General forms of the Kähler and superpotenials that lead to consistent low energy brokenSupersymmetry originating from N = 1 Supergravity have been classified and used formodel building since more than three decades. We point out the incompleteness of thisclassification when hidden sector vacuum expectation values are of the order of the Planckmass. Focusing in this paper mainly on the case of minimal Kähler potential, we adopta rigorous approach that retrieves on the one hand the known forms, and demonstrateon the other hand the existence of a whole set of new forms for the superpotential ofwhich we give a complete classification. The latter forms involve a new type of chiralsuperfields having the unusual property of belonging neither to the hidden sector nor tothe conventional observable sector. Comparing the obtained forms with the conventionalones, we argue how new possibilities for model building can arise, and discuss the gravitymediation of soft as well as additional hard (but parametrically small) Supersymmetrybreaking, in the presence of the new type of chiral superfields. In the simplest case,we study the vacuum structure, characterize the masses and couplings of the scalarcomponents to the hidden and observable sectors and discuss briefly the physical rolethey could play. In the generic case, we estimate the magnitude and possible consequencesof the hard breaking of Supersymmetry in terms of the interplay between hidden andvisible sectors mass scales.

Background: Major depressive disorder (MDD) is a serious public health problem with high lifetime prevalence (4.4-20%) in the general population. The monoamine hypothesis is the most widespread etiological theory of MDD. Also, recent scientific data has emphasized the importance of immuno-inflammatory pathways in the pathophysiology of MDD. The lack of data on the magnitude of brain neuroinflammation in MDD is the main limitation of this inflammatory hypothesis. Our team has previously demonstrated the relevance of [18F] DPA-714 as a neuroinflammation biomarker in humans. We formulated the following hypotheses for the current study: (i) Neuroinflammation in MDD can be measured by [18F] DPA-714; (ii) its levels are associated with clinical severity; (iii) it is accompanied by anatomical and functional alterations within the frontal-subcortical circuits; (iv) it is a marker of treatment resistance. Methods: Depressed patients will be recruited throughout 4 centers (Bordeaux, Montpellier, Tours, and Toulouse) of the French network from 13 expert centers for resistant depression. The patient population will be divided into 3 groups: (i) experimental group-patients with current MDD (n = 20), (ii) remitted depressed group-patients in remission but still being treated (n = 20); and, (iii) control group without any history of MDD (n = 20). The primary objective will be to compare PET data (i.e., distribution pattern of neuroinflammation) between the currently depressed group and the control group. Secondary objectives will be to: (i) compare neuroinflammation across groups (currently depressed group vs. remitted depressed group vs. control group); (ii) correlate neuroinflammation with clinical severity across groups; (iii) correlate neuroinflammation with MRI parameters for structural and functional integrity across groups; (iv) correlate neuroinflammation and peripheral markers of inflammation across groups. Discussion: This study will assess the effects of antidepressants on neuroinflammation as well as its role in the treatment response. It will contribute to clarify the putative relationships between neuroinflammation quantified by brain neuroimaging techniques and peripheral markers of inflammation. Lastly, it is expected to open innovative and promising therapeutic perspectives based on anti-inflammatory strategies for the management of treatment-resistant forms of MDD commonly seen in clinical practice. Clinical trial registration (reference: NCT03314155) https://www.clinicaltrials.gov/ct2/show/NCT03314155?term=neuroinflammation&cond=depression&cntry=FR&rank=1.

The relation of white matter hyperintense lesions to episodic memory impairment in patients with Parkinson's disease (PD) is still controversial. We aimed at evaluating the relation between white matter hyperintense lesions and episodic memory decline in patients with PD. In this multicentric prospective study, twenty-one normal controls, 15 PD patients without mild cognitive impairment (MCI) and 13 PD patients with MCI were selected to conduct a clinico-radiological correlation analysis. Performance during episodic memory testing, age-related white matter changes score, total manual and automated white matter hyperintense lesions volume and lobar white matter hyperintense lesions volumes were compared between groups using the Kruskal-Wallis and Wilcoxon signed-rank tests, and correlations were assessed using the Spearman test. MCI PD patients had impaired free recall. They also had higher total, left prefrontal and left temporal white matter hyperintense lesions volumes than normal controls. Free recall performance was negatively correlated with the total white matter hyperintense lesions volume, either manually or automatically delineated, but not with the age-related white matter changes score. Using automated segmentation, both the left prefrontal and temporal white matter hyperintense lesions volumes were negatively correlated with the free recall performance. Early episodic memory impairment in MCI PD patients may be related to white matter hyperintense lesions, mainly in the prefrontal and temporal lobes. This relation is influenced by the method used for white matter hyperintense lesions quantification. Automated volumetry allows for detecting those changes.