What is the experimental hypothesis and null hypothesis of these two articles:

(Article 1)

What are the experimental hypothesis and null hypothesis of these two articles?

(Article 1), retrieved from: https://www.medicalnewstoday.com/articles/bipolar-and-autism#summary

Similar gene expression patterns in the brain can be observed in ASD and bipolar disorder, leading to occasional misdiagnosis. The true relationship between these two conditions and the prevalence of co-occurrence remain uncertain due to the frequency of misdiagnoses.

Early and accurate treatment significantly lowers the risk of negative complications associated with both bipolar disorder and ASD, enhancing the likelihood of individuals leading normal, productive lives.

Those worried about themselves or someone they know potentially having either condition should seek a comprehensive diagnosis from a medical professional.

(Article 2)

Whole-genome studies involving large cohorts of affected individuals are revealing genetic connections among autism, schizophrenia, and bipolar disorder. Investigations into Copy Number Variations (CNVs) and rare alleles indicate an overlap between autism and schizophrenia, while analyses of common Single Nucleotide Polymorphism (SNP) variants show a connection between schizophrenia and bipolar disorder. These findings challenge the notion that these disorders are entirely unrelated and suggest shared underlying pathogenic mechanisms.

The research also supports the idea that schizophrenia has a more pronounced neurodevelopmental aspect compared to bipolar disorder, placing it on a continuum of decreasing neurodevelopmental impairment between conditions such as mental retardation and autism on one end and bipolar disorder on the other [74].

The discovery of both rare and common alleles associated with distinct psychiatric disorders poses challenges to their diagnosis and research methodologies. Recent genetic data indicate common pathophysiological mechanisms, emphasizing the need for further exploration in future research. While the disorders may not be phenomenologically identical, the presence of shared risk factors, such as rare CNVs like NRXN1 deletions linked to mental retardation, autism, and schizophrenia, underscores the importance of understanding the interconnectedness.

It is evident that extensive future investigations are necessary, and it is crucial not to be confined by current categorical diagnostic systems. These studies should explore the correlation between genes and other biological variables with dimensional measures of key psychopathological domains across existing diagnostic categories. The growing body of data emphasizes the need to consider a broader clinical spectrum, encompassing autism and mental retardation/cognitive impairment, in addition to the functional psychoses of schizophrenia and bipolar disorder [8].

retrieved from:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784305/