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Etiopathogenesis of Alzheimer's disease

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Presentation on theme: "Etiopathogenesis of Alzheimer's disease"— Presentation transcript:

1 Etiopathogenesis of Alzheimer's disease

2 Introduction Alzheimer’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.

3 What 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.

4 To understand Alzheimer’s disease, it’s important to know a bit about the brain…

5 Cells of the nervous system
Neurons 2.Neuroglia cells Astrocyte Oligodentrocytes Ependymal cells Microglia

6 Neurons The 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.

7 Structure of the neuron


9 Etiology 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






15 Other crucial parts…. Hippocampus: where short-term memories are converted to long-term memories Thalamus: receives sensory and limbic information and sends to cerebral cortex Hypothalamus: monitors certain activities and controls body’s internal clock Limbic system: controls emotions and instinctive behavior (includes the hippocampus and parts of the cortex)

16 Etiology for AD Unknown Aging Familial cause

17 AD and brain Amyloid plaques Neuro fibrillary tangles
Loss of connection between cells and cell death Genetic factor Cellular and other cause

18 Amyloid plaque Amyloid precursor protein (APP) is the precursor to amyloid plaque. APP sticks through the neuron membrane.

19 Contd…. Enzymes cut the APP into fragments of protein, including beta-amyloid.

20 Contd… Beta-amyloid fragments come together in clumps to form plaques.

21 Contd.. In AD, many of these clumps form, disrupting the work of neurons. This affects the hippocampus and other areas of the cerebral cortex.


23 Neurofibrillary 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.



26 Genetic factor Presenillin -1 and 2 genes are muted to cause over production of betaamyloid(cell damage/death/inflammation) Apolipoprotein E (ApoE) gene on chromosome 19 Four allele of apolipoprotein –E that is Apo E-2,3,4. Role in cholesterol transport E4 associated with AD but E2 is protective

27 Contd.... – 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).

28 Cellular and others …. Aging causes formation of free radicals
HT, obesity, smoking, atherosclerosis, high cholesterol and homocysteine increase the risk of AD.

29 Conclusion The neural damage in AD is irreversible, and
hence the disease cannot be cured. There is no effective drug for relieving symptoms, and no prospect of one in the near future.


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