Mild Cognitive Impairment in Patients with Moderate to Severe Chronic Plaque Psoriasis

Gisondi, Paolo; Sala, Francesca Della; Alessandrini, Franco; Avesani, Virginia; Zoccatelli, Giada; Beltramello, Alberto; Moretto, Giuseppe; Gambina, Giuseppe; Girolomoni, Giampiero

doi:10.1159/000357220

Cited by 50 publications

(55 citation statements)

References 42 publications

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“…It may also explain the high incidence of neuropsychiatric symptoms in psoriasis, namely the anxiety, irritability and depressive symptoms associated with CNS dysfunction [33]. This suggests potential usefulness of mental training, e.g.…”

Section: Discussionmentioning

confidence: 99%

Cognitive impairment in patients with severe psoriasis

Marek-Józefowicz

Jaracz

Placek

et al. 2017

pdia

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IntroductionPsoriasis is a chronic inflammatory skin disease, in which an important role is played by psychological factors.AimTo evaluate the frontal cognitive functions in patients with psoriasis.Material and methodsThe study included 188 subjects (97 patients with psoriasis and 91 healthy controls). To assess the dorsolateral prefrontal cortex functions, the Trail Making Test and the Stroop test were applied. Severity of psoriasis was assessed by means of the PASI index.ResultsCompared to healthy subjects, psoriatics scored lower in neuropsychological tests assessing memory and executive functions.ConclusionsCognitive dysfunction disclosed by neuropsychological assessment of frontal functions was evident in patients with psoriasis.

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Section: Discussionmentioning

confidence: 99%

Cognitive impairment in patients with severe psoriasis

Marek-Józefowicz

Jaracz

Placek

et al. 2017

pdia

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“…Both mechanisms would make the correlation stronger but for different reasons. Although the specific cellular/biochemical mechanisms for such changes in correlation are unknown, they are likely to share similar mechanisms that underlie brain dysfunction in other autoimmune or inflammatory brain disorders (Selmi et al, 2016), including neuropsychiatric lupus (Belmont et al, 1996, Menon et al, 1999, Omdal et al, 2005), rheumatoid arthritis (Shin et al, 2012), Sjögren's syndrome (Tezcan et al, 2016), and psoriasis (Gisondi et al, 2014). A special case is autoimmune encephalitis where the investigation of cellular autoimmune mechanisms has progressed appreciably (Armangue et al, 2015, Boronat et al, 2013, Clemente-Casares et al, 2016, Dalmau and Rosenfeld, 2008, Dalmau and Rosenfeld, 2014, Linnoila et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Brain Correlates of Human Leukocyte Antigen (HLA) Protection in Gulf War Illness (GWI)

et al. 2016

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BackgroundWe recently reported that six alleles from class II genes of the Human Leukocyte Antigen (HLA) confer protection from Gulf War Illness (GWI) (Georgopoulos et al., 2015). The most significant effect is exerted on Neurological-Cognitive-Mood (NCM), Pain, and Fatigue symptoms, such that higher number of copies of the protective alleles are associated with lower symptom severity. Here we tested the hypothesis that this effect is exerted by modulating the strength of neural synchronicity.MethodsEighty-one Gulf War veterans (65 with GWI and 16 healthy controls) underwent a magnetoencephalography (MEG) scan to assess the strength of brain synchronicity by computing zero-lag crosscorrelations (and their Fisher z transforms) between prewhitened MEG time series. A high-resolution HLA genotyping determined the number of copies, k, of the 6 protective alleles above in each participant. We tested the hypothesis above by regressing NCM, Pain and Fatigue symptom severity against the interaction term, k × z (HLA-related effect), while including z (non-HLA-related effect), gender and age as covariates. The k × z and z terms assessed HLA- and non-HLA-related effects, respectively, of neural synchronicity on symptom severity. The distributions of these effects in sensor space were visualized using statistical heatmaps.FindingsWe found significant, graded HLA- and non-HLA-related effects: (a) NCM > Pain > Fatigue for HLA-related effects, (b) NCM > Fatigue > Pain for non-HLA-related effects, and (c) HLA-related > non-HLA-related effects for all symptoms. These effects had widespread but distinct distributions in sensor space that allowed the orderly separation of the 6 terms (3 symptom domains × 2 HLA factors) in a multidimensional plot, where one dimension separated the symptoms and the other the HLA relation.InterpretationThese findings demonstrate the presence of substantial, widespread, distinct and orderly HLA- and non-HLA-related neural influences on NCM, Pain and Fatigue symptom severity in GWI.FundingU.S. Department of Veterans Affairs and University of Minnesota.

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“…The impact of psoriasis plaques on self-esteem and mood is well-described and the role of psychological stress as a trigger of psoriasis recurrence is also robustly documented 144 . However, measurable signs of subtle cognitive impairment are also observed in psoriasis patients 145, 146 , even during the early phases of the disease 145 .…”

Section: The Cns Is a Major Source Of Superautoantigensmentioning

confidence: 99%

Evolution, immunity and the emergence of brain superautoantigens

Nataf¹

2017

F1000Res

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While some autoimmune disorders remain extremely rare, others largely predominate the epidemiology of human autoimmunity. Notably, these include psoriasis, diabetes, vitiligo, thyroiditis, rheumatoid arthritis and multiple sclerosis. Thus, despite the quasi-infinite number of "self" antigens that could theoretically trigger autoimmune responses, only a limited set of antigens, referred here as superautoantigens, induce pathogenic adaptive responses. Several lines of evidence reviewed in this paper indicate that, irrespective of the targeted organ (e.g. thyroid, pancreas, joints, brain or skin), a significant proportion of superautoantigens are highly expressed in the synaptic compartment of the central nervous system (CNS). Such an observation applies notably for GAD65, AchR, ribonucleoproteins, heat shock proteins, collagen IV, laminin, tyrosine hydroxylase and the acetylcholinesterase domain of thyroglobulin. It is also argued that cognitive alterations have been described in a number of autoimmune disorders, including psoriasis, rheumatoid arthritis, lupus, Crohn's disease and autoimmune thyroiditis. Finally, the present paper points out that a great majority of the "incidental" autoimmune conditions notably triggered by neoplasms, vaccinations or microbial infections are targeting the synaptic or myelin compartments. On this basis, the concept of an immunological homunculus, proposed by Irun Cohen more than 25 years ago, is extended here in a model where physiological autoimmunity against brain superautoantigens confers both: i) a crucial evolutionary-determined advantage via cognition-promoting autoimmunity; and ii) a major evolutionary-determined vulnerability, leading to the emergence of autoimmune disorders in Homo sapiens. Moreover, in this theoretical framework, the so called co-development/co-evolution model, both the development (at the scale of an individual) and evolution (at the scale of species) of the antibody and T-cell repertoires are coupled to those of the neural repertoires (i.e. the distinct neuronal populations and synaptic circuits supporting cognitive and sensorimotor functions). Clinical implications and future experimental insights are also presented and discussed.

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Mild Cognitive Impairment in Patients with Moderate to Severe Chronic Plaque Psoriasis

Cited by 50 publications

References 42 publications

Cognitive impairment in patients with severe psoriasis

Cognitive impairment in patients with severe psoriasis

Brain Correlates of Human Leukocyte Antigen (HLA) Protection in Gulf War Illness (GWI)

Evolution, immunity and the emergence of brain superautoantigens

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