Literature DB >> 25091367

CNS involvement in V30M transthyretin amyloidosis: clinical, neuropathological and biochemical findings.

Luís F Maia1, Rui Magalhães2, Joel Freitas3, Ricardo Taipa4, Manuel Melo Pires4, Hugo Osório5, Daniel Dias6, Helena Pessegueiro7, Manuel Correia3, Teresa Coelho8.   

Abstract

OBJECTIVES: Since liver transplant (LT) was introduced to treat patients with familial amyloid polyneuropathy carrying the V30M mutation (ATTR-V30M), ocular and cardiac complications have developed. Long-term central nervous system (CNS) involvement was not investigated. Our goals were to: (1) identify and characterise focal neurological episodes (FNEs) due to CNS dysfunction in ATTR-V30M patients; (2) characterise neuropathological features and temporal profile of CNS transthyretin amyloidosis.
METHODS: We monitored the presence and type of FNEs in 87 consecutive ATTR-V30M and 35 non-ATTR LT patients. FNEs were investigated with CT scan, EEG and extensive neurovascular workup. MRI studies were not performed because all patients had cardiac pacemakers as part of the LT protocol. We characterised transthyretin amyloid deposition in the brains of seven ATTR-V30M patients, dead 3-13 years after polyneuropathy onset.
RESULTS: FNEs occurred in 31% (27/87) of ATTR-V30M and in 5.7% (2/35) of the non-ATTR transplanted patients (OR=7.0, 95% CI 1.5 to 33.5). FNEs occurred on average 14.6 years after disease onset (95% CI 13.3 to 16.0) in ATTR-V30M patients, which is beyond the life expectancy of non-transplanted ATTR-V30M patients (10.9, 95% CI 10.5 to 11.3). ATTR-V30M patients with FNEs had longer disease duration (OR=1.24; 95% CI 1.07 to 1.43), renal dysfunction (OR=4.65; 95% CI 1.20 to 18.05) and were men (OR=3.57; 95% CI 1.02 to 12.30). CNS transthyretin amyloidosis was already present 3 years after polyneuropathy onset and progressed from the meninges and its vessels towards meningocortical vessels and the superficial brain parenchyma, as disease duration increased.
CONCLUSIONS: Our findings indicate that CNS clinical involvement occurs in ATTR-V30M patients regardless of LT. Longer disease duration after LT can provide the necessary time for transthyretin amyloidosis to progress until it becomes clinically relevant. Highly sensitive imaging methods are needed to identify and monitor brain ATTR. Disease modifying therapies should consider brain TTR as a target. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Entities:  

Keywords:  Amyloid; Clinical Neurology; Neuropathology; Neuropathy

Mesh:

Substances:

Year:  2014        PMID: 25091367     DOI: 10.1136/jnnp-2014-308107

Source DB:  PubMed          Journal:  J Neurol Neurosurg Psychiatry        ISSN: 0022-3050            Impact factor:   10.154


  28 in total

1.  Epileptic seizures as a presentation of central nervous system involvement in TTR Val30Met-FAP.

Authors:  Ana Franco; Carla Bentes; Mamede de Carvalho; Pedro Pereira; José Pimentel; Isabel Conceição
Journal:  J Neurol       Date:  2016-10-11       Impact factor: 4.849

Review 2.  Leading RNA Interference Therapeutics Part 1: Silencing Hereditary Transthyretin Amyloidosis, with a Focus on Patisiran.

Authors:  Simoneide S Titze-de-Almeida; Pedro Renato de Paula Brandão; Ingrid Faber; Ricardo Titze-de-Almeida
Journal:  Mol Diagn Ther       Date:  2020-02       Impact factor: 4.074

Review 3.  Current and future treatment of amyloid diseases.

Authors:  M Ankarcrona; B Winblad; C Monteiro; C Fearns; E T Powers; J Johansson; G T Westermark; J Presto; B-G Ericzon; J W Kelly
Journal:  J Intern Med       Date:  2016-05-10       Impact factor: 8.989

4.  Age-dependent cognitive dysfunction in untreated hereditary transthyretin amyloidosis.

Authors:  Ana Martins da Silva; Sara Cavaco; Joana Fernandes; Raquel Samões; Cristina Alves; Márcio Cardoso; Jeffery W Kelly; Cecília Monteiro; Teresa Coelho
Journal:  J Neurol       Date:  2017-12-05       Impact factor: 4.849

5.  Semi-quantitative models for identifying potent and selective transthyretin amyloidogenesis inhibitors.

Authors:  Stephen Connelly; David E Mortenson; Sungwook Choi; Ian A Wilson; Evan T Powers; Jeffery W Kelly; Steven M Johnson
Journal:  Bioorg Med Chem Lett       Date:  2017-05-26       Impact factor: 2.823

Review 6.  Current and Future Treatment Approaches in Transthyretin Familial Amyloid Polyneuropathy.

Authors:  Philippe Kerschen; Violaine Planté-Bordeneuve
Journal:  Curr Treat Options Neurol       Date:  2016-12       Impact factor: 3.598

7.  The identification of a transthyretin variant p.D38G in a Chinese family with early-onset leptomeningeal amyloidosis.

Authors:  Kuan Fan; Haixia Zhu; Hongbo Xu; Ping Mao; Lamei Yuan; Hao Deng
Journal:  J Neurol       Date:  2018-11-23       Impact factor: 4.849

Review 8.  Targeting protein aggregation for the treatment of degenerative diseases.

Authors:  Yvonne S Eisele; Cecilia Monteiro; Colleen Fearns; Sandra E Encalada; R Luke Wiseman; Evan T Powers; Jeffery W Kelly
Journal:  Nat Rev Drug Discov       Date:  2015-09-04       Impact factor: 84.694

Review 9.  Amyloidosis in Heart Failure.

Authors:  Sandra Ihne; Caroline Morbach; Laura Obici; Giovanni Palladini; Stefan Störk
Journal:  Curr Heart Fail Rep       Date:  2019-12

Review 10.  Transthyretin familial amyloid polyneuropathy: an update.

Authors:  Violaine Plante-Bordeneuve
Journal:  J Neurol       Date:  2017-12-16       Impact factor: 4.849

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