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.
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
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
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
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
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK499922/
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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.
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
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
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
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
https://www.ncbi.nlm.nih.gov/books/NBK499922/
medtigo
Alzheimer Disease
Updated :
January 4, 2023
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.
https://www.ncbi.nlm.nih.gov/books/NBK499922/
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