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ALZHIEMER’S DISEASE

BY CH. SRUTHI12Z31R0080

ALZHEIMER'S DISEASE

Alzheimer's disease is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. A neurodegenerative type of dementia, the disease starts mild and gets progressively worse.

WHAT HAPPENS IN ALZHEIMER’S DISEASE?

Usually, in alzheimers the brain gets shrinked off due to the death of nerve cells because of the formation of amyloid plaques and neurofibrillary tangles.

ANATOMY OF BRAIN• Brain is the most powerful organ in our

body.It normally appears in a jelly texture.• It mainly has 3 parts.They are:cerebrum- thinking, solving, feelingCerebellum- coordination and balanceBrain stem- automatic

functions(breathing,heart rate,blood pressure)

Outer layer of the brain has a wrinkled surface which is called CORTEX.Its functions include sensation,smell,storing memories,etc.

• The structural and functional unit of brain is neuron cells. These neurons gets destroyed during alzheimers disease.

• Signals travelling through neurons due to impulse are the main reasons for memories, feelings, and thoughts.

• As in alzheimers disease these neuronal cells gets destroyed, there will be drastic effects on feelings, memories, and thoughts.so in alzheimers patients, memory is lost.

NEURO TRANSMISSION

PATHO PHYSIOLOGY

• The pathophysiology of alzheimers disease includes:

Amyloid HypothesisCholinergic hypothesisExcitotoxicity hypothesisOxidative stress hypothesis

AMYLOID HYPOTHESIS

Amyloid precursor protein is mainly involved in the pathogenesis of alzhiemers disease.

Beta secretases act on APP protein and it results in formation of amylin protein.

Mutation in amylin protein and gamma secretases action on amylin protein also results in formation of amyloid deposits.

Plaques form when protein pieces calledbeta-amyloid (BAY-tuh AM-uh-loyd) clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells.

•Beta-amyloid is chemically "sticky" and gradually builds up into plaques.

•The most damaging form of beta-amyloid may be groups of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at synapses. They may also activate immune system cells that trigger inflammation and devour disabled cells.

Tau proteins are another reason for pathogenesis of Alzheimer’s disease.

CHOLINERGIC HYPOTHESIS:

Loss of cholinergic neurons is another well established pathogenesis in Alzhiemer’s disease. By the later stage of this disease, number of cholinergic neurons is dramatically reduced (75% loss of cholinergic neurons in whole body).

EXCITOTOXIC HYPOTHESIS

Excessive activation of NMDA receptors by Glutamate causes neuronal degeneration , due to excessive ca and glutamate release.

OXIDATIVE STRESS HYPOTHESIS

Earliest Alzheimer's - changes may begin 20 years or more before diagnosis.Mild to moderate Alzheimer's stages - generally last from 2 - 10 years.Severe Alzheimer's - may last from 1 - 5 years.

STAGES OF ALZHEIMER’S DISEASE

DIAGNOSIS OF ALZHEIMER’S DISEASE

There is no single test that can show whether a person has Alzheimer's.

Doctors may: Take a history (ask about symptoms and daily activities)Do a physical examination to find any signs of, for example, a stroke, heart condition or kidney disease, andCheck neurological function, e.g. by testing balance, senses and reflexes.Depending on what the doctor thinks could need checking, other diagnostics are: Sending off for tests of blood and urine samplesArranging brain scans (possibly including CT, MRI and EEG).

TREATMENT

ANTI-CHOLINESTERASES: TacrineRivastigmineDonepazilGallamineAlantamine

ERGOT ALKALOIDS :Dihydroergotamine

NOOTROPIC DRUGS:PiracetamAneracetam NSAIDS:IbuprufenIndomethacinPrednisolone

AMOEBICIDAL AGENTS:Clioquinol

PHARMACOLOGY OF ANTI CHOLINESTERASES:

MECHANISM OF ACTION: When Acetocholine is released into the synapse, it binds to it's receptor on the post-synaptic membrane, and is then broken down by the enzyme Acetocholinesterase. An Anticholinesterase prolongs the life-span of the Acetocholine in the synapse by inhibiting the enzyme that would break it down (Acetocholinesterase), allowing it to bind with the remaining receptors and thereby increase the effect on the target neuron. This helps to compensate for the loss of receptors due to the autoimmune reaction.

SIDE EFFECTS

Trouble breathing.Swelling of your face, lips, tongue, or throat.Hives.Nausea.Diarrhea.Vomiting.Indigestion.Loss of appetite and weight loss.

CONTRAINDICATIONS: Administration of reversible cholinoesterase

inhibitors is contraindicated with those that have urinary retention due to obstruction.

THERAPEUTIC USES: • Antagonists for residual neuromuscular block• Treatment of Myasthenia gravis• Treatment of Paralytic ileus• Glaucoma

CONCLUSION:

I here by conclude that, alzhiemer’s disease is a neurodegenerative disease characterized by formation of amyloid plaques and neuro fibrillary tangles, which can be treated by using anti-cholinesterase inhibitors. However, the disease cannot be cured completely by the usage of these drugs as they are able to manage the symptoms only.

THANK YOU.