Aberrant salience (AS) is considered as a predisposing factor in early psychosis. Although it has been frequently examined in the general population as a measure of vulnerability to psychotic disorder, empirical evidence on AS in prodromal phases of psychosis is still relatively scarce. Thus, the aims of this research were (1) to investigate any significant association of AS with functioning, psychopathology and treatment components of an "early intervention in psychosis" program in a sample of young community help-seekers at Ultra-High Risk (UHR) of psychosis along a 1-year follow-up period, and (2) to longitudinally monitor the stability of AS across the 1 year of follow-up. Participants (87 UHR), aged 13–35 years, completed the Aberrant Salience Inventory (ASI), the Comprehensive Assessment of At-Risk Mental States (CAARMS) and the brief version of the Schizotypal Personality Questionnaire (SPQ-B) at baseline and after the 1 year of follow-up. Spearman correlation analyses among psychopathological parameters and specialized treatment components were performed. A multiple linear regression analysis was also carried out. After a 1-year follow-up period, UHR subjects had a statistically relevant decrease in ASI total scores. This was significantly related to the number of individual cognitive-behavioral therapy (CBT) sessions and the number of family psychoeducational sessions offered to UHR participants and their family members during the same 12-month period. In conclusion, AS is clinically relevant in UHR individuals. However, it seems to improve over time along with the delivery of tailored, specialized psychosocial interventions for early psychosis.

Parkinson's disease (PD) with cognitive impairment (PDCI) is essentially diagnosed through clinical and neuropsychological examinations. There is a need to identify biomarkers to foresee cognitive decline in them. We performed label-free unbiased nontargeted proteomics (Q-TOF LC/MS-MS) on the CSF of non-neurological control; PDCI; PD; and normal pressure hydrocephalus (NPH) patients, followed by targeted ELISA for validation. Of the 281 proteins identified, 42 were differentially altered in PD, PDCI, and NPH. With a certain overlap, 28 proteins were altered in PDCI and 25 proteins were altered in NPH. Five significantly upregulated proteins in PDCI were fibrinogen, gelsolin, complement factor-H, and apolipoproteins A-I and A-IV, whereas carnosine dipeptidase-1, carboxypeptidase-E, dickkopf-3, and secretogranin-3 precursor proteins were downregulated. Those uniquely altered in NPH were the insulin-like growth factor-binding protein, ceruloplasmin, α-1 antitrypsin, VGF nerve growth factor, and neural cell adhesion molecule L1-like protein. The ELISA-derived protein concentrations correlated with neuropsychological scores of certain cognitive domains. In PDCI, the Wisconsin card sorting percentile correlated negatively with fibrinogen. Intraperitoneal injection of native fibrinogen caused motor deficits in C57BL/6J mice as assessed by the pole test. Thus, a battery of proteins such as fibrinogen-α-chain, CFAH, and APOA-I/APOA-IV alongside neuropsychological assessment could be reliable biomarkers to distinguish PDCI and NPH.