2IntroductionAlzheimer’s is the most common cause of dementia in adult life and is associated with the selective damage of brain regions and neural circuits critical for memory and cognition.The pathogenesis of this disease is complex, and involves many molecular, cellular, and physiological pathologies.
3What is AD?Alzheimer’s disease (AD) is a devastating illness characterized by progressive memory loss, impaired thinking, personality change, and inability to perform routine tasks of daily living.
4To understand Alzheimer’s disease, it’s important to know a bit about the brain…
5Cells of the nervous system Neurons2.Neuroglia cellsAstrocyteOligodentrocytesEpendymal cellsMicroglia
6NeuronsThe brain has billions of neurons, each with an axon and many dendrites.To stay healthy, neurons must communicate with each other, carry out metabolism, and repair themselves.AD disrupts all three of these essential jobs.
9Etiology and risk factors Although the risk of developing AD increases with age – in most people with AD, symptoms first appear after age 60 – AD is not a part of normal aging. It is caused by a fatal disease that affects the brain.Family history
15Other crucial parts….Hippocampus: where short-term memories are converted to long-term memoriesThalamus: receives sensory and limbic information and sends to cerebral cortexHypothalamus: monitors certain activities and controls body’s internal clockLimbic system: controls emotions and instinctive behavior (includes the hippocampus and parts of the cortex)
23Neurofibrillary tangles Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules.In AD, tau changes, causing microtubules to twist together in helical fashion , and tau proteins clump together to form neurofibrillary tangles.
26Genetic factorPresenillin -1 and 2 genes are muted to cause over production of betaamyloid(cell damage/death/inflammation)Apolipoprotein E (ApoE) gene on chromosome 19Four allele of apolipoprotein –E that is Apo E-2,3,4.Role in cholesterol transportE4 associated with AD but E2 is protective
27Contd....– ApoE4 promotes the formation of neuritic plaques;also binds to beta-amyloid to make it insoluble.-Apo E-4 increase the risk of person to develop late onset of AD– E4 neither necessary nor sufficient to cause AD (many people have apoE4 gene, but do not have AD).
28Cellular and others …. Aging causes formation of free radicals HT, obesity, smoking, atherosclerosis, high cholesterol and homocysteine increase the risk of AD.
29Conclusion The neural damage in AD is irreversible, and hence the disease cannot be cured.There is no effective drug for relievingsymptoms, and no prospect of one in the nearfuture.