Alzheimer's disease
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Transcript of Alzheimer's disease
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Alzheimer’s Disease
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What is Alzheimer’s disease Incidence & PrevalenceSigns & SymptomsCausesMechanismsDiagnosisTreatment & Management
Outline
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Neurodegenerative dementia causing memory loss & cognitive decline.
Cause shrinkage of the brain.
Discovered by German psychiatrist & neuro-pathologist Alois Alzheimer in 1906.
Most common cause of dementia in adults.
Introduction
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Mostly diagnosed in people over 65 years of age
(Late-onset Alzheimer’s disease).
Early-onset AD may occur within 30-60 years.
In 2006, throughout the world 26.6 million
people were affected.
Within 2050, among 85 people, 1 will be affected
globally.
Statistics of AD
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Memory loss.Difficulty performing familiar tasks.Problems with language.Disorientation to time & space.Poor/decreased judgment.Problems with abstract thinking.Misplacing things.Changes in mood & behavior.Changes in personality.Loss of initiative.
Signs & Symptoms
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1. Genetic cause
2. Cholinergic hypothesis
3. Amyloid hypothesis
4. Tau hypothesis
5. Others
Causes
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Genetic Cause:
Involvement of Amyloid precursor protein(APP),
Presenilin 1 & Presenilin 2.
Carrying APOEε4 causes 40-80% of Late-onset AD.
Other genes responsible for causing AD are-
CLU, PICALM, CR1, BIN1, MS4A, ABCA7, EPHA1, CD33,
CD2AP, ATP5H, EXOC4, CTNA3, RNF219, TREM2 etc.
Causes
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Cholinergic Hypothesis:
Reduced synthesis of neurotransmitter ,
acetylcholin.
Large scale aggregation of amyloids.
Results in neuroinflammation & degeneration
of neurons.
Causes
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Amyloid Hypothesis:
Deposition of β-Amyloid proteins.
APP present on chromosome 21 together with
Down syndrome causes 90% of Early-onset AD.
N-APP triggers self destruct pathway by binding
to a neuronal receptor, Death Receptor 6 (DR6).
Causes
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Tau Hypothesis:
Degeneration of tau proteins.
Formation of neurofibrillary tangles.
Initiation of AD.
Causes
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Others:
Involvement of Herpes simplex virus carrying
susceptible version of apoE gene.
Oxidative stress in brain.
Dys-hemostasis of bio metal metabolism.
Causes
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Formation of β-Amyloid plaques:
Normally, α-secretase produces APP & γ-secretase
creates another shorter version of APP which is then
degraded.
In case of AD, β-secretase together with γ-secretase
produces longer, sticky form of β-amyloid proteins (Aβ).
Accumulation of Aβ proteins produce senile plaques.
Mechanism
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Enzymes act on the APP (amyloid precursor protein) and cut it into fragments. The beta-amyloid fragment is crucial in
the formation of senile plaques in AD.
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Formation of Neurofibrillary Tangles:
In neurons, signal transduction occurs through
microtubules which are stabilized by tau proteins.
In AD, tau proteins are degenerated.
& causes microtubules to disintegrate.
Leads to formation of neurofibrillary
tangles of tau proteins.
Causes neuron degeneration.
Mechanism
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Based on patient’s history, relatives’ history & observation of his behavior.
Assessment of intellectual functioning by memory tests.
Exclusion of other cerebral pathology of dementia using-
Computed tomography (CT) Magnetic resonance imaging (MRI) Single photon emission computed
tomography (SPECT)Positron emission tomography (PET)
Diagnosis
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.
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No known treatment found yet as, death of brain cells can’t be halted or reversed.
Some therapeutic drugs are available that can help a patient to live ably. Those includes-
• Donepezil• Alantamine• Rivastigmine• Tacrine• Menantine etc.
Treatment & Management
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Some potential treatment may involve-Application of chaperone molecules.Gene therapy in reversing memory loss.Application of Dab2 protein, which exhibits
neuroprotective effects.Regulation of TGF- β1/SMAD signaling.
Most important thing an AD patient needs is proper nursing & care.
Treatment & Management
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