Alzheimer's disease.pptx

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

2. 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 of above three areas gets degenerated or destroyed . Reason: Formation of  Amyloid plaques between neurons. Formation of Neurofibrillary plexus/tangles within neurons.

3. 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 of amyloid precursor protein (APP). amyloid precursor protein (APP ) App is a protein found in large amounts in brain tissue. Function: cellular growth and other functions.

4. 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

5. 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.

6. 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.

7. definition P athologist ‘ A lois A lzheimer’ first described this disease and is, therefore named after him. A lzheimer'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 D efinition: A lzheimer'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 A lzheimer'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. C haracterized by difficulty in remembering recent events. I t is characterized by short term memory loss, poor thinking ability. [Note: Dementia= l oss 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.]

8. 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. T here 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. P ersonality changes occur, which include emotional outbursts, wandering and agitation. T he severity of these changes increases with disease progression. S lowly many other areas of the brain get involved, the brain shrinks and loses function thus person becomes bedridden, helpless and non-responsive.

9. Etiology (continued….) Other risk factors for alzheimer’s disease: Age. Family history. Head trauma/injury. Brain infection.

10. 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

11. Clinical manifestations of ad T he early signs of the disease include forgetting recent events or conversations. A s the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks. O ther symptoms include: M emory lapses (forgetting). R epeat statements and questions over and over. H ave trouble finding the right words to identify objects, express thoughts or take part in conversations. I nability to perform routine tasks. L oss of judgement. NCJ @ AMAN P ersonality or behaviour changes. T rouble sleeping. D ifficulty concentrating and thinking.

12. Diagnosis Diagnosis Physical exam. Blood test. Magnetic Resonance Imaging(MRI). Computerized Tomography Scan(CT-Scan).

13. treatment 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. Memantine (Namenda ): It improves memory and brain function. Aducanumab: It reduces the amount of beta-amyloid plaques.

14. Thank you NCJ @ AMAN