This review aims to identify the mechanistic relationships related to periodontal diseases and its possible association with changes in human milk composition and the composition and function of infants’ gut microbiome.

Maternal health conditions, especially inflammatory, are associated with altered human milk composition. It is not known whether maternal oral inflammatory diseases, including periodontal diseases, deleteriously affect human milk composition.

A narrative review was conducted according to SANRA, the Scale for the Assessment of Narrative Review Articles, guidelines. PubMed, Google Scholar, and Cochrane database of systematic reviews were searched from September 2019 up to December 2023 using keywords such as breast/human milk, maternal health/infections, and periodontal diseases. Reference lists of relevant articles were also screened. Our primary outcome of interest was human milk composition (i.e., any changes in macronutrients, immunological components, etc.). Secondary outcomes included changes in human milk microbiome and subsequent changes in the infant gut microbiome. Outcomes were synthesized using a narrative approach where the existing evidence and current literature were summarized. No risk of bias assessment of the studies was performed in this review.

The search yielded no studies investigating the relationship between periodontal diseases in nursing mothers and changes in human milk composition. However, a dose–response relationship exists between the severity of periodontal diseases and the risk of adverse pregnancy outcomes such as preterm birth. Mastitis and diabetes affected milk lipids. Immunoglobulin A (sIgA) was increased in mastitis, whereas reduced concentrations were reported in diabetes. Potential biological pathways through which periodontal diseases can negatively affect human milk composition include the systemic dissemination of inflammatory cytokines like IL-6, PGE2, and tumor necrosis factor (TNF)-β that can be up-regulated by bacterial by-products. This biological plausibility needs to be investigated, given the potentially negative impact on the quality of human milk that could be caused by periodontal inflammation.

Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.

To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.

Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.

Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.

AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.

The Comprehensive Assessment of Neurodegeneration and Dementia (COMPASS-ND) cohort study of the Canadian Consortium on Neurodegeneration in Aging (CCNA) is a national initiative to catalyze research on dementia, set up to support the research agendas of CCNA teams. This cross-country longitudinal cohort of 2310 deeply phenotyped subjects with various forms of dementia and mild memory loss or concerns, along with cognitively intact elderly subjects, will test hypotheses generated by these teams.

The COMPASS-ND protocol, initial grant proposal for funding, fifth semi-annual CCNA Progress Report submitted to the Canadian Institutes of Health Research December 2017, and other documents supplemented by modifications made and lessons learned after implementation were used by the authors to create the description of the study provided here.

The CCNA COMPASS-ND cohort includes participants from across Canada with various cognitive conditions associated with or at risk of neurodegenerative diseases. They will undergo a wide range of experimental, clinical, imaging, and genetic investigation to specifically address the causes, diagnosis, treatment, and prevention of these conditions in the aging population. Data derived from clinical and cognitive assessments, biospecimens, brain imaging, genetics, and brain donations will be used to test hypotheses generated by CCNA research teams and other Canadian researchers. The study is the most comprehensive and ambitious Canadian study of dementia. Initial data posting occurred in 2018, with the full cohort to be accrued by 2020.

Availability of data from the COMPASS-ND study will provide a major stimulus for dementia research in Canada in the coming years.

We sought to investigate the relationship between neuroticism and depression in an elderly cohort. In this paper, we describe the methods of an National Institute of Mental Health—NIMH-supported study and present findings among the cohort enrolled to date.

We used the NEO Personality Inventory to assess neuroticism, and we employed several cognitive neuroscience-based measures to examine emotional control.

Compared with a group of 27 non-depressed older control subjects, 33 older depressed subjects scored higher on measures of state and trait anxiety and neuroticism. On our experimental neuroscience-based measures, depressed subjects endorsed more negative words compared with controls on an emotional characterization test. In addition, we found a significant group-by-congruency effect on an emotional interference test where subjects were asked to identify the face's emotional expression while ignoring the words “fear” or “happy” labeled across the face.

Thus, in this preliminary work, we found significant differences in measures of neuroticism and emotional controls among older adults with and without depression.