临床抑郁症

An Analysis of the Affective Disorders (Revised Hypothesis)

Abstract

Theresa Hannon

The principal purpose of this Study is to assert that either or both of the Prokineticins fail to be degraded in the case of the Affective Disorders. Although genetic defects in PROKR2 (the Gene responsible for synthesizing Prokineticin 2 Receptor protein) are usually associated with Kallmann Syndrome, this study intends to indicate that the Single Nucleotide Polymorphism (SNP) rs6053303 was homozygous in 4 out of 7 Affective Disorder Genomes. Concerning Kallmann Syndrome, Dode C et al. have noted that this Disorder is caused by insufficient prokineticinsignalling through PROKR2. By comparison, Hannon proposes that the Affective Disorders may be caused by PROKR2’s failure to degrade either or both of the Prokineticins.

Other Researchers have found that exogenous mRNA can be internalized by cells and translated into functioning protein. PROKR2 mRNA has been sequenced (NCBI, ‘Nucleotide’, NM_144773.2); arguably this could be used to restore function to the Prokineticin 2 Receptor and thereby control both of the Affective Disorders (Endogenous Depression and Bipolar Disorder).