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One very crucial function of Cathepsin B that is emphasized on is its ability to break down the proteins that cause [http://en.wikipedia.org/wiki/Amyloid amyloid plaque], the root cause of Alzheimer’s disease systems.  Cathepsin B has a built in protective mechanism against Alzheimer’s disease.  Cathepsin B functions by “snipping” apart proteins which are closely associated with the amyloid protein that forms the amyloid plaques. Once, Cathepsin B breaks down these amyloid plaques, it signals other enzymes to further degrade the protein.  An experiment with mice was conducted by Dr. Li Gan's lab at the University of California San Francisco in which Dr. Gan's lab found that cutting out the Cathepsin B gene increased the plaque deposition in mice with Alzheimers disease symptoms.  The mice showed the human form of  amyloid [http://en.wikipedia.org/wiki/Amyloid_precursor_protein amyloid precursor protein, APP].  These researchers also discovered that Cathepsin B build up within the amyloid plaques and that it acted to decrease levels in neurons.  The researchers also found that introducing a pathological form APP called APP1-42 into the neurons drastically increased cathepsin B in young and middle aged mice with human APP, but not old mice.  From this observation, the researchers concluded that the upregulation of Cathepsin B could represent a protective mechanism that fails with aging and a failure like this could mean that it plays a role in late-onset sporadic Alzheimer’s disease.   

Another mechanism of action that Cathepsin B takes on is its function to regulate [http://en.wikipedia.org/wiki/Angiogenesis angiogenic] threshold of [http://en.wikipedia.org/wiki/Endothelium endothelial]  cells.  Cathepsin B has the ability to suppress the [http://en.wikipedia.org/wiki/Intrinsic_and_extrinsic_properties intrinsic] angiogenic switch.  When bovine retinal endothelial cells (BREC) are cultured between two layers of collagen, the BRECS can produce both proangiogenic factors ([http://en.wikipedia.org/wiki/Vascular_endothelial_growth_factor cascular endothelial growth factor]) and antioangiogenic factors ([http://en.wikipedia.org/wiki/Endostatin endostatin]).  Cathepsin B can suppress the production of VEGF and increase the levels of endostatin.  Under these specific conditions the tube formation is low, but it can be induced by adding VEGF.  Blocking Cathepsin B activity allows for the release of endogenous control mechanism and VEGF levels increase and the endostatin levels decrease.  A diagram representation of how Cathepsin B allows for this mechanism to occur is shown.  

== Medical Implications  ==

Cathepsin B is very important in the field of medicine.  The regulatory secretory pathway of neurons is the major source of toxic beta-amyloid peptides that accumulate in Alzheimer’s disease.  Also, Cathepsin B has been shown to play a role in numerous cardiovascular diseases.