Those are exceptions rather than the rule for rare disease. Ashkenazi Jews had a bottleneck effect; SSD is a gain of function, etc. They other thing they have in common is a relatively high allele frequency in the general population.

For interference where a heterozygote would be effected (and therefore selected again) most variants would be de novo; so a homozygous mutant would require simultaneous and identical de novo mutations to occur in the same individual.

Sort of. Protocadherins are like address codes in the developing brain. So the problem is having 2 different sets of instructions for migrating neurons. Hence heterozygotes have disease and homozygotes (even if mutant) are normal. even if co-expressed absent mosiacism the prediction would be disease. However, for reasons I mentioned in the original post human examples would be hard to find because the event of 2 identical yet independent mutations would be highly improbable.

In diseases with recurrent mutations there is usually a mechanistic reason (Gain of function in achondroplasia) that wouldn't apply here.

Here is an even older paper describing this before we found any examples.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1686061/

Yes; the best studied mechanism for this is cellular interference.

PCDH19 is the classic human disease example. It's a protocadherin (cell surface protein that affects migration, signaling, etc) on the X chromosome. When both normal and abnormal PCDH19 is present (XX heterozygotes) affected individuals have epilepsy and developmental delay because neurons with different variants behave differently and have trouble forming networks with each other. XY males, regardless of whether there is a mutant or wt allele are normal. XXY males or mosaic males have the same phenotype as heterozygous females.

This is an illustration: https://www.ncbi.nlm.nih.gov/books/NBK98182/figure/depienne.f4/

EFNB1 is another example: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605834/

OLD paper postulating this: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1686061/

Edit: I know you said you're not interested in sex chromosomes, but this disease mechanism applies just as easily to autosomal genes. We can predict based on males that a true mutant homozygote would be unaffected while a compound heterozygote would be affected.

The problem with finding an autosomal example is being homozygous outside of a consanguinous situation is exceedingly improbable. Not only do both alleles need to develop a disease causing mutation, but they need to mutate in the same way by chance. Most recessive diseases we see are caused by a compound heterozygous state; which while not wild type, it also not homozygous.