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 What is Alzheimer’s disease
 Incidence & Prevalence
 Signs & Symptoms
 Causes
 Mechanisms
 Diagnosis
 Treatment & Management
 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.
 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.
 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.
1. Genetic cause
2. Cholinergic hypothesis
3. Amyloid hypothesis
4. Tau hypothesis
5. Others
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.
Cholinergic Hypothesis:
Reduced synthesis of neurotransmitter , acetylcholin.
Large scale aggregation of amyloids.
Results in neuroinflammation & degeneration of
neurons.
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).
Tau Hypothesis:
 Degeneration of tau proteins.
 Formation of neurofibrillary tangles.
 Initiation of AD.
Others:
 Involvement of Herpes simplex virus carrying
susceptible version of apoE gene.
 Oxidative stress in brain.
 Dys-hemostasis of bio metal metabolism.
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.
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.
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.
 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)
.
 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.
 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.
Alzheimer's disease

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Alzheimer's disease

  • 1.
  • 2.  What is Alzheimer’s disease  Incidence & Prevalence  Signs & Symptoms  Causes  Mechanisms  Diagnosis  Treatment & Management
  • 3.  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.
  • 4.  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.
  • 5.  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.
  • 6. 1. Genetic cause 2. Cholinergic hypothesis 3. Amyloid hypothesis 4. Tau hypothesis 5. Others
  • 7. 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.
  • 8. Cholinergic Hypothesis: Reduced synthesis of neurotransmitter , acetylcholin. Large scale aggregation of amyloids. Results in neuroinflammation & degeneration of neurons.
  • 9. 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).
  • 10. Tau Hypothesis:  Degeneration of tau proteins.  Formation of neurofibrillary tangles.  Initiation of AD.
  • 11. Others:  Involvement of Herpes simplex virus carrying susceptible version of apoE gene.  Oxidative stress in brain.  Dys-hemostasis of bio metal metabolism.
  • 12. 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.
  • 13. 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.
  • 14. 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.
  • 15.
  • 16.  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)
  • 17. .
  • 18.  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.
  • 19.  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.