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AUTOANTIBODIES IN ALZHEIMER DISEASE;
  1. Ramin Nilforooshan1,
  2. Angela Vincent2,
  3. Jessica Eccles3,
  4. Rosie Pettingill4,
  5. Philippa Pettingill5,
  6. Lamia Ali6,
  7. Naji Tabet7
  1. 1 Brain Science research Unit, ACU, Holloway Hill, Chertsey, KT16 0AE, UK
  2. 2 Neurosciences Group, Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, UK
  3. 3 Brighton and Sussex Medical School, BN1 9RR, UK
  4. 4 Neurosciences Group, Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, UK
  5. 5 Neurosciences Group, Department of Clinical Neurology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, UK
  6. 6 Brain Science research Unit, ACU, Holloway Hill, Chertsey, KT16 0AE, UK
  7. 7 Cognitive Treatment and Research Unit, Sussex Partnership NHS Foundation Trust, Brighton and Sussex Medical School, BN1 9RR, UK

Abstract

Aims There is increasing evidence to support the relevance of immune system in the pathogenesis of Alzheimer Disease (AD) and also there is growing evidence for importance of specific antibodies in some neurological disorders. Antibodies against Voltage Gated Potassium Channels (VGKC) and Glutamic Decarboxylase (GAD) are of interest for AD. The presence of these antibodies is thought to be related to cognitive impairment and memory problems. In our study we attempted to find a relationship between these antibodies in individuals with AD compared with healthy controls.

Method Twenty two patients with diagnosis of mild to moderate AD aged 65 and above were recruited from a memory clinic. Controls (22) were partners/carers of recruited patients who had no complaints of memory impairment and had a Mini Mental State Examination (MMSE) of 29 and above. Antibodies were measured by radioimmuo-precipitaion assay.

Results AD and control group did not differ significantly in age (p=0.593) and gender (0.674) but as expected the median MMSE scores (p≤0.001) did. We could not find any statistically significant difference between level of VGKC-ab (p=0.490) or GAD (p=0.330) between patients and controls. NMDA antibodies were negative in both groups. One of the patients (84 year old, female, MMSE 20/30 none smoker with no medical history and only 6 months history of memory decline) had strong positive Hippocampal Neurons (G) antibodies. This was observed on the strong immunocytochemical staining of the hippocampal neurons.

Conclusion It is still unclear for how long these antibodies are being identified in acute onset of many neurological diseases including amnesia or psychosis. We know that pathophysiology of AD starts many years before the clinical presentations. It may be the case that positive antibodies can be found in a very early stage of mild cognitive impairment.

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