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Alzheimer's disease (Risk factors (Smoking (Protective effect…

- - - - Tau protein gets misfolded or hyperphosphorylated leads to formation of Tau threads and PHFs which become tangled inside the cells
        
        results in instable axons and interferes with protein synthesis
  - - - leads to inflammation, apoptosis, and disfunctioning extra cellular matrix
  - - - extravasation of plasmin, thrombin, RBCs, lymphocytes, autoantibodies, pathogens into brain tissue
        
        Neuronal injury+synaptic dysfunction+loss of neurons= Neurodegeneration
  - - - Release of cytokines, chemokines, caspases, ROS and activation of complement system by microglia
        
        Neuronal degeneration and contributes to disease severity and progression
- - - - Increase the risk of AD
  - - - Extravasation of proteins into brain tissue
        
        Cell damage, reduction in neuronal or synaptic function, apoptosis, and increased Abeta accumulation
  - - - Insulin can increase deposition of Abeta and tau proteni phosphorylation
  - - - Nicotine induces increases in nAChR, counterbalancing the loss of nAChR in AD
  - - - Fish, fruit, and vegetables are rich in antioxidants which reduce lipid peroxidation
    - - Increases cerebral blood flow, oxygen extraction, glucose utilization, and activation of growth factors promoting structural brain changes, such as increased capillary density
    - - Cognitively stimulating activities reduce the risk of AD
- - - - little more common
        
        increases AD risk
    - - least common
        
        reduce AD risk
    - - most common
        
        seems like it has no effect
  - - - amyloid-beta peptide build up
        
        amyloid-beta plaque
        
        tau proteins malfunction
        
        neurofibrillary tangles
        
        abnormal brain functions
      - can be cleaved up into alpha, beta and gamma
        
        beta
        
        produced and released in extracellular space
        
        C99 peptide in cell membrane
        
        gamma
        
        alpha
        
        'normal' cleavage
        
        produced and released into extracellular space
        
        C83 peptide
      - signal transduction receptor
    - - PSEN2
      - PSEN1
- - - - Accumulation of mutations
  - - - Oxidative stress
  - - - Accumulation of missfolded proteins
        
        Senile (amyloid-beta) plaques
        
        Missfolded Tau proteins
- - - - Low task demands
        
        Unimpaired working memory performances with age
      - High task demands
        
        Poorer performances in older individuals
    - - Measure of intracerebral communication
      - Facilitated by hubs
        
        Degenerate with age
        
        Reduced functional integrity of frontal neural circuits
        
        Less flexible and efficient working memory control processes
    - - Reduction of dopamine
        
        Leads to impaired cognitive performance
        
        Progressive loss of dopamine cell bodies in the substantia nigra
  - - - Cortical thinning, decreased brain tissue surface, or progressive reduction of brain volume
        
        Shrinkage of neurons, reduction of synaptic spines, and a reduced number of synapses
    - - Loss of myelin
        
        Deterioration of fiber connections
        
        Decreased length of myelinated axons and a reduction in white matter volume
      - Decline shows an inverted U-shape, with the volume increasing until 50 years of age, after which it decreases
- - - - moderate to severe AD
      - counterbalance the neurotransmitter disturbance
        
        don't stop underlying decline
      - improve symptoms of memory loss and problems with thinking and reasoning
  - - - interfere with pathogenic steps
        
        deposition of extracellular amyloid beta plaques
        
        recruiting the immune system
        
        prevent beta-amyloid from clumping
        
        intracellular neurofibrillary tangle formation
        
        inflammation
        
        oxidative damage
        
        iron deregulation
        
        cholesterol metabolism
  - - - being studied now
    - - being studied now