Complete pathophysiology of Alzheimer Disease for B.Pharm and D.Pharm Students and also for medical students. Definition, Etiology, Pathogenesis, Clinical Manifestations, Diagnosis, Pharmacological and Non Pharmacological Treatments. D.Pharm Students, B.Pharm Students, Pharmacoogy and Medical Students.

1. CENTRAL NERVOUS SYSTEM
DISORDERS
ALZHEIMER’S DISEASE
A PRESENTATION BY:
AMAN GUPTA
LECTURER
GCRG COLLEGE OF PHARMACY, LUCKNOW
NCJ @ AMAN

3. ALZHEIMER’S DISEASE
ALZHEIMER’S DISEASE = A DISEASE OF CNS.
IT MAINLY AFFECTS 3 AREAS OF BRAIN:
• FRONTAL LOBE. (INTELLIGENCE, JUDGEMENT & BEHAVIOUR)
• PARIETAL LOBE. (LANGUAGE)
• TEMPORAL LOBE & HIPPOCAMPUS. (MEMORY).
IN THIS DISEASE, NEURONS OFABOVE THREE AREAS GETS DEGENERATED OR
DESTROYED.
REASON:
• FORMATION OF AMYLOID PLAQUES BETWEEN NEURONS.
• FORMATION OF NEUROFIBRILLARY PLEXUS/TANGLES WITHIN NEURONS.

4. AMYLOID PLAQUES
AMYLOID = BETA-AMYLOID PROTEIN.
PLAQUES = COLLECTION OF PIECES.
AMYLOID PLAQUES = A COLLECTION/AGGREGATE OF VARIOUS PIECES OF BETA-
AMYLOID PROTEIN.
BETA-AMYLOID PROTEIN
BETA-AMYLOID IS A PROTEIN PRODUCED DUE TO BREAKDOWN OFAMYLOID
PRECURSOR PROTEIN (APP).
AMYLOID PRECURSOR PROTEIN (APP)
APP IS A PROTEIN FOUND IN LARGE AMOUNTS IN BRAIN TISSUE.
FUNCTION: CELLULAR GROWTH AND OTHER FUNCTIONS.

5. BREAKDOWN OF APP DUE TO UNKNOWN REASONS.
(FORMATION OF BETA-AMYLOID PROTEIN PIECES)
COLLECTION/AGGREGATION OF BETA-AMYLOID PROTEIN PIECES TO FORM AMYLOID PLAQUES.
(AMYLOID PLAQUES)
THESE AMYLOID PLAQUES GETS DEPOSITED IN BETWEEN NEURONS AND BREAKS DOWN THEIR
CONNECTION DISRUPTS NORMAL FUNCTIONING OF NEURONS.
APP inside
brain tissue

7. NEUROFIBRILLARY PLEXUS/TANGLES
NEUROFIBRILLARY = NEURO (WITHIN NEURON) + FIBRILLARY (FIBER LIKE)
PLEXUS/TANGLES = NETWORK.
NEUROFIBRILLARY PLEXUS/TANGLES = NETWORK OF FIBER LIKE STRUCTURE WITHIN THE
NEURONS.
NEUROFIBRILLARY PLEXUS/TANGLES
NEUROFIBRILLARY PLEXUS/TANGLES = THESE ARE ABNORMAL COLLECTION OF A
PROTEIN CALLED “TAU”.
TAU PROTEIN
TAU PROTEIN = A PROTEIN FOUND WITHIN THE NEURONS.
FUNCTION:
• THESE PROTEINS BINDS WITH MICROTUBULES OF NEURONS.
• HELPS IN TRANSFER OF NUTRIENTS AND MOLECULES FROM CELL BODY TO AXON AND
DENDRITES & THUS HEALTHY FUNCTIONING OF NEURONS.

9. BUT, IN ALZHEIMER DISEASE,
DUE TO SOME UNKNOWN REASONS, TAU PROTEIN BEGINS TO DETACH FROM
MICROTUBULES,
AND ATTACH TO OTHER TAU MOLECULES TO FORM FILAMENTS/FIBRE LIKE
PLEXUS/TANGLES/NETWORK.
IN THE END, THESE PLEXUS ARE CONNECTED, WHICH GIVES RISE TO TANGLES
INSIDE THE NEURONS.
THE TANGLES INTERFERE WITH THE NORMAL FUNCTIONING OF THE NEURONS AND
DISRUPTS THEIR FUNCTION LEADING TO ALZHEIMER.

11. DEFINITION
• Pathologist ‘Alois Alzheimer’ first described this disease and is, therefore named after him.
• Alzheimer's disease (AD) is the most common form of ‘Dementia’.
Irreversible + Progressive + Neurodegenerative disease
AD
Slowly destroys memory + thinking skills + ability to carry simple tasks
Definition: Alzheimer's disease is an irreversible progressive neurodegenerative disease, caused due to formation of amyloid plaques and
neurofibrillary tangles with in brain tissue, that slowly destroys memory and thinking skills and ability to carry out the simplest tasks.
Or NCJ @ AMAN
• Alzheimer's disease is a chronic neurodegenerative disease that usually starts slowly.
• Caused due to formation of amyloid plaques and neurofibrillary tangles with in brain tissue.
• Characterized by difficulty in remembering recent events.
• It is characterized by short term memory loss, poor thinking ability.
[Note: Dementia= Loss of intellectual abilities such as thinking remembering and reasoning that is severe enough to interface with daily
functioning it occurs in patients above age of 65 years.]

13. ETIOLOGY OF AD
• AD IS CAUSED DUE TO FORMATION OF AMYLOID PLAQUES AND
NEUROFIBRILLARY TANGLES WITH IN BRAIN TISSUE.
• AD destroys neurons (nerve cells) of the brain that control memory, including the
hippocampus, which controls short-term memory leading to short term memory failure.
• There is a decrease in ability to perform familiar tasks.
• AD affects mainly three areas of brain: (temporal lobe, frontal lobe and parietal lobe)
responsible for memory, behaviour, intelligence and language.
• Personality changes occur, which include emotional outbursts, wandering and agitation.
• The severity of these changes increases with disease progression.
• Slowly many other areas of the brain get involved, the brain shrinks and loses function thus
person becomes bedridden, helpless and non-responsive.

14. ETIOLOGY (CONTINUED….)
OTHER RISK FACTORS FOR ALZHEIMER’S DISEASE:
• AGE.
• FAMILY HISTORY.
• HEAD TRAUMA/INJURY.
• BRAIN INFECTION.

15. PATHOPHYSIOLOGY OF AD
Due to the etiological factors.
Changes occurs in the proteins of the nerve cells of few parts of the brain.
Accumulation of amyloid plaque and neurofibrillary tangles[abnormal protein] inside the neurons.
Degeneration of neurons.
Loss of nerve cells[leading to shrinkage of brain].
Dementia, Loss of memory, thinking skills and other important functions.
AD
NCJ @ AMAN

16. CLINICAL MANIFESTATIONS OF AD
• The early signs of the disease include forgetting recent events or conversations.
• As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to
carry out everyday tasks.
Other symptoms include:
• Memory lapses (forgetting).
• Repeat statements and questions over and over.
• Have trouble finding the right words to identify objects, express thoughts or take part in conversations.
• Inability to perform routine tasks.
• Loss of judgement. NCJ @ AMAN
• Personality or behaviour changes.
• Trouble sleeping.
• Difficulty concentrating and thinking.

17. DIAGNOSIS
DIAGNOSIS
• Physical exam.
• Blood test.
• Magnetic Resonance Imaging(MRI).
• Computerized Tomography Scan(CT-Scan).

18. TREATMENT
1. Cholinesterase Inhibitors: Cholinesterase is an enzyme which breaks down acetylcholine.
Cholinesterase inhibitors inhibits cholinesterase and prevents break down of acetylcholine.
Acetylcholine increases communication between neurons and reduces symptoms of AD. For example:
Donepezil, Galantamine and Rivastigmine.
2. Memantine (Namenda): It improves memory and brain function.
3. Aducanumab: It reduces the amount of beta-amyloid plaques.

19. THANK YOU
NCJ @ AMAN