APP

Jamshed Arslan, Pharm D, PhD

By Michalina Hanzel, PhD

By Jamshed Arslan, Pharm. D., PhD.

By Jamshed Arslan Pharm.D.

By Christina Towers, PhD.

By Jamshed Arslan Pharm.D.

The neurodegenerative disorder, Alzheimer's disease, is responsible for 60 to 80% of all dementia cases.¹   Neurodegeneration occurs in response to the accumulation of amyloid-β plaques and neurofibrillary tangles composed of hyperphosphorylated tau.

Alzheimer’s Disease (AD) is a neurodegenerative disorder that is characterized by an abundance of the beta-amyloid peptide in the brain.  When AD was first discovered, it was determined that beta-amyloid was produced as a result of the proteolysis of the amyloid precursor protein (APP).  Aside from its role in AD, the single-pass transmembrane APP has a high expression level in the brain and tends to concentrate at the synapses of neurons.  Because of this localization, it has been suggested that APP plays a role in synapse formation and potentially plasticity.  However, the

An epidemiological association between traumatic brain injury (TBI) and Alzheimer's disease (AD) has long been established.  Interestingly, an increase in beta amyloid  (one hallmark of AD) directly following TBI has been observed.  In fact, it has been reported that with a greater level of TBI comes a higher risk of developing AD, or other neurodegenerative disorders, in the future.  Roberts et al first presented research that beta amyloid plaques found in TBI patients are very similar to those found in AD patients.

Niemann-Pick type C1 (NPC1) mediates low-density cholesterol transport from late endosomes and lysosomes to other areas of the cell via receptor mediation endocytosis.  Although cholesterol moves freely inside the cell, it cannot independently export out of the lysosome, which is where NPC1 steps in.