The son of a man who does not have Huntington's develops Huntington's after age

Could of gotten the gene from the mother, it could of been passed down in the family and started to become active, or he could be the only one in the family with that gene.

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Autosomal dominant phenotypes can manifest in the offspring when the father does
not show signs of the condition:
1. The disease allele could have come from his mother. That is, the father could
have been homozygous hh, or the son could be homozygous for the
Huntington’s allele (HH), giving rise to an earlier and more vigorous onset.
2. Due to genetic anticipation, the original father may have not had enough CAG
repeats to cross the threshold of penetrance required to show symptoms of
Huntington’s. More repeats may have been formed in the germ cells down the
generational line.
3. Genotypically, both could be heterozygous Hh, but disease onset (the
phenotype in question) frequently onsets earlier in later generations than in the
parental generations. Theoretically, the father could still in fact begin to show
signs of Huntington’s, but merely hasn’t done so yet.

2) The offspring will show signs of the disease earlier than the father mostly due to
increased trinucleotide repeats. The penetrance and onset of the disease is increased as
the number of CAG repeats increases. The offspring will have increased numbers of the
CAG repeats due to the phenomena of genetic anticipation, whereby certain disorders
(especially trinucleotide repeat disorders) onset earlier as the disease is passed down
the lineage due to increased repeats of the CAG codon, bringing the number of repeats
farther past the disease threshold, thereby increasing the disease’s penetrance as the
lineage continues.

These repeats often appear in the ORF of the mutated gene, causing protein changes by
changing the amino acid sequence of the proteins (the proteins’ primary structure).