Alzheimer’s Disease and treatment

Dementia and Treatment of Alzheimer’s Disease

Alzheimer’s disease is a brain disorder that progressively worsens over time. It’s characterized by changes in the brain that lead to deposits of certain proteins. Alzheimer’s disease causes the brain to shrink and brain cells to eventually die. It is the most common cause of dementia—a gradual decline in memory, thinking, behavior, and social skills. About 6.5 million people in the United States age 65 and older live with Alzheimer’s disease. Among them, more than 70% are 75 years old and older. Of the about 55 million people worldwide with dementia, 60% to 70% are estimated to have Alzheimer’s disease. The early signs of the disease include forgetting recent events or conversations. Over time, it progresses to serious memory problems and loss of the ability to perform everyday tasks. Medicines may improve or slow the progression of symptoms. Programs and services can help support people with the disease and their caregivers. There is no treatment that cures Alzheimer’s disease. In advanced stages, severe loss of brain function can cause dehydration, malnutrition, or infection. These complications can result in death.


Dementia is a condition that impairs cognitive functions, including memory, problem-solving, motor skills, social skills, and emotional control.

Alzheimer’s disease:


It is a neurodegenerative disorder that causes dementia and is the most common cause of dementia in older people. It is characterized by shrinking of the cortex and subcortical regions, the accumulation of -amyloid protein, and neurofibrillary tangles inside cells made of “tau” protein.



Cholinergic activators, such as cholinergic agonists and anti-cholinesterases, have been used to augment brain ACh levels in Alzheimer’s disease, but they come with peripheral side effects. Four cerebroselective anti-ChEs have been introduced over the past two decades, and three are widely used in Alzheimer’s disease. They are rivastigmine, donepezil and Galantamine.

Tacrine was the first centrally-acting anti-ChE used in Alzheimer’s disease, but it has gone out of use due to hepatotoxicity.


A carbamate form of physostigmine that blocks both AChE and BuChE. However, it targets the G1 isoform of AChE more strongly, which is found in more than one part of the brain. Rivastigmine is highly lipid-soluble, enters the brain easily, and produces mild peripheral side effects. It is indicated in mild-to-moderate cases of Alzheimer’s disease but not in advanced disease.


It is a cerebroselective and reversible anti-AChE that produces measurable improvement in several cognitive and non-cognitive scores in Alzheimer’s disease, which is maintained for up to two years. It is generally well tolerated and is not hepatotoxic.


Selectively inhibits cerebral AChE and has some direct agonistic action on nicotinic receptors as well. It produces cognitive and behavioral benefits in Alzheimer’s disease that are comparable to rivastigmine and donepezil.


It is a newer NMDA receptor antagonist that slows functional decline in moderate-to-severe Alzheimer’s disease, but the benefit in milder disease is unclear. Symptom relief is similar to or lesser than anti-AChEs. It appears to block excitotoxicity.

Disclaimer: This article is for informational purposes only and should not be taken as medical advice. Always consult with a healthcare professional before making any decisions related to medication or treatment.

Disclaimer: This article is for informational purposes only and does not constitute medical advice. Always seek the advice of a healthcare provider with any questions regarding a medical condition.

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