Cognitive decline in a patient with anti-glutamic acid decarboxylase autoimmunity; case report

Masahito Takagi, Hiroshi Yamasaki, Keiko Endo, Tetsuya Yamada, Keizo Kaneko, Yoshitomo Oka, Etsuro Mori

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Background: Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme for producing γ-aminobutyric acid, and it has been suggested that antibodies against GAD play a role in neurological conditions and type 1 diabetes. However, it is not known whether dementia appears as the sole neurological manifestation associated with anti-GAD antibodies in the central nervous system.Case presentation: We describe the clinical, neuropsychological, and neuroradiological findings of a 73-year-old female with cognitive dysfunction and type 1A diabetes. Observation and neuropsychological studies revealed linguistic problems, short-term memory disturbance, and frontal dysfunction. MRI showed no significant lesion except for confluent small T2-hyperintensity areas localized in the left basal ganglia. 18F-fluorodeoxy glucose-positron emission tomography (FDG-PET) and 123I-N-isopropyl-p-iodoamphetamine-single photon emission computed tomography (IMP-SPECT) studies showed bifrontal hypometabolism and hypoperfusion. Immunomodulating therapy with intravenous high-dose immunoglobulin resulted in no remission of the cognitive symptoms.Conclusions: Cognitive dysfunction may develop as an isolated neurological manifestation in association with type 1A diabetes and anti-GAD autoimmunity. A systematic study with extensive neuropsychological assessment is indicated in patients with type 1 diabetes and anti-GAD autoimmunity.

Original languageEnglish
Article number156
JournalBMC Neurology
Publication statusPublished - 2011 Dec 21


  • Anti-glutamic acid decarboxylase antibodies
  • Cognitive decline
  • Frontal dysfunction
  • Stiff person syndrome
  • Working memory

ASJC Scopus subject areas

  • Clinical Neurology


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