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.

1. ALZHEIMER’S DISEASE
PRESENTED BY- SARAS H. TIWARI
(M.PHARM SEM-I)
(DEPT OF PHARMACOLOGY)
GUIDED BY- DR. SHIVANI R. DESAI
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2. CONTENTS
• History
• Introduction
• Sign and Symptoms
• Causes
• Pathophysiology
• Risk Factor
• Complications
• Diagnosis
• Treatment
• References
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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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4. Ctd..
• 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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6. SIGN & SYMPTOMS(3)
MEMORY
LOSS
Thinking
and
reasoning
Making
judgments
and
decisions
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Planning and
performing
familiar tasks
Changes in
personality and
behavior
Preserved
skills

7. CAUSES(3)
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GENETIC
LIFE-
STYLE
ENVIORN-
MENTAL
• PHYSICAL
• MENTAL
• STRESS
• SLEEP- WAKE
CYCLES
• APOE e4
• PSEN 1
• PSEN 2
• TRISOMY 21
• HEAVY
METALS
• PESTICIDES
• AIR
POLLUTION

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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9. Ctd…
AchDA
9
DA
Ach
Alzheimer’s
Disease
Normal
1. CHOLINERGIC HYPOTHESIS:- Low level of Ach in brain
leads to AD that results in loss of memory.

10. Ctd…
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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11. Ctd…
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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15. TREATMENT(5,3)
1. Non-pharmacological :-
• Creating a safe and supportive environment
• Exercise
• Nutrition
2. Pharmacological treatment :-
• Cholinesterase inhibitors: Tacrine , Donepezil, Rivastigmine, Galantamine.
• NMDA receptor blocker : Memantine.
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16. Ctd…
• 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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17. Ctd…
• 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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