ArticleBMC neurology2011
Cognitive decline in a patient with anti-glutamic acid decarboxylase autoimmunity; case report.
Article in BMC neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Associations between glutamic acid decarboxylase antibodies, oxidative stress markers, and cognitive capacity in adolescents who stutter.Saudi journal of biological sciences · 2023Article
- Case report: Successful autologous hematopoietic stem cell transplantation in a patient with GAD antibody-spectrum disorder with rapidly progressive dementia.Frontiers in neurology · 2023Article
- Serum glutamate decarboxylase antibodies and neurological disorders: when to suspect their association?Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Observational
- Brain and Muscle Metabolic Changes by FDG-PET in Stiff Person Syndrome Spectrum Disorders.Frontiers in neurology · 2021Article
- Diagnostic Value of Structural and Functional Neuroimaging in Autoimmune Epilepsy.Contrast media & molecular imaging · 2020Review
- Autoimmune epilepsy: findings on MRI and FDG-PET.The British journal of radiology · 2019Review
- Evaluation of incidence and clinical features of antibody-associated autoimmune encephalitis mimicking dementia.Behavioural neurology · 2014Article
- Cognitive dysfunction associated with anti-glutamic acid decarboxylase autoimmunity: a case-control study.BMC neurology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlutamic 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.
conclusionsCognitive 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.
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