AD is type of neurodegenerative disorder. Loss of cholinergic neurons leads to memory impairment and It is a leading cause of dementia. This progressive and unstoppable disease mainly seen in old age patient.
3. HISTORY(1)
• In 1906, Dr. Alois Alzheimer a German psychiatrist found a different type of
mental illness in his patient Auguste Deter.
• He examined Ms. Deter’s brain microscopically using new stains that revealed
the presence of some protein like structure.
• Now we call it amyloid plaques and neurofibrillary tangles.
Dr. Alois Alzheimer Auguste Deter
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• Dr. Emil Kraepelin included Miss. Deter’s case in the 1910 edition of his widely
respected psychiatry textbook.
• It was Kraepelin who named this dementia on the name of Dr. Alois Alzheimer.
• November is National Alzheimer’s Disease Awareness Month as well as National
Caregivers Month.
• And 21 Sep is known as National Alzheimer’s Day.
Dr. Emil Kraepelin
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5. INTRODUCTION(3)
• AD is progressive neurodegenerative disorder that destroys memory.
• It is most common cause of Dementia.
• Cholinergic neurons in brain are degenerated.
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8. PATHOPHYSIOLOGY(4)
• Pathophysiology of AD is not clear.
• Three pathogenic AD hypothesis are discussed below-
1. Cholinergic hypothesis.
2. The amyloid plaques hypothesis.
3. The tau protein neurofibrillary tangles hypothesis.
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2. The Amyloid plaques :-
• Beta secretase enzyme degrade the APP which are sticky in nature.
• They combined with each other and form insoluble plaques between
neurons.
• That leads to impairment in neuronal chemical transmission.
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3. Neurofibrillary tangles:-
• Tau protein stabilizes the microtubule from which chemical messengers
move.
• Degeneration of this protein causes destabilization of microtubule.
• Chemical messengers fail to transmit the signal.
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12. RISK FACTORS(3)
Family history and Genetics
Age & Sex
Mild Cognitive Impairment
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Past Head trauma & Down syndrome
Life style and Heart health
Life long learning and Social engagement
13. COMPLICATIONS(3)
• Inhaling food or liquid into the lungs (aspiration)
• Pneumonia and other infections
• Falls
• Fractures
• Bedsores
• Malnutrition or dehydration
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14. DIAGNOSIS(3)
1. Physical and neurological exam
2. Lab tests
3. Mental status and neuropsychological testing
4. Brain imaging
Magnetic resonance imaging (MRI)
Computerized tomography (CT).
Fluorodeoxyglucose (FDG) PET
Amyloid PET imaging
Tau Pet imaging
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• Cholinesterase inhibitors:
These Drugs are use for enhancing the Ach level in brain.
It acts by Inhibiting Acetylcholine esterase enzyme.
Tacrine was first drug approved for treating AD.
But its use has declined due to its Hepatotoxic potential and need of frequent
dosing.
Donepezil, Rivastigmine, Galantamine are newer in this category useful in AD.
They are less toxic than Tacrine.
Donepezil is also the current drug of choice.
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• NMDA receptor blocker:
Memantine is an orally active weak antagonist of NMDA receptors.
It was originally introduced as an Anti-viral drug.
After that it resurrected as a potential inhibitor of excitotoxicity.
It produces a modest cognitive improvement in moderate to severe AD.
It does not appear to be neuroprotective.
It has a long plasma half- life.
Adverse effects include Headache, Dizziness, Drowsiness, Constipation,
Shortness of breath.
It is used in combination with cholinesterase inhibitors.
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18. REFERENCE
1. Hippius H, Neundörfer G. “The Discovery of Alzheimer's disease”, Dialogues Clin
Neurosci. 2003;5:101–8.
2. Jack CR Jr, Albert MS, Knopman DS, et al. “Introduction to the recommendations
from the National Institute on Aging-Alzheimer's Association workgroups on
diagnostic guidelines for Alzheimer's disease”, Alzheimers Dement. 20117:257-62
3. https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/symptoms-
causes/syc-20350447
4. Spires-Jones TL, Hyman BT. “The intersection of amyloid beta and tau at synapses
in Alzheimer’s disease”, Neuron. 2014;82(4):756–71.
5. Gupta. S, Garg. G. “ Review of pharmacology”, “12th edition”, “The health sciences
publisher” 2018, pg. no. 229.
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