Fig 1: Pathology of AD showing plaques and tangles.
Some would say a soul is the collective memories and personality traits of an individual. So, what is left if those memories and traits are erased? You and I might be far from old and senile (well I’m not old). But you know someone near & dear to you, who will have to deal with this existential crisis in their golden years. Alzheimer’s disease currently has two culprits, Beta amyloid (Aβ) which can form plaques on the brain and Tau protein, whose over expression can cause neurons to tangle up (NFT).
These pathologies appear to be affected by the APOE gene, certain variations of which are now recognized as dead-ringers for Alzheimer’s. The mechanism however is still very much in the process of being understood. More so, when considering the role of Tau.
Fig 2: Constant expression of plaque causing Aβ with varying levels of Tau shows little difference in pathology. Plaques and tangles remain present. Thus deletion or over expression of Tau is not enough to prevent AD pathology.
Although the signs of Alzheimer’s on a cellular level remained steady while playing with the knobs of Tau expression, the authors did find a difference is the cell & organism survivability. Hypothesizing that Tau helps the neuron deal with excitotoxicity, the damage to nerve cells through stimulation.
Don’t lose hope, although it’s difficult to get a full picture, we may have enough glimpses to make a clinical difference. Eventhough, we don’t quite understand the role between APOE, lipoproteins and Alzheimer’s pathology, on a higher symbolic level APOE is a great predictor of who is at risk for AD and sometimes even when. Best move for now is probably just to get your parents genotyped and planning active mental lifestyles for them, there should be a fix by the time I’m grey.
Petri Dish Talk 