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Journal of Neurology

, Volume 265, Issue 4, pp 968–969 | Cite as

Early-onset subcortical ischemic vascular dementia in an adult with mtDNA mutation 3316G>A

  • Giuseppe Lanza
  • Mariagiovanna Cantone
  • Sabrina Musso
  • Eugenia Borgione
  • Carmela Scuderi
  • Raffaele Ferri
Letter to the Editors

Dear Sirs,

The term subcortical ischemic vascular disease (SIVD) identifies a clinically homogeneous group of patients at risk for future vascular dementia (VaD) [1]. However, while cerebrovascular changes are common findings in aged subjects with or without dementia, etiology of dementing disorders in younger patients is challenging and often undetermined. We report a young woman without any conventional vascular risk factor, with a typical neuroimaging pattern of SIVD, and a clinical-cognitive profile of VaD.

A 59-year old woman complained about a 6-year history of progressive cognitive deterioration, along with apathy and depressive symptoms. Family and past medical history were uneventful. She did not take any medication. General and neurological examinations were within normal limits, except for diffuse brisk tendon reflexes. A comprehensive neuropsychological battery disclosed a global cognitive decline involving multiple domains (especially at executive functions,...

Notes

Compliance with ethical standards

Conflicts of interest

The authors declare that they have no conflict of interest.

Ethical standards

The authors state that they acted in accordance with the ethical standards of the 1964 Helsinki declaration and its later amendments.

References

  1. 1.
    Jokinen H, Kalska H, Ylikoski R, Madureira S, Verdelho A, van der Flier WM, Scheltens P, Barkhof F, Visser MC, Fazekas F, Schmidt R, O’Brien J, Waldemar G, Wallin A, Chabriat H, Pantoni L, Inzitari D, Erkinjuntti T, LADIS Group (2009) Longitudinal cognitive decline in subcortical ischemic vascular disease: the LADIS Study. Cerebrovasc Dis 27:384–391.  https://doi.org/10.1159/000207442 CrossRefPubMedGoogle Scholar
  2. 2.
    Hsu MJ, Sheu JR, Lin CH, Shen MY, Hsu CY (2010) Mitochondrial mechanisms in amyloid beta peptide-induced cerebrovascular degeneration. Biochim Biophys Acta 1800:290–296.  https://doi.org/10.1016/j.bbagen.2009.08.003 CrossRefPubMedGoogle Scholar
  3. 3.
    Grazina M, Silva F, Santana I, Santiago B, Mendes C, Simões M, Oliveira M, Cunha L, Oliveira C (2004) Frontotemporal dementia and mitochondrial DNA transitions. Neurobiol Dis 15:306–311CrossRefPubMedGoogle Scholar
  4. 4.
    Ji L, Hou X, Han X (2001) Prevalence and clinical characteristics of mitochondrial tRNAleu(UUR) nt 3243 A→G and nt 3316 G→A mutations in Chinese patients with type 2 diabetes. Diabetes Res Clin Pract 54:S35–S38CrossRefPubMedGoogle Scholar
  5. 5.
    Kaminsky YG, Tikhonova LA, Kosenko EA (2015) Critical analysis of Alzheimer’s amyloid-beta toxicity to mitochondria. Front Biosci (Landmark Ed) 20:173–197CrossRefGoogle Scholar
  6. 6.
    Carnevale D, Mascio G, D’Andrea I et al (2012) Hypertension induces brain beta amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature. Hypertension 60:188–197CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Oasi Research Institute – IRCCSTroinaItaly

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