A Theory of Huntington's Disease: Phenocopy, Frame Shift and Rate Equation

18-11 Radburn Road, Fair Lawn, NJ 07410, USA

*Corresponding Author: Eugen Tarnow, 18-11 Radburn Road, Fair Lawn, NJ 07410, USA, Phone: +16462290787, Email: [email protected]

Received Date: October 08, 2024

Published Date: January 03, 2025

Citation: Tarnow E. (2025). A Theory of Huntington's Disease: Phenocopy, Frame Shift and Rate Equation. Mathews J Psychiatry Ment Health. 10(1):48.

Copyrights: Tarnow E. (2025).

ABSTRACT

Huntington’s disease (HD) is one of the most well defined “repeat diseases”, associated with a short repeated genetic sequence, CAG. Recent research points to the possibility that HD is caused by a frame shift. Here is presented three pieces of evidence that supports the frame shift hypothesis. First, taking into account that a phenocopy of HD has a different repeat that is associated with a different gene, I suggest that the Huntingtin gene is not important for HD, only the repeat sequence is. Second, taking into account that a phenocopy of HD has a CTG repeat rather than a CAG repeat, and that the toxin should be the same for both disease types and that the third base in a codon is the least important, I propose the reading frame is shifted for the repeat expansions and the A/T difference occurs on the least important third base. The most likely sense and antisense reading frames are then (GCA)_n and (GCT)_n and the corresponding amino acid is polyalanine as previously suggested. Third, I suggest that the age of onset relationship follows a rate equation based on the frame shift. If the concentration is proportional to the probability of creating a polyalanine of length m in a repeat expansion of length n, the corresponding equation is borne out by the data on age of onset and repeat length and m is found to be about 30.6 (the onset for infinite age).

Keywords: Huntington’s Disease, CAG, Kinetics, Repeat Expansions.