Most of the knowledge on the genetic component of dementia comes from research on Alzheimer’s disease and psychosis (AD + P). Three different cohort studies show that psychosis in Alzheimer’s disease aggregates in families. The heritability is estimated to be between 30 and 61 %. A stricter definition of AD + P, requiring multiple symptoms and persistence, strengthens the familial aggregation. A genome-wide association study has produced some indication that genes that have been linked with schizophrenia also may be implicated in psychosis in Alzheimer’s disease. In linkage studies, specific loci on several chromosomes, such as chromosomes 2, 7, 8 and 15, have been linked to AD + P. ApoE status, which is strongly associated with increased risk of AD, does not seem to be associated with an increased risk of AD + P .
Neuroimaging and postmortem studies indicate that neurobiological changes in AD+P are more prominent in the neocortex than in the medial temporal lobe, where we find the early signs of AD. Magnetic resonance imaging studies have shown that there is a decrease in grey matter volume in AD+P, particularly in the frontal regions. The association between white matter hyperintensities and AD+P has been investigated, but the results are inconclusive. Positron emission tomography (PET) studies have demonstrated hypometabolism in neocortical regions, in particular in frontal and prefrontal cortex .