Tomasz Sobów

Medical University of Lodz

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Maria Barcikowska

Polish Academy of Sciences

Tomasz Gabryelewicz

Mossakowski Medical Research Institute, Polish Academy of Sciences

CŻ

Cezary Żekanowski

Polish Academy of Sciences

Iwona Kłoszewska

Medical University of Lodz

Anna Barczak

Polish Academy of Sciences

Małgorzata Chodakowska-Żebrowska

Central Clinical Hospital

Mariusz Berdyński

Mossakowski Medical Research Institute, Polish Academy of Sciences

Adam Wysokiński

Medical University of Lodz

Monika Sieruta

Medical University of Lodz

Paweł P. Liberski

Medical University of Lodz

Cooperative Institutions

Polish Academy of Sciences

Mossakowski Medical Research Institute, Polish Academy of Sciences

Medical University of Lodz

King's College London

UNSW Sydney

Neuroscience Research Australia

New Chemical Syntheses Institute

Karolinska Institutet

Centralny Szpital Kliniczny

Central Clinical Hospital

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The use of tetrabenazine for the treatment of drug-induced tardive dyskinesia – report of four cases

Aktualności Neurologiczne (2016)

Ewa Szczepocka Radosław Magierski Tomasz Sobów Adam Wysokiński

Tardive dyskinesias are defined as a syndrome of involuntary, irregular, hyperkinetic movement disorders, including mixed movement disorders of the face and the mouth as well as choreoathetoid movements of the trunk and limbs. They are a serious and usually irreversible side effect of chronic neuroleptic treatment and affect approximately 15–20% of patients. Treatment attempts using amantadine, levetiracetam, piracetam, clonazepam, propranolol, vitamin B6, vitamin E, ondansetron, botulinum toxin and Ginkgo biloba were made. However, in many cases the treatment efficacy has not been confirmed in long-term studies in larger groups of patients. Tetrabenazine, registered in Poland for the treatment of hyperkinetic motor disorders in the Huntington’s disease, is one of the available therapeutic options. We present the course and the effects of tetrabenazine therapy in four patients with antipsychotic-induced tardive dyskinesias. Based on the experience gained during the research program using tetrabenazine, we believe that the use of this agent should be limited to patients in a stable mental condition, with no current symptoms of depression or active psychotic symptoms. In our opinion, suicidal tendencies or thoughts and a history of neuroleptic malignant syndrome are absolute contraindications. The off-label use of tetrabenazine requires a written informed consent of the patient and careful monitoring of their mental and neurological condition.

Tetrabenazine

Tardive dyskinesia

Amantadine

Ziprasidone

Movement Disorders

10.15557/an.2016.0025

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Citations (2)

Mutations in MAPT and PGRN in polish patients with frontotemporal lobar degeneration

Pharmacological Reports (2009)

Mariusz Berdyński Małgorzata Chodakowska-Żebrowska Tomasz Gabryelewicz Tomasz Sobów Małgorzata Kobryś

Frontotemporal lobar degeneration

10.1016/s1734-1140(09)70190-2

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Sigma nonopioid intracellular receptor 1 mutations cause frontotemporal lobar degeneration–motor neuron disease

Annals of Neurology (2010)

Agnes A. Luty John B. Kwok Carol Dobson‐Stone Clement T. Loy Kirsten Coupland

Frontotemporal lobar degeneration (FTLD) is the most common cause of early-onset dementia. Pathological ubiquitinated inclusion bodies observed in FTLD and motor neuron disease (MND) comprise trans-activating response element (TAR) DNA binding protein (TDP-43) and/or fused in sarcoma (FUS) protein. Our objective was to identify the causative gene in an FTLD-MND pedigree with no mutations in known dementia genes.A mutation screen of candidate genes, luciferase assays, and quantitative polymerase chain reaction (PCR) was performed to identify the biological role of the putative mutation. Neuropathological characterization of affected individuals and western blot studies of cell lines were performed to identify the pathological mechanism of the mutation.We identified a nonpolymorphic mutation (c.672*51G>T) in the 3'-untranslated region (UTR) of the Sigma nonopioid intracellular receptor 1 (SIGMAR1) gene in affected individuals from the FTLD-MND pedigree. The c.672*51G>T mutation increased gene expression by 1.4-fold, corresponding with a significant 1.5-fold to 2-fold change in the SIGMAR1 transcript or Sigma-1 protein in lymphocyte or brain tissue. Brains of SIGMAR1 mutation carriers displayed a unique pathology with cytoplasmic inclusions immunopositive for either TDP-43 or FUS but not Sigma-1. Overexpression of SIGMAR1 shunted TDP-43 and FUS from the nucleus to the cytoplasm by 2.3-fold and 5.2-fold, respectively. Treatment of cells with Sigma-1 ligands significantly altered translocation of TDP-43 by up to 2-fold.SIGMAR1 is a causative gene for familial FTLD-MND with a unique neuropathology that differs from other FTLD and MND cases. Our findings also suggest Sigma-1 drugs as potential treatments for the TDP-43/FUS proteinopathies.

Frontotemporal lobar degeneration

Inclusion bodies

10.1002/ana.22274

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Citations (184)

Mutations in presenilin 1, presenilin 2 and amyloid precursor protein genes in patients with early-onset Alzheimer's disease in Poland

Experimental Neurology (2003)

Cezary Żekanowski Maria Styczyńska Beata Pepłońska Tomasz Gabryelewicz Dorota Religa

PSEN1

Early-onset Alzheimer's disease

10.1016/s0014-4886(03)00384-4

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Citations (93)

PGRN and MAPT gene mutations cause of frontotemporal lobar dementia in Polish population

Journal of the Neurological Sciences (2013)

Mariusz Berdyński Anna Barczak A. Filipek-Gliszczynska Tomasz Gabryelewicz Monika Mandecka

Frontotemporal lobar degeneration

10.1016/j.jns.2013.07.1257

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APOE, CYP46, PRNP and PRND: Genetic polymorphisms in Alzheimer's disease and mild cognitive impairment

European Psychiatry (2008)

Marcin Flirski Monika Sieruta Tomasz Sobów Paweł P. Liberski Iwona Kłoszewska

Homocysteine (Hcy) is harmful to neurons and blood vessels, including the cerebral microvasculature. It is possible that such effects contribute to the cascade of events that leads to cognitive decline, dementia, and depression in later life. Hcy is produced during the metabolism of the essential amino-acid methionine, which also involves a methyl group transfer derived from folate and choline metabolism. Its plasma level can be influenced by factors such as age, vitamin deficiency, renal function, and a common mutation in the methylenetetrahydrofolate reductase (MTHFR) gene, where cytosine is replaced by thymidine (C→T) at nucleotide position 677. Subjects with the TT genotype have higher homocysteine levels and may be particularly prone to experiencing depression as a result of high plasma Hcy and dysfunction of methylation metabolic pathways critical to the synthesis of noradrenaline and serotonin. We designed the present study to investigate whether older women with the TT genotype would have higher depression and lower cognitive scores than women with CT and CC genotypes. A total of 240 community-dwelling women aged 70 years or over volunteered to take part in the study – 29 carried the TT genotype, 113 the CT and 98 the CC genotype. The Beck Depression Inventory (BDI) score for subjects with the TT genotype was statistically similar to the other groups (P = 0.609). Plasma Hcy showed a modest and significant correlation with BDI scores (r = 0.21) that was independent from age, B12 and folate levels. There was no association between beck anxiety inventory (BAI) scores and MTHFR genotype or homocysteine levels. The cognitive assessment of participants included measures of verbal memory, memory for faces, verbal fluency, visuo-spatial abilities and the cognitive section of the Cambridge Examination For Mental Disorders Of The Elderly (CAMCOG) – MTHFR genotype had no clear association with cognitive scores. These results indicate that, in isolation, the MTHFR C677T gene variation does not play an important role in the modulation of mood and cognitive performance in later life.

Depression

10.1016/j.eurpsy.2008.01.308

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Effect of APOE ε4 Allele on Cortical Thicknesses and Volumes: The AddNeuroMed Study

Journal of Alzheimer s Disease (2010)

Yawu Liu Teemu Paajanen Eric Westman Lars‐Olof Wahlund Andrew Simmons

The apolipoprotein E (APOE) ε4 allele is a risk factor for Alzheimer's disease (AD), but its effect on brain volumes is controversial. We explored the effect of the ε4 allele on regional cortical thickness and volume measurements using an automated p

Apolipoprotein E

Orbitofrontal cortex

Gyrus

Caudate nucleus

10.3233/jad-2010-100201

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Citations (89)

Earlier Onset of Alzheimer's Disease: Risk Polymorphisms Within PRNP, PRND, CYP46, and APOE Genes

Journal of Alzheimer s Disease (2009)

Ewa Golańska Krystyna Hułas-Bigoszewska Monika Sieruta Izabela Zawlik Monika Witusik‐Perkowska

We studied eight polymorphisms within APOE, PRNP, PRND, and CYP46 genes in 213 Polish late-onset patients with Alzheimer's disease (AD) and 171 non-demented elderly controls. A latent classification approach, grade-of-membership analysis, was taken t

PRNP

Apolipoprotein E

10.3233/jad-2009-1055

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Citations (21)

Level of thyroid-stimulating hormone in elderly patients with unipolar depression – case–control analysis

Psychiatria i Psychologia Kliniczna (2019)

Adam Wysokiński Łukasz Kroc Elizaveta Fife Iwona Kłoszewska Tomasz Sobów

Depression

Thyroid-stimulating hormone

10.15557/pipk.2019.0006

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Citations (0)