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Background
Alzheimer disease is a neurological condition that causes a gradual decline in behavioral and cognitive abilities such as memory, interpretation, language, concentration, thinking, and decisions.
Alzheimer is the most prevalent dementia, contributing to two-thirds of dementia cases in persons 65 and older.
Early onset before age 65 is rare and occurs in less than 10% of Alzheimer patients. There is no cure for Alzheimer, although a recent development has shown progress in slowing cognitive decline.
Epidemiology
The global incidence of dementia is estimated at 24 million individuals, which is expected to double by 2050. Alzheimer disease is predicted to cost $172 billion in health care costs in the United States annually. After the age of 65, the risk of Alzheimer increases every five years.
The age-specific incidence rises significantly from less than 1% per year before age 65 to 6% per year beyond age 85. The prevalence rate rises from 10% at age 65 to 40% after age 85. Women have a slightly greater incidence rate of Alzheimer disease, especially after age 85.
Anatomy
Pathophysiology
Alzheimer disease is characterized by the buildup of aberrant neurofibrillary tangles and neuritic plaques in the brain. An increase in beta-amyloid 42 levels produce amyloid aggregation, which causes neurotoxicity. Beta-amyloid 42 promotes aggregate fibrillary amyloid protein production over normal APP breakdown.
The APP gene is found on chromosome 21, related to familial Alzheimer disease. Amyloid deposition occurs in Alzheimer disease surrounding meningeal and cerebral arteries, as well as gray matter. Gray matter deposits are multifocal and create miliary structures known as plaques.
Tau is hyperphosphorylated because of extracellular beta-amyloid aggregation, leading to tau aggregates’ production. Tau aggregates generate neurofibrillary tangles, which are tangled paired helical filaments. They begin in the hippocampus and can spread across the cerebral cortex. Tau-aggregates accumulate within neurons.
Braak and Braak created a staging approach based on the topographic staging of neurofibrillary tangles into six phases. This Braak staging is an essential aspect of the National Institute on Aging and Reagan Institute neuropathological criteria for Alzheimer diagnosis. Tangles are more strongly linked to Alzheimer disease than plaques.
Alzheimer disease is an autosomal dominant condition has complete penetrance. Mutations in three genes have been associated with the autosomal dominant type of the disease: the AAP gene on chromosome 21, Presenilin1 on chromosome 14, and Presenilin2 on chromosome 1. APP mutations may enhance beta-amyloid peptide production and aggregation.
PSEN1 & PSEN2 mutations cause beta-amyloid aggregation by interfering with gamma-secretase processing. Mutations in these three genes are responsible for 5% to 10% of all cases and early-onset Alzheimer disease predominance.
Etiology
Alzheimer is a neurological condition that causes neuronal cell loss over time. It usually begins in the hippocampus’s entorhinal cortex. Both early and late-onset Alzheimer disease has a hereditary component.
Trisomy 21 is a risk factor for developing dementia at a young age. Alzheimer disease has been linked to several risk factors. The primary risk factor for Alzheimer disease is becoming older.
Traumatic brain injury, older parental age, depression, cardiovascular and cerebrovascular illness, a family history of dementia, smoking, elevated homocysteine levels, and the presence of the APOE e4 allele have all been linked to an increased risk of Alzheimer disease.
Genetics
Prognostic Factors
Alzheimer is usually progressing. A person diagnosed with Alzheimer disease at age 65 has an average life expectancy of 4 to 8 years.
Some people with Alzheimer might live for up to 20 years after the first symptoms appear. Pneumonia is the leading cause of mortality in Alzheimer disease.
Clinical History
Age:
Associated Comorbidities:
Acuity of Presentation:
Physical Examination
The objective of the physical examination is to evaluate different aspects of an individual’s health and neurological condition. Below are key elements of the physical examination for Alzheimer’s disease:
Neurological Examination:
Vital Signs:
General Physical Examination:
Gait and Mobility Assessment:
Sensory Examination:
Functional Assessment:
Psychiatric Assessment:
Laboratory and Ancillary Tests:
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Various conditions that may be considered in the differential diagnosis of Alzheimer’s disease include:
Vascular Dementia (VaD):
Vascular dementia results from compromised blood flow to the brain, often due to strokes or other vascular issues. Symptoms can overlap with those of Alzheimer’s disease.
Lewy Body Dementia (LBD):
LBD is characterized by the presence of Lewy bodies in the brain, leading to cognitive and motor symptoms. It shares certain features with both Alzheimer’s disease and Parkinson’s disease.
Frontotemporal Dementia (FTD):
FTD encompasses a group of disorders that predominantly affect the frontal and temporal lobes of the brain, causing changes in personality, behavior, and language. Memory loss may not be as apparent in the early stages.
Parkinson’s Disease Dementia (PDD):
Individuals with Parkinson’s disease may develop dementia as the condition progresses. Cognitive impairment may manifest as memory loss and executive dysfunction.
Normal Pressure Hydrocephalus (NPH):
NPH is characterized by an abnormal accumulation of cerebrospinal fluid in the brain, leading to gait disturbances, urinary incontinence, and cognitive decline.
Huntington’s Disease:
Huntington’s disease is a genetic disorder resulting in progressive degeneration of nerve cells in the brain, causing both motor and cognitive symptoms.
Chronic Traumatic Encephalopathy (CTE):
CTE is associated with repeated head injuries, as observed in athletes participating in contact sports, and can result in cognitive and behavioral changes.
Metabolic and Endocrine Disorders:
Conditions such as hypothyroidism, vitamin B12 deficiency, and metabolic disorders can induce cognitive impairment and should be ruled out.
Infections:
Chronic infections, such as neurosyphilis or HIV-related dementia, can induce cognitive decline.
Depression and Anxiety:
Mood disorders, especially in older adults, may occasionally present with cognitive symptoms that could be confused with dementia.
Medication Side Effects:
Some medications, particularly those with anticholinergic effects, may contribute to cognitive impairment.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Medication Management:
Non-Pharmacological Approaches:
Supportive Care and Education:
Healthy Lifestyle Practices:
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
non-pharmacological-treatment-of-alzheimer-disease
Lifestyle modifications:
Use of Cholinesterase Inhibitors in the treatment of Alzheimer Disease
Cholinesterase inhibitors are a class of medications commonly used in the treatment of Alzheimer’s disease. They increase the levels of acetylcholine, a neurotransmitter involved in memory and cognitive function.
Donepezil (Aricept, Aricept ODT):
Rivastigmine (Exelon, Exelon Patch):
Galantamine (Razadyne, Razadyne ER):
Donepezil transdermal (Adlarity):
Use of Anti-amyloid beta monoclonal antibodies in the treatment of Alzheimer Disease
Anti-amyloid beta monoclonal antibodies represent a newer class of medications designed to target and remove beta-amyloid plaques, which are characteristic pathological features of Alzheimer’s disease (AD).
Aducanumab (Aduhelm):
Lecanemab (Leqembi):
Use of NMDA antagonist in the treatment of Alzheimer Disease
Memantine (Namenda, Namenda XR):
Use of Combination Drugs in the treatment of Alzheimer Disease
Combination drugs, such as Memantine/Donepezil (brand name: Namzaric), are formulations that combine multiple medications to treat Alzheimer’s disease. Namzaric specifically combines two active ingredients: memantine, an NMDA receptor antagonist, and donepezil, a cholinesterase inhibitor.
Memantine/Donepezil (Namzaric):
Â
Use of Nutritional Supplement in the treatment of Alzheimer Disease
Axona, also known for its active ingredient Caprylidene, is a nutritional supplement that has been explored in the context of Alzheimer’s disease management. It is a medical food designed to provide an alternative energy source for the brain.
Caprylidene (Axona):
Use of Diagnostic Imaging Agents in Alzheimer Disease
Diagnostic imaging agents are not used in treating Alzheimer’s disease; instead, they are used in diagnosing and evaluating the disease. These agents are radiopharmaceuticals designed for positron emission tomography (PET) imaging to visualize and detect the beta-amyloid plaques in brain, a hallmark of Alzheimer’s disease.
deep-brain-stimulation-in-the-treatment-of-alzheimer-disease
Deep brain stimulation (DBS) is not widely established as a standard treatment for Alzheimer’s disease. Deep brain stimulation involves implanting electrodes into the specific areas of the brain and connecting them to a pulse generator placed under the skin. The electrodes deliver electrical impulses to modulate abnormal brain activity. The use of deep brain stimulation in Alzheimer’s disease has been explored in research and clinical trials, but the results have been mixed, and the procedure is not yet considered a routine or proven treatment. Alzheimer’s disease is a neurodegenerative disorder, and its underlying mechanisms involve widespread changes and damage in the brain. While DBS has shown promise in addressing certain symptoms in other neurological conditions, its application to Alzheimer’s disease is still under investigation. The clinical trials have explored the potential benefits of deep brain stimulation in Alzheimer’s disease. These studies often focus on targeting specific brain regions involved in memory and cognition. The results of studies have been variable, with some showing potential cognitive improvements and others showing limited or no benefits. The variability in outcomes may be influenced by factors such as patient selection, stimulation parameters, and the stage of Alzheimer’s disease.
phases-of-management-of-alzheimer-disease
Acute Phase Management:
Acute Phase Management:
Medication
Oral- mild-to-moderate Initial dose: 1.5 mg capsule orally every 12hr; increase it up to 1.5 mg/dose every 2 weeks Do not exceed the dose up to 6 mg orally every 12 hours Maintenance dose: 3-6 mg capsule orally every 12 hours Transdermal- mild, moderate, and severe Initial dose: Apply the patch 4.6 mg every 24 hours; increase it up to 9.5 mg every 24 hours minimum 4 weeks; further after additional 4 weeks increase dose up to 13.3 mg patch Mild-to-moderate: 9.5-13.3 mg every 24 hours Moderate-to-severe: 13.3 mg every 24 hours Replace with new patch every 24 hours
Initial Conventional: 4 mg orally 2 times a day ER: 8 mg orally once a day Maintenance Conventional: Titrate to 8-12 mg orally two times and increase up to 4 mg every 12 hours for <4 weeks ER: 16-24 mg orally once a day and increase by 8 mg a day for <4 weeks
10 mg of memantine two times a day or 28 mg of memantine ER once a day; and donepezil 10 mg once a day: 28 mg Memantine ER and donepezil 10 mg orally once a day every evening
5 mg tablet orally may be increased up to 5 mg/day each week. Maintenance dose: 20 mg/day orally twice a day 7 mg PO Capsule-ER may be increased up to 7 mg/day each week Maintenance dose: 28 mg/day orally daily
apply a 5 mg patch once in a week; and increase up to 10 mg patch once a week after 4-6 weeks
Mild/moderate: 5 mg orally daily, may increase up to10 mg after 4-6 weeks Moderate/severe: 5 mg/day orally, increase up to 10 mg/day after 4-6 weeks; and after 3 months increase up to 23 mg/day Administration Take at bedtime and dissolve the drug under the tongue and follow with water
Dose Adjustments
Dose Modification Renal Impairment: Not Available Hepatic Impairment: Not Available
Take 10-15 mg of medication orally every other day to once a day
Indicated for Alzheimer's Disease
100 mg orally three times a day
Senile Dementia and Memory/Cognitive Impairment
100 mg orally three times a day
1.6 to 9.6 grams/day orally
Administer orally twice daily at a dosage range of 50-200 mcg
Indicated for Alzheimer Disease
Administered every four weeks as intravenously infused nearly 21 days apart
Dosing titration regimen:
1-2 Infusions: 1 mg/kg intravenously every 4 weeks
3-4 Infusions: 3 mg/kg intravenously every 4 weeks
5-6 Infusions: 6 mg/kg intravenously every 4 weeks
7 and beyond Infusions: 10 mg/kg intravenously every 4 weeks
Initial dosing involves the administration of 10 grams one time a day over a period of two days
To gradually increase the dosage, it is recommended to administer the drug in 10 grams increments every 2 days until a total of 40 grams is reached, to be taken one time daily on seventh day
It is important to consider a slower titration rate if the patient encounters any adverse events
a maintenance dosage of 40 grams one time a day is recommended to sustain therapeutic efficacy
20 mg given 2 to 3 times daily
Take an initial dose of 10 mg orally four times daily if possible, in between food up to 6 weeks
The maintenance dose may raise up to 20 mg orally four times daily
It may further raise up to 120 mg and 160 mg daily may be done in 6-week intervals
3.6 mg, 7.2 mg, 10.8 mg MSF were given orally to 27 healthy volunteers (between the ages 50 to 72 years) in a randomised, placebo-controlled phase I research. The individuals got the same dosages three times a week for two weeks after a single dose phase and a one-week wash-out period
6
g
Orally 
once a day
1
month
off-label:
In-vivo data suggests intraperitoneal administration of 500 mg/kg for every third day
It is indicated for mild to moderate Alzheimer’s disease
In-vivo studies suggests that administer dose of 5 mg orally every 12 hours for the starting 4 weeks of the investigation and then dose of 10 mg orally every 12 hours for the remaining 4 weeks
Phase II studies were conducted on colorectal, metastatic breast, and non-small-cell lung malignancies. However, there was an end of development in favor of a second-generation analog that had a higher safety rating. Alzheimer's disease therapy was also investigated with this medication. Following the conclusion of the trial, epothilone D's examination of Alzheimer's disease was discontinued
Indicated for the treatment of mild cognitive impairment or mild dementia in Alzheimer disease patients:
10 mg/kg IV infused over approximately 1 hour, given once every two weeks
Note:
This drug has received accelerated approval due to observed reductions in amyloid beta plaques in treated patients
Sustained approval for this indication may hinge upon confirmation of clinical benefits in a subsequent confirmatory trial
It is crucial to confirm the presence of amyloid beta pathology before initiating this treatment
2.5
mg/kg
Tablets
Orally 
once a day
2
weeks
Off-label/br
Loading dose: 2.5mg/kg orally for two weeks
Maintenance dose: 1mg/kg orally for two weeks
Posiphen is under Phase 2/3 clinical trial
Future Trends
Alzheimer disease is a neurological condition that causes a gradual decline in behavioral and cognitive abilities such as memory, interpretation, language, concentration, thinking, and decisions.
Alzheimer is the most prevalent dementia, contributing to two-thirds of dementia cases in persons 65 and older.
Early onset before age 65 is rare and occurs in less than 10% of Alzheimer patients. There is no cure for Alzheimer, although a recent development has shown progress in slowing cognitive decline.
The global incidence of dementia is estimated at 24 million individuals, which is expected to double by 2050. Alzheimer disease is predicted to cost $172 billion in health care costs in the United States annually. After the age of 65, the risk of Alzheimer increases every five years.
The age-specific incidence rises significantly from less than 1% per year before age 65 to 6% per year beyond age 85. The prevalence rate rises from 10% at age 65 to 40% after age 85. Women have a slightly greater incidence rate of Alzheimer disease, especially after age 85.
Alzheimer disease is characterized by the buildup of aberrant neurofibrillary tangles and neuritic plaques in the brain. An increase in beta-amyloid 42 levels produce amyloid aggregation, which causes neurotoxicity. Beta-amyloid 42 promotes aggregate fibrillary amyloid protein production over normal APP breakdown.
The APP gene is found on chromosome 21, related to familial Alzheimer disease. Amyloid deposition occurs in Alzheimer disease surrounding meningeal and cerebral arteries, as well as gray matter. Gray matter deposits are multifocal and create miliary structures known as plaques.
Tau is hyperphosphorylated because of extracellular beta-amyloid aggregation, leading to tau aggregates’ production. Tau aggregates generate neurofibrillary tangles, which are tangled paired helical filaments. They begin in the hippocampus and can spread across the cerebral cortex. Tau-aggregates accumulate within neurons.
Braak and Braak created a staging approach based on the topographic staging of neurofibrillary tangles into six phases. This Braak staging is an essential aspect of the National Institute on Aging and Reagan Institute neuropathological criteria for Alzheimer diagnosis. Tangles are more strongly linked to Alzheimer disease than plaques.
Alzheimer disease is an autosomal dominant condition has complete penetrance. Mutations in three genes have been associated with the autosomal dominant type of the disease: the AAP gene on chromosome 21, Presenilin1 on chromosome 14, and Presenilin2 on chromosome 1. APP mutations may enhance beta-amyloid peptide production and aggregation.
PSEN1 & PSEN2 mutations cause beta-amyloid aggregation by interfering with gamma-secretase processing. Mutations in these three genes are responsible for 5% to 10% of all cases and early-onset Alzheimer disease predominance.
Alzheimer is a neurological condition that causes neuronal cell loss over time. It usually begins in the hippocampus’s entorhinal cortex. Both early and late-onset Alzheimer disease has a hereditary component.
Trisomy 21 is a risk factor for developing dementia at a young age. Alzheimer disease has been linked to several risk factors. The primary risk factor for Alzheimer disease is becoming older.
Traumatic brain injury, older parental age, depression, cardiovascular and cerebrovascular illness, a family history of dementia, smoking, elevated homocysteine levels, and the presence of the APOE e4 allele have all been linked to an increased risk of Alzheimer disease.
Alzheimer is usually progressing. A person diagnosed with Alzheimer disease at age 65 has an average life expectancy of 4 to 8 years.
Some people with Alzheimer might live for up to 20 years after the first symptoms appear. Pneumonia is the leading cause of mortality in Alzheimer disease.
Age:
Associated Comorbidities:
Acuity of Presentation:
The objective of the physical examination is to evaluate different aspects of an individual’s health and neurological condition. Below are key elements of the physical examination for Alzheimer’s disease:
Neurological Examination:
Vital Signs:
General Physical Examination:
Gait and Mobility Assessment:
Sensory Examination:
Functional Assessment:
Psychiatric Assessment:
Laboratory and Ancillary Tests:
Various conditions that may be considered in the differential diagnosis of Alzheimer’s disease include:
Vascular Dementia (VaD):
Vascular dementia results from compromised blood flow to the brain, often due to strokes or other vascular issues. Symptoms can overlap with those of Alzheimer’s disease.
Lewy Body Dementia (LBD):
LBD is characterized by the presence of Lewy bodies in the brain, leading to cognitive and motor symptoms. It shares certain features with both Alzheimer’s disease and Parkinson’s disease.
Frontotemporal Dementia (FTD):
FTD encompasses a group of disorders that predominantly affect the frontal and temporal lobes of the brain, causing changes in personality, behavior, and language. Memory loss may not be as apparent in the early stages.
Parkinson’s Disease Dementia (PDD):
Individuals with Parkinson’s disease may develop dementia as the condition progresses. Cognitive impairment may manifest as memory loss and executive dysfunction.
Normal Pressure Hydrocephalus (NPH):
NPH is characterized by an abnormal accumulation of cerebrospinal fluid in the brain, leading to gait disturbances, urinary incontinence, and cognitive decline.
Huntington’s Disease:
Huntington’s disease is a genetic disorder resulting in progressive degeneration of nerve cells in the brain, causing both motor and cognitive symptoms.
Chronic Traumatic Encephalopathy (CTE):
CTE is associated with repeated head injuries, as observed in athletes participating in contact sports, and can result in cognitive and behavioral changes.
Metabolic and Endocrine Disorders:
Conditions such as hypothyroidism, vitamin B12 deficiency, and metabolic disorders can induce cognitive impairment and should be ruled out.
Infections:
Chronic infections, such as neurosyphilis or HIV-related dementia, can induce cognitive decline.
Depression and Anxiety:
Mood disorders, especially in older adults, may occasionally present with cognitive symptoms that could be confused with dementia.
Medication Side Effects:
Some medications, particularly those with anticholinergic effects, may contribute to cognitive impairment.
Medication Management:
Non-Pharmacological Approaches:
Supportive Care and Education:
Healthy Lifestyle Practices:
Emergency Medicine
Neurology
Nutrition
Lifestyle modifications:
Neurology
Psychiatry/Mental Health
Cholinesterase inhibitors are a class of medications commonly used in the treatment of Alzheimer’s disease. They increase the levels of acetylcholine, a neurotransmitter involved in memory and cognitive function.
Donepezil (Aricept, Aricept ODT):
Rivastigmine (Exelon, Exelon Patch):
Galantamine (Razadyne, Razadyne ER):
Donepezil transdermal (Adlarity):
Neurology
Psychiatry/Mental Health
Anti-amyloid beta monoclonal antibodies represent a newer class of medications designed to target and remove beta-amyloid plaques, which are characteristic pathological features of Alzheimer’s disease (AD).
Aducanumab (Aduhelm):
Lecanemab (Leqembi):
Neurology
Neurosurgery
Memantine (Namenda, Namenda XR):
Neurology
Neurosurgery
Combination drugs, such as Memantine/Donepezil (brand name: Namzaric), are formulations that combine multiple medications to treat Alzheimer’s disease. Namzaric specifically combines two active ingredients: memantine, an NMDA receptor antagonist, and donepezil, a cholinesterase inhibitor.
Memantine/Donepezil (Namzaric):
Â
Neurology
Nutrition
Axona, also known for its active ingredient Caprylidene, is a nutritional supplement that has been explored in the context of Alzheimer’s disease management. It is a medical food designed to provide an alternative energy source for the brain.
Caprylidene (Axona):
Neurology
Diagnostic imaging agents are not used in treating Alzheimer’s disease; instead, they are used in diagnosing and evaluating the disease. These agents are radiopharmaceuticals designed for positron emission tomography (PET) imaging to visualize and detect the beta-amyloid plaques in brain, a hallmark of Alzheimer’s disease.
Neurology
Deep brain stimulation (DBS) is not widely established as a standard treatment for Alzheimer’s disease. Deep brain stimulation involves implanting electrodes into the specific areas of the brain and connecting them to a pulse generator placed under the skin. The electrodes deliver electrical impulses to modulate abnormal brain activity. The use of deep brain stimulation in Alzheimer’s disease has been explored in research and clinical trials, but the results have been mixed, and the procedure is not yet considered a routine or proven treatment. Alzheimer’s disease is a neurodegenerative disorder, and its underlying mechanisms involve widespread changes and damage in the brain. While DBS has shown promise in addressing certain symptoms in other neurological conditions, its application to Alzheimer’s disease is still under investigation. The clinical trials have explored the potential benefits of deep brain stimulation in Alzheimer’s disease. These studies often focus on targeting specific brain regions involved in memory and cognition. The results of studies have been variable, with some showing potential cognitive improvements and others showing limited or no benefits. The variability in outcomes may be influenced by factors such as patient selection, stimulation parameters, and the stage of Alzheimer’s disease.
Neurology
Acute Phase Management:
Acute Phase Management:
Alzheimer disease is a neurological condition that causes a gradual decline in behavioral and cognitive abilities such as memory, interpretation, language, concentration, thinking, and decisions.
Alzheimer is the most prevalent dementia, contributing to two-thirds of dementia cases in persons 65 and older.
Early onset before age 65 is rare and occurs in less than 10% of Alzheimer patients. There is no cure for Alzheimer, although a recent development has shown progress in slowing cognitive decline.
The global incidence of dementia is estimated at 24 million individuals, which is expected to double by 2050. Alzheimer disease is predicted to cost $172 billion in health care costs in the United States annually. After the age of 65, the risk of Alzheimer increases every five years.
The age-specific incidence rises significantly from less than 1% per year before age 65 to 6% per year beyond age 85. The prevalence rate rises from 10% at age 65 to 40% after age 85. Women have a slightly greater incidence rate of Alzheimer disease, especially after age 85.
Alzheimer disease is characterized by the buildup of aberrant neurofibrillary tangles and neuritic plaques in the brain. An increase in beta-amyloid 42 levels produce amyloid aggregation, which causes neurotoxicity. Beta-amyloid 42 promotes aggregate fibrillary amyloid protein production over normal APP breakdown.
The APP gene is found on chromosome 21, related to familial Alzheimer disease. Amyloid deposition occurs in Alzheimer disease surrounding meningeal and cerebral arteries, as well as gray matter. Gray matter deposits are multifocal and create miliary structures known as plaques.
Tau is hyperphosphorylated because of extracellular beta-amyloid aggregation, leading to tau aggregates’ production. Tau aggregates generate neurofibrillary tangles, which are tangled paired helical filaments. They begin in the hippocampus and can spread across the cerebral cortex. Tau-aggregates accumulate within neurons.
Braak and Braak created a staging approach based on the topographic staging of neurofibrillary tangles into six phases. This Braak staging is an essential aspect of the National Institute on Aging and Reagan Institute neuropathological criteria for Alzheimer diagnosis. Tangles are more strongly linked to Alzheimer disease than plaques.
Alzheimer disease is an autosomal dominant condition has complete penetrance. Mutations in three genes have been associated with the autosomal dominant type of the disease: the AAP gene on chromosome 21, Presenilin1 on chromosome 14, and Presenilin2 on chromosome 1. APP mutations may enhance beta-amyloid peptide production and aggregation.
PSEN1 & PSEN2 mutations cause beta-amyloid aggregation by interfering with gamma-secretase processing. Mutations in these three genes are responsible for 5% to 10% of all cases and early-onset Alzheimer disease predominance.
Alzheimer is a neurological condition that causes neuronal cell loss over time. It usually begins in the hippocampus’s entorhinal cortex. Both early and late-onset Alzheimer disease has a hereditary component.
Trisomy 21 is a risk factor for developing dementia at a young age. Alzheimer disease has been linked to several risk factors. The primary risk factor for Alzheimer disease is becoming older.
Traumatic brain injury, older parental age, depression, cardiovascular and cerebrovascular illness, a family history of dementia, smoking, elevated homocysteine levels, and the presence of the APOE e4 allele have all been linked to an increased risk of Alzheimer disease.
Alzheimer is usually progressing. A person diagnosed with Alzheimer disease at age 65 has an average life expectancy of 4 to 8 years.
Some people with Alzheimer might live for up to 20 years after the first symptoms appear. Pneumonia is the leading cause of mortality in Alzheimer disease.
Age:
Associated Comorbidities:
Acuity of Presentation:
The objective of the physical examination is to evaluate different aspects of an individual’s health and neurological condition. Below are key elements of the physical examination for Alzheimer’s disease:
Neurological Examination:
Vital Signs:
General Physical Examination:
Gait and Mobility Assessment:
Sensory Examination:
Functional Assessment:
Psychiatric Assessment:
Laboratory and Ancillary Tests:
Various conditions that may be considered in the differential diagnosis of Alzheimer’s disease include:
Vascular Dementia (VaD):
Vascular dementia results from compromised blood flow to the brain, often due to strokes or other vascular issues. Symptoms can overlap with those of Alzheimer’s disease.
Lewy Body Dementia (LBD):
LBD is characterized by the presence of Lewy bodies in the brain, leading to cognitive and motor symptoms. It shares certain features with both Alzheimer’s disease and Parkinson’s disease.
Frontotemporal Dementia (FTD):
FTD encompasses a group of disorders that predominantly affect the frontal and temporal lobes of the brain, causing changes in personality, behavior, and language. Memory loss may not be as apparent in the early stages.
Parkinson’s Disease Dementia (PDD):
Individuals with Parkinson’s disease may develop dementia as the condition progresses. Cognitive impairment may manifest as memory loss and executive dysfunction.
Normal Pressure Hydrocephalus (NPH):
NPH is characterized by an abnormal accumulation of cerebrospinal fluid in the brain, leading to gait disturbances, urinary incontinence, and cognitive decline.
Huntington’s Disease:
Huntington’s disease is a genetic disorder resulting in progressive degeneration of nerve cells in the brain, causing both motor and cognitive symptoms.
Chronic Traumatic Encephalopathy (CTE):
CTE is associated with repeated head injuries, as observed in athletes participating in contact sports, and can result in cognitive and behavioral changes.
Metabolic and Endocrine Disorders:
Conditions such as hypothyroidism, vitamin B12 deficiency, and metabolic disorders can induce cognitive impairment and should be ruled out.
Infections:
Chronic infections, such as neurosyphilis or HIV-related dementia, can induce cognitive decline.
Depression and Anxiety:
Mood disorders, especially in older adults, may occasionally present with cognitive symptoms that could be confused with dementia.
Medication Side Effects:
Some medications, particularly those with anticholinergic effects, may contribute to cognitive impairment.
Medication Management:
Non-Pharmacological Approaches:
Supportive Care and Education:
Healthy Lifestyle Practices:
Emergency Medicine
Neurology
Nutrition
Lifestyle modifications:
Neurology
Psychiatry/Mental Health
Cholinesterase inhibitors are a class of medications commonly used in the treatment of Alzheimer’s disease. They increase the levels of acetylcholine, a neurotransmitter involved in memory and cognitive function.
Donepezil (Aricept, Aricept ODT):
Rivastigmine (Exelon, Exelon Patch):
Galantamine (Razadyne, Razadyne ER):
Donepezil transdermal (Adlarity):
Neurology
Psychiatry/Mental Health
Anti-amyloid beta monoclonal antibodies represent a newer class of medications designed to target and remove beta-amyloid plaques, which are characteristic pathological features of Alzheimer’s disease (AD).
Aducanumab (Aduhelm):
Lecanemab (Leqembi):
Neurology
Neurosurgery
Memantine (Namenda, Namenda XR):
Neurology
Neurosurgery
Combination drugs, such as Memantine/Donepezil (brand name: Namzaric), are formulations that combine multiple medications to treat Alzheimer’s disease. Namzaric specifically combines two active ingredients: memantine, an NMDA receptor antagonist, and donepezil, a cholinesterase inhibitor.
Memantine/Donepezil (Namzaric):
Â
Neurology
Nutrition
Axona, also known for its active ingredient Caprylidene, is a nutritional supplement that has been explored in the context of Alzheimer’s disease management. It is a medical food designed to provide an alternative energy source for the brain.
Caprylidene (Axona):
Neurology
Diagnostic imaging agents are not used in treating Alzheimer’s disease; instead, they are used in diagnosing and evaluating the disease. These agents are radiopharmaceuticals designed for positron emission tomography (PET) imaging to visualize and detect the beta-amyloid plaques in brain, a hallmark of Alzheimer’s disease.
Neurology
Deep brain stimulation (DBS) is not widely established as a standard treatment for Alzheimer’s disease. Deep brain stimulation involves implanting electrodes into the specific areas of the brain and connecting them to a pulse generator placed under the skin. The electrodes deliver electrical impulses to modulate abnormal brain activity. The use of deep brain stimulation in Alzheimer’s disease has been explored in research and clinical trials, but the results have been mixed, and the procedure is not yet considered a routine or proven treatment. Alzheimer’s disease is a neurodegenerative disorder, and its underlying mechanisms involve widespread changes and damage in the brain. While DBS has shown promise in addressing certain symptoms in other neurological conditions, its application to Alzheimer’s disease is still under investigation. The clinical trials have explored the potential benefits of deep brain stimulation in Alzheimer’s disease. These studies often focus on targeting specific brain regions involved in memory and cognition. The results of studies have been variable, with some showing potential cognitive improvements and others showing limited or no benefits. The variability in outcomes may be influenced by factors such as patient selection, stimulation parameters, and the stage of Alzheimer’s disease.
Neurology
Acute Phase Management:
Acute Phase Management:
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