same way
- Things may be placed in unusual places
- May lose things and not be able to retrace their steps to find them
- May accuse others of stealing
- These behaviors may increase in frequency over time
- Typical: Often misplaces things, such as glasses or remote controls.
8. Decreased or poor judgment
- Changes in judgement or decision-making
- Poor money judgment or may offer large sums to telemarketers
- May pay little attention to grooming or hygiene
- Typical: occasionally makes bad decisions
9. Quit working or socializing
- Detach yourself from hobbies, social activities, work projects or sports
- Difficulty keeping up with a favorite sports team or remembering how to accomplish a favorite hobby.
- May avoid being social activities
- Typical: Sometimes tired of work, family, and social obligations.
10. Changes in mood and personality
- Suspicious
- Depressed
- Fearful or anxious
- Anxiety about working at home with friends or being outside of your comfort zone
- Typical: develops very specific ways of doing things, becomes irritable when routine is disrupted
Stages of Alzheimer’s Disease
Alzheimer’s disease may go through the following stages [25][26]:
Mild Alzheimer’s disease (early stage)
- May function independently: may drive work or may be separate from social activities
- Memory loss: familiar words locations of objects names of new people recent reading
- Difficulties noted by family, friends and physicians: Challenges with activities at home or difficulties with work schedules
- 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, delusional, compulsive, repetitive behaviors
- Exacerbated memory loss: Amnesia about personal history can’t recall addresses, phone numbers, or the high schools they graduated from
- Reduced independence: Difficulty controlling bowel movements Increased risk of mind wandering or loss of dependence, choosing appropriate clothing for the event or season Increased confusion
- Impaired cognition and abstract thinking
- Restlessness and agitation
- Wandering, “sundown syndrome”
- Inability to perform activities of daily living
- Impaired judgement
- Inappropriate social behavior
- Lack of insight, abstract thinking
- Repetitive behavior
- Voracious appetite
Severe Alzheimer’s disease (late stage)
- Decreased responsiveness to the environment: Decreased ability to communicate, may speak in small phrases, decreased awareness of experiences and surroundings
- Dependence on caregiver: decreased physical function: walking, sitting and swallowing; increased vulnerability to infectious incontinence
- Emaciation, indifference to food
- Inability to communicate
- Urinary and fecal incontinence
- Seizures
Associated Co-morbidities
High levels of comorbidity were associated with poor self-care, reduced mobility and incontinence. Increased comorbidities were associated with lower cognitive scores observed by the Mini-Mental State Examination. [27]
- Vascular Disease
- Thyroid Disease
- Sleep Apnea
- Osteoporosis
- Glaucoma
- Cancer
- Rheumatoid Arthritis & NSAIDs
- Depression
Medications
Listed below are some common medications used to treat Alzheimer’s symptoms. There are other treatments, such as antioxidants, anti-inflammatory drugs, and estrogen replacement therapy in women, that can prevent or delay the onset of the disease. [28][29]
- Donepezil – (Aricept) has only modest benefits, but it does help slow loss of function and reduce the burden on caregivers. It is equally effective in patients with and without apolipoprotein E4. It may even have some benefits for patients with moderate to severe Alzheimer’s disease.
- Rivastigmine – (Exelon) targets two enzymes (the main ones being acetylcholinesterase and butyrylcholinesterase). The drug may be especially beneficial for patients with rapidly progressive disease. Even in patients with advanced disease, the drug slowed or slightly improved the disease state. (Rivastigmine may cause significantly more side effects than donepezil, including nausea, vomiting, and headache.
- Galantamine – (Reminyl) Galantamine not only protects the cholinergic system, but also acts on nicotine receptors, which are also depleted in Alzheimer’s disease. It improves behaviors of daily living and mental function, including in patients with mild to advanced moderate Alzheimer’s disease and those with both Alzheimer’s and vascular dementia. Some studies suggest that the effects of galantamine may last a year or more, and may even increase over time.
- Tacrine – (Cognex) Only modest benefit, no benefit in patients with the apolipoprotein E4 gene. In high doses, it can also damage the liver. In general, newer cholinergic-protective drugs that do not pose much risk to the liver are now being used to treat Alzheimer’s disease.
- Memantine – (Namenda) targets the N-methyl-aspartate receptor for moderate to severe Alzheimer’s disease.
- Selegiline – (Eldepryl) used to treat Parkinson’s disease appears to prolong the time to the next stage of disability.
Diagnostic Tests/Lab Tests/Lab Values
Currently, the diagnosis of Alzheimer’s relies primarily on signs and symptoms of mental decline. Primary care physicians and physical therapists can screen for signs of dementia, and the next section describes tools for identifying signs of dementia or Alzheimer’s disease in patients. the following Current research advances are used to rule out other possible diagnoses while confirming the progression of Alzheimer’s disease. Onset occurs between the ages of 40 and 90, most often after the age of 65. [30]
Biomarkers
Experts are developing “biological markers” to identify the presence of disease. Examples of biomarkers being investigated for disease confirmation are beta-amyloid and tau levels in cerebrospinal fluid and changes in brain injury. These Biomarkers have been suggested to change throughout the course of the disease. Biomarkers have not been validated.
Neuro-imaging
Standard imaging used to detect changes in a patient’s brain includes magnetic resonance imaging (MRI) and computed tomography (CT). Imaging is mainly used to rule out other conditions that, although similar to Alzheimer’s disease, require different treatment, such as tumors, small or large strokes and trauma or fluid in the brain. Cerebrospinal fluid (CSF) The protein CSF can be seen with a lumbar puncture or spinal tap. Changes in cerebrospinal fluid involving two proteins, beta-amyloid and tau, promote abnormal deposits in the brain throughout stages of Alzheimer’s disease, study shows related to disease. One challenge the researchers faced was the observed variability in protein levels between institutions. Research is currently underway to develop criteria for CSF protein associated with Alzheimer’s disease.
Genetic Testing
Three genetically rare genes have been linked to causing Alzheimer’s disease, such as amyloid precursor protein (APP) Presenilin-1 (PS-1) Presenilin-2 (PS-2). Another gene associated with a higher risk of Alzheimer’s disease is apolipoprotein 4 (APOE-4). genetic testing is not It is currently recommended outside of research because there are currently no treatments that can alter the course of Alzheimer’s disease.
Society of Nuclear Medicine and Molecular Imaging (SNMMI) Standards for Amyloid Imaging:
Structural Imaging
- People with Alzheimer’s shrink dramatically as disease progresses
- Significant shrinkage of the hippocampus may be a sign of early-onset Alzheimer’s
- No criteria were developed for values of reduced size to indicate Alzheimer’s disease
Functional Imaging
- Positron emission tomography (PET) and other functional methods show reduced brain cell activity in AD patients
- Lower blood sugar observed in areas important for memory learning and problem solving
- No criteria for inactivity values for confirming Alzheimer’s disease
Molecular Imaging
- Biological clues may indicate progression of Alzheimer’s disease before changes in brain structure or function, memory, thinking and reasoning
- Pittsburgh Compound B (PIB) Amyvid Vizamyl or Neuraceq have been developed since 2012 to identify amyloid plaques. Although amyloid plaques can be identified on positron emission tomography (PET), this cannot be used as a diagnostic criterion because not all individuals with amyloid plaques are symptomatic.
- Therefore, the use of tracers for the diagnosis of Alzheimer’s patients is not currently recommended.
Screening Tools
Objective tools have been validated in physical therapy practice to screen for AD, such as the Mini-Cog Mini-Mental State Examination (MMSE) Clock Mapping and Neurobehavioral Cognitive Status Examination. A pilot study develops a research protocol to help detect dementia early Diseases were identified using the Timed Up-and-Go (TUG) test and a verbal task of naming different animals [31].
Screening tools can be selected based on sensitivity, specificity, and time to administer the screen.
The mini-mental status exam has been validated for detecting possible dementia, but the timing of the test prevented doctors from using it. MMSE takes 5-12 minutes to administer and consists of 20 questions in 5 categories to observe directed memory attention concentration language and Construction [32].
- Cut off scores: (out of 25)
- ≥ 24 = no impairment
- 18-23 = mild impairment
- ≤ 17 = severe impairment
- < 23 is generally considered a sign of cognitive impairment and is associated with at least 79% of dementia diagnoses (Lancu & Olmer 2006) [33]
Mini-Cog takes 2-4 minutes to manage and combines build (clock drawing) and memory. [34]
- Below are current findings on how well the tests perform in terms of sensitivity to judge the differential diagnosis of AD, and it is best to group these tests together in order to exclude the possibility of dementia or AD.
- A score < 3 indicates clinically significant cognitive impairment on a scale of 10
[35]
Causes
The exact cause of Alzheimer’s disease remains unknown. Early-onset Alzheimer’s is believed to be caused by genetic mutations. Late-onset Alzheimer’s disease is caused by complex changes in the brain over a period of time. It is believed that combined with Factors from environmental genetics and lifestyle. The importance of individual factors to an individual may vary in each person with the disorder. See Risk Factors under Features/Clinical Presentation above for more information. [36]
Systemic Involvement
The most noticeable symptoms initially are those related to cognition and memory. However, Alzheimer’s disease can affect other parts of the body, causing symptoms beyond those affecting memory and cognition. Depending on the brain region, there are usually obvious signs of abnormal movement affected by disease. The presence of tremor may be associated with an increased risk of cognitive decline, the presence of bradykinesia with an increased risk of functional decline, and the presence of postural gait disturbance with an increased risk of hospitalization and death. also Patients may experience sleep, eating, and sexual behavior disturbances. [37]
Medical Management
There is currently no cure for Alzheimer’s disease, so medical management focuses on maintaining quality of life, maximizing function, enhancing cognition, creating a safe environment, and promoting self-engagement [38]. Maximizing function in dementia includes monitoring the patient’s Health and cognition Patient and family education Initiation of drug and non-pharmacological treatments.
- Cognitive symptom treatment
- Although disease progression cannot be changed, it can be slowed with the drugs listed above
- Behavioral and Psychological Symptom Treatment
- Agitation, aggression, depression, and psychosis are the leading reasons for assisted living or nursing home placements.
- Assessment of sudden onset behavior is important to improve patient comfort, safety and well-being.
- Monitoring Alzheimer’s disease
- Patients should return to the clinic regularly so that doctors can monitor the course of Alzheimer’s disease (behavioral and cognitive changes).
- Regular follow-up appointments allow treatment to be adjusted to meet the patient’s needs.
- Non-medical/social issues that patients need to address:
- Need for ongoing support & information
- A living will or power of attorney
- Review finances/plans for future and end-of-life care
- Alternative Treatment
- In addition to the medicines prescribed by doctors, there are also concerns about alternative treatments. If any problems come to your attention, your doctor should be notified.
- Importance of Caregiver
- Many caregivers seek to meet the needs of physicians and patients, which increases the incidence of stress and depression. Physicians should continue to monitor the status of caregivers, watch for burnout and provide them with resources.
- Aducanumab
- This is a monoclonal antibody drug against amyloid beta, designed to treat Alzheimer’s disease. Sold under the brand name Aduhelm, it targets isolated forms of amyloid beta (Aβ) in the brains of Alzheimer’s patients to reduce their accumulation. [39]
- The drug was approved by the Food and Drug Administration under the accelerated approval pathway in June 2021. The drug is the first of its kind approved to treat Alzheimer’s disease and the first new treatment for the disease since 2003, the FDA reported. Aducanumab has also been reported Becoming the first drug to address the pathophysiology of Alzheimer’s disease. [39]
Physical Therapy Management
[40]
It is important to modify risk factors that can be changed through lifestyle activities. High blood pressure has been shown to interact with specific genotypes at risk for Alzheimer’s disease. This interaction increases cognitive health in midlife and the elderly. Therefore, when at risk, it is very important to control blood pressure, which can be done through exercise [41].
Physical activity is important in the life of a person with Alzheimer’s disease, and the sooner the better. “Given recent clinical evidence, early application of physical activity to attenuate pathological processes and cognitive decline is imperative Trials have shown that interventions applied earlier in the Alzheimer’s disease course are more likely to achieve disease remission, while those applied later, after the onset of neuronal degeneration, have significant but more limited effects. “[42]
A community-based exercise program has been shown to improve several areas of life for people with Alzheimer’s disease. In a study by Vreugdenhil et al. Community-dwelling Alzheimer’s patients add daily home exercise program and supervised walking to usual care plan. Those who participated in additional exercise improved cognitive activity and instrumental activities of daily living [43].
It has been suggested that aerobic exercise in the form of walking and upper-body cycling ergometers is especially helpful in improving exercise tolerance and quality of life in patients with Alzheimer’s disease [44]. In addition to cardio training, strength training is also supported Research. The combination of these two activities has shown greater improvements in cognition than aerobic training alone [45].
People with dementia are at higher risk of falls than the average population of community-dwelling older adults. [46] A study showed that poor vision leads to poorer executive function, which in turn leads to inadequate balance control, thus demonstrating that The importance of assessing executive function in addition to vision and balance in older adults with Alzheimer’s dementia. [47]
Preliminary research has been done looking at fall prevention training for people with intellectual disabilities such as Alzheimer’s disease. Using a modified Otago exercise program is effective in reducing the risk of falls in some adults with intellectual disabilities, a study finds Disability [48]. A pilot study found that the Berg Balance Scale has relative reliability values that support its use in a clinical setting. However, MDC values for this population have not been determined [49]. More research is needed in this area to best assess fall risk in this population.
Often, when a physical therapist works with a patient diagnosed with Alzheimer’s disease, the patient may be in a structured living situation because they have progressed to a stage of the disease that their caregivers cannot give appropriate attention to patients because they need. Physical therapy can provide patients with activities they can perform successfully and can also help improve their breathing flexibility and endurance. Restlessness and mind-wandering can be classic symptoms of Alzheimer’s patients and can be managed with physical therapy Therapy (release some energy with exercise). These exercises can help reduce the nocturnal wanderings known as sundowners.
Transition care [50] provides a time-limited, goal-oriented and treatment-centred package of services for older adults after discharge that includes low-intensity therapy (such as physical therapy and occupational therapy), social work and nursing support, or individual care. it is designed Improve independence and function to delay their entry into residential aged care. A qualitative study demonstrated better outcomes for older patients (over 80 years) who had family involvement assisting with physical therapy care in a transitional care setting [51].
Group therapy can also be successful for people with Alzheimer’s disease, but the treatment cannot provide more stimulation than the patient can handle. Repetition and encouragement are also very important to maintain the patient’s confidence and help remember practise. Knowing the patient is important for the therapist because it enables better communication by using words and terminology that a particular patient may be more familiar with. The preferred practice pattern is 5E: Impaired motor function and sensory integrity associated with progression Diseases of the central nervous system. Physiotherapists can use the Global Exacerbation Scale to assess the extent of dementia. When Alzheimer’s patients receive a comprehensive cognitive stimulation program, it enhances neuroplasticity in patients. exercise can It also helps to improve the patient’s activity balance and ROM as well as improve mood [52].
Staying physically and socially active may help reduce your risk of dementia as well as keep you mentally active. A randomized controlled trial showed favorable results of an exercise and gardening intervention program for older adults with depression and memory problems [53].
Dietary Management
It has been found that maintaining a healthy diet may help prevent or slow the progression of Alzheimer’s disease. A diet low in fat, high in omega-3 oils, and high in dark vegetables and fruits is recommended, while adding vitamin C to the diet along with coenzyme Q10 and folic acid may help Reduce the risk of Alzheimer’s disease. No single aspect of the diet appears to provide neuroprotection, but rather these items work together to reduce the risk of AD. [54] There is also interest in the use of antioxidants such as vitamin E and ginkgo and anti-inflammatory Medicines and estrogen replacement therapy for women. [55]
Differential Diagnosis
- Pick’s Disease
- Lewy Body Dementia
- Frontotemporal Dementia
- Dementia from multiple medications
- Other potentially reversible causes of dementia
Low Resource Health Settings
More than half of people with dementia live in low- and middle-income countries. Alzheimer’s disease, other dementias and non-communicable diseases are expected to continue to burden health systems across Sub-Saharan Africa as country populations age and infectious diseases spread Mortality and morbidity decreased [56]. The number of people living with Alzheimer’s disease and dementia in general is estimated to be growing at a much faster rate in upper-middle-income, lower-middle-income, and low-income countries (LMICs) than in high-income countries [57]. general lack of awareness The disease spreads in the population, so patients do not seek medical care and do not receive the treatment they need. As such, it is underrecognized, underdisclosed and underregulated, especially in low- and middle-income countries [58]. The living environment also usually poses little cognitive challenge because Families may not understand the behavior of their relatives [59]. Cognitive and functional assessment tools used in many low- and middle-income countries were originally developed and validated in high-income countries. It needs to be tuned for more efficient use in LMIC [60].
References
- ↑ Anand, R., Gill, K.D. and Mahdi, A.A. (2014) ‘Therapeutics of Alzheimers disease: past, present and future’, Neuropharmacology, 76, 27-50
- ↑ Alzheimer’s Disease & Dementia [Internet]. Alzheimer’s Association. [cited 2017Apr1]. Available from:http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Alzheimer’s Disease & Dementia [Internet]. Alzheimer’s Association. [cited 2017Apr1]. Available from: http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp
- ↑ Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
- ↑ actionalz. What is Alzheimer’s Disease?. Available from: http://www.youtube.com/watch?v=9Wv9jrk-gXc [last accessed 08/12/12]
- ↑ Jump up to:7.0 7.1 7.2 wenk, G.L. (2003) ‘Neuropathological changes in Alzheimers disease’, Journal of clinical psychiatry, 64, 7-10
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Reitz C, Mayeux R. Alzheimer disease: Epidemiology, diagnostic criteria, risk factors and biomarkers. Biochem Pharmacol. 2014, 88; 4: 640-651. Accessed 21 November 2018.
- ↑ Jump up to:10.0 10.1 10.2 10.3 Alzheimer’s Facts and Figures [Internet]. Latest Facts; Figures Report | Alzheimer’s Association. 2021 [cited 2022 Jan29]. Available from: http://www.alz.org/facts/
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Latest Alzheimer’s Facts and Figures [Internet]. Latest Facts & Figures Report | Alzheimer’s Association. 2016 [cited 2017Apr1]. Available from: http://www.alz.org/facts/
- ↑ Naharci MI, Buyukturan O, Cintosun U, Doruk H, Tasci I. Functional status of older adults with dementia at the end of life: Is there still anything to do?. Indian journal of palliative care. 2019 Apr;25(2):197.
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Latest Alzheimer’s Facts and Figures [Internet]. Latest Facts; Figures Report | Alzheimer’s Association. 2016 [cited 2017Apr1]. Available from: http://www.alz.org/facts/
- ↑ Traumatic Brain Injury | Signs, Symptoms, and Diagnosis [Internet]. Dementia. [cited 2017Apr1]. Available from: http://www.alz.org/dementia/traumatic-brain-injury-head-trauma-symptoms.asp
- ↑ Latest Alzheimer’s Facts and Figures [Internet]. Latest Facts; Figures Report | Alzheimer’s Association. 2016 [cited 2017Apr1]. Available from: http://www.alz.org/facts/
- ↑ Duthie A, Chew D, Soiza RL. Non-psychiatric comorbidity associated with Alzheimer’s disease. Qjm [Internet]. 2011 [cited 2017Apr1];104(11):913–20. Available from: https://academic.oup.com/qjmed/article/104/11/913/1563428/Non-psychiatric-comorbidity-associated-with
- ↑ Duthie A, Chew D, Soiza RL. Non-psychiatric comorbidity associated with Alzheimer’s disease. Qjm [Internet]. 2011 [cited 2017Apr1];104(11):913–20. Available from: https://academic.oup.com/qjmed/article/104/11/913/1563428/Non-psychiatric-comorbidity-associated-with
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Know the 10 Signs of Alzheimer’s Disease [Internet]. Know the 10 Signs of Alzheimer’s Disease. [cited 2017Apr3]. Available from: http://alz.org/10-signs-symptoms-alzheimers-dementia.asp
- ↑ Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
- ↑ Stages of Alzheimer’s Symptoms [Internet]. Alzheimer’s Association. [cited 2017Apr1]. Available from: http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
- ↑ Duthie A, Chew D, Soiza RL. Non-psychiatric comorbidity associated with Alzheimer’s disease. Qjm [Internet]. 2011 [cited 2017Apr1];104(11):913–20. Available from: https://academic.oup.com/qjmed/article/104/11/913/1563428/Non-psychiatric-comorbidity-associated-with
- ↑ Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Alzheimer’s & Dementia Testing Advances | Research Center [Internet]. Alzheimer’s Association. [cited 2017Apr3]. Available from: http://www.alz.org/research/science/earlier_alzheimers_diagnosis.asp
- ↑ 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.
- ↑ Benson AD, Slavin MJ, Tran T-T, Petrella JR. Screening for Early Alzheimer’s Disease: Is There Still a Role for the Mini-Mental State Examination? The Primary Care Companion [Internet]. [cited 2017Apr1]; Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1079697/
- ↑ Rehab Measures – Mini-Mental State Examination [Internet]. The Rehabilitation Measures Database. [cited 2017Apr1]. Available from: http://www.rehabmeasures.org/Lists/RehabMeasures/DispForm.aspx?ID=912
- ↑ Borson S, Scanlan JM, Chen P, Ganguli M. The Mini-Cog as a Screen for Dementia: Validation in a Population-Based Sample. Journal of the American Geriatrics Society. 2003;51(10):1451–4.
- ↑ Borson S, Scanlan JM, Chen P, Ganguli M. The Mini-Cog as a Screen for Dementia: Validation in a Population-Based Sample. Journal of the American Geriatrics Society. 2003;51(10):1451–4.
- ↑ About Alzheimer’s Disease: Causes [Internet]. National Institutes of Health. U.S. Department of Health and Human Services; [cited 2017Apr3]. Available from: https://www.nia.nih.gov/alzheimers/topics/causes
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ 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
- ↑ Jump up to:39.0 39.1 “FDA Grants Accelerated Approval for Alzheimer’s Drug”. U.S. Food and Drug Administration (FDA) (Press release). 7 June 2021. Accessed on 29 January 2022. Available from: https://www.fda.gov/news-events/press-announcements/fda-grants-accelerated-approval-alzheimers-drug
- ↑ 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
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Phillips, C. et al. “The Link Between Physical Activity And Cognitive Dysfunction In Alzheimer Disease”. Physical Therapy 95.7 (2015): 1046-1060. Web. 1 Apr. 2017.
- ↑ Vreugdenhil, Anthea et al. “A Community-Based Exercise Programme To Improve Functional Ability In People With Alzheimer’S Disease: A Randomized Controlled Trial”. Scandinavian Journal of Caring Sciences 26.1 (2011): 12-19. Web. 1 Apr. 2017.
- ↑ Mahmoud S. “Role of aerobic exercise training in changing exercise tolerance and quality of life in Alzheimer’s disease”. European journal of general medicine. 2011;8(1):1-6. Web. 1 Apr. 2017.
- ↑ Manckoundia, Patrick et al. “Impact Of Ambulatory Physiotherapy On Motor Abilities Of Elderly Subjects With Alzheimer’s Disease”. Geriatrics;; Gerontology International 14.1 (2013): 167-175. Web. 1 Apr. 2017.
- ↑ Renfro M, Bainbridge D, Smith M. Validation of Evidence-Based Fall Prevention Programs for Adults with Intellectual and/or Developmental Disorders: A Modified Otago Exercise Program. Frontiers in Public Health. 2016;4. Web. 1 Apr. 2017.
- ↑ 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.
- ↑ Muir-Hunter S, Graham L, Montero Odasso M. Reliability of the Berg Balance Scale as a Clinical Measure of Balance in Community-Dwelling Older Adults with Mild to Moderate Alzheimer Disease: A Pilot Study. Physiotherapy Canada. 2015;67(3):255-262. Web. 1 Apr. 2017.
- ↑ Renfro M, Bainbridge D, Smith M. Validation of Evidence-Based Fall Prevention Programs for Adults with Intellectual and/or Developmental Disorders: A Modified Otago Exercise Program. Frontiers in Public Health. 2016;4. Web. 1 Apr. 2017.
- ↑ Transition Care Programme. Aging and aged care.Accessed from ☀https://agedcare.health.gov.au/programs-services/flexible-care/transition-care-programme on 4/12/2019.
- ↑ Lawler K, Taylor NF, Shields N. Family-assisted therapy empowered families of older people transitioning from hospital to the community: a qualitative study. Journal of physiotherapy. 2019 Jun 13.
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Makizako H, Tsutsumimoto K, Makino K, Nakakubo S, Liu-Ambrose T, Shimada H. Exercise and Horticultural Programs for Older Adults with Depressive Symptoms and Memory Problems: A Randomized Controlled Trial. Journal of Clinical Medicine. 2020 Jan;9(1):99.
- ↑ Goodman CC, Fuller KS. Pathology: implications for the physical therapist. St. Louis, MO: Elsevier Saunders; 2015.
- ↑ Porth C. Pathopysiology Concepts of Altered Health States. Philadelphia PA: Lippincott and Wilkins; 2005.
- ↑ 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.
- ↑ Global Prevalence. Available from: https://www.dementiastatistics.org/statistics/global-prevalence/ ( Accessed, 20/09/2021).
- ↑ 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.
- ↑ 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).
- ↑ 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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