Diseases that run in families usually have genetic causes.
In these patients' brains, as with the patient who had the Christchurch variant, there were extensive amyloid plaques but very few neurofibrillary tangles. This observation confirmed that the tangles are responsible for the cognitive loss and that there are several ways to"disconnect" amyloid and neurofibrillary tangle accumulation.
Finding medicines that might mimic the protective effects of the Christchurch variant or the reelin mutation could help delay Alzheimer's disease symptoms for all patients.
Although there is still discussion of how much slowing of decline is clinically significant, these successes provide support for the amyloid hypothesis. They also suggest that other strategies will be needed for optimal treatment.
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