Subjective cognitive decline (SCD) has been described as a probable early stage of dementia, as it has consistently appeared to precede the onset of objective cognitive impairment. SCD is related to many risk factors, including genetic predisposition for dementia. The Apolipoprotein (APOE) ε4 allele, which has been thoroughly studied, seems to explain genetic risk for SCD only partially. Therefore, we aimed to summarize existing data regarding genetic factors related to SCD, beyond APOE ε4, in order to improve our current understanding of SCD. We conducted a PRISMA systematic search in PubMed/MEDLINE and Embase databases using the keywords \"subjective cognitive decline\" and \"genetic predisposition\" with specific inclusion and exclusion criteria. From the 270 articles identified, 16 were finally included for the qualitative analysis. Family history of Alzheimer\'s disease (AD) in regard to SCD was explored in eight studies, with conflicting results. Other genes implicated in SCD, beyond APOE ε4, were investigated in six studies, which were not strong enough to provide clear conclusions. Very few data have been published regarding the association of polygenic risk for AD and SCD. Thus, many more genes related to AD must be studied, with polygenic risk scores appearing to be really promising for future investigation.

BACKGROUND: The aging of the worlds population leads to an increase in the prevalence of age-related diseases, including cognitive impairment. At the stage of dementia, therapeutic interventions become usually ineffective. Therefore, researchers and clinical practitioners today are looking for methods that allow for early diagnosis of cognitive impairment, including techniques that are based on the use of biological markers.
OBJECTIVE: The aim of this literature review is to delve into scientific papers that are centered on modern laboratory tests for Alzheimers disease, including tests for biological markers at the early stages of cognitive impairment.
METHODS: The authors have carried out a descriptive review of scientific papers published from 2015 to 2023. Studies that are included in the PubMed and Web of Science electronic databases were analyzed. A descriptive analysis was used to summarized the gleaned information.
RESULTS: Blood and cerebrospinal fluid (CSF) biomarkers, as well as the advantages and disadvantages of their use, are reviewed. The most promising neurotrophic, neuroinflammatory, and genetic markers, including polygenic risk models, are also discussed.
CONCLUSIONS: The use of biomarkers in clinical practice will contribute to the early diagnosis of cognitive impairment associated with Alzheimers disease. Genetic screening tests can improve the detection threshold of preclinical abnormalities in the absence of obvious symptoms of cognitive decline. The active use of biomarkers in clinical practice, in combination with genetic screening for the early diagnosis of cognitive impairment in Alzheimers disease, can improve the timeliness and effectiveness of medical interventions.

This study aimed to systematically review current models for communicating polygenic scores (PGS) and psycho-behavioral outcomes of receiving PGSs.
Original research on communicating PGSs and reporting on psycho-behavioral outcomes was included. Search terms were applied to 5 databases and were limited by date (2009-2021).
In total, 28 articles, representing 17 studies in several disease settings were identified. There was limited consistency in PGS communication and evaluation/reporting of outcomes. Most studies (n = 14) presented risk in multiple ways (ie, numerically, verbally, and/or visually). Three studies provided personalized lifestyle advice and additional resources. Only 1 of 17 studies reported using behavior change theory to inform their PGS intervention. A total of 8 studies found no evidence of long-term negative psychosocial effects up to 12 months post result. Of 14 studies reporting on behavior, 9 found at least 1 favorable change after PGS receipt. When stratified by risk, 7 out of 9 studies found high PGS was associated with favorable changes including lifestyle, medication, and screening. Low-risk PGS was not associated with maladaptive behaviors (n = 4).
PGS has the potential to benefit health behavior. High variability among studies emphasizes the need for developing standardized guidelines for communicating PGSs and evaluating psycho-behavioral outcomes. Our findings call for development of best communication practices and evidence-based interventions informed by behavior change theories.

The genetic basis of mood disorders can, theoretically, provide diagnostic information in scenarios of clinical uncertainty. Therefore, we examined the available body of knowledge on the association between polygenic risk scores for bipolar disorder (BP-PRSs) and pediatric bipolar spectrum and related disorders. We performed a literature search through PubMed in March of 2020. The following variables were extracted from relevant studies: population age, study sample size, source of polygenic risk scores, source of data, the primary goal of the study, the assessments used during the course of the study, and the main findings/outcomes of each study. BP-PRSs were associated with deficits in executive functioning and the diagnosis of attention deficit/hyperactivity disorder (ADHD). Three studies included in our analysis directly compared major depressive disorder (MDD)-PRSs to BP-PRSs in youth. Results showed that MDD-PRSs, and not BP-PRSs, were associated with ADHD symptoms, internalizing problems, and social problems. ADHD-PRSs were associated with conduct problems, depressive symptomatology, and externalizing disorders symptoms. Findings revealed that ADHD-PRSs were more clearly associated with emotional reactivity, emotional dysregulation, and irritability-frequent correlates of pediatric BP disorder. These findings suggest that ADHD-PRSs may have an important contribution to the development of mood related problems in youth.

Studies testing the effect of single genetic variants on substance use have had modest success. This paper reviewed 39 studies using polygenic measures to test interaction with any type of environmental exposure (G×E) in alcohol, tobacco, and cannabis use. Studies using haplotype combinations, sum scores of candidate-gene risk alleles, and polygenic scores (PS) were included. Overall study quality was moderate, with lower ratings for the polygenic methods in the haplotype and candidate-gene score studies. Heterogeneity in investigated environmental exposures, genetic factors, and outcomes was substantial. Most studies (N = 30) reported at least one significant G×E interaction, but overall evidence was weak. The majority (N = 26) found results in line with differential susceptibility and diathesis-stress frameworks. Future studies should pay more attention to methodological and statistical rigor, and focus on replication efforts. Additional work is needed before firm conclusions can be drawn about the importance of G×E in the etiology of substance use.