The Neuroimmunology of Cortical Disease (Dementia, Epilepsy, and Autoimmune Encephalopathies)

  • Julie L. Roth
  • Brian R. Ott
  • John N. Gaitanis
  • Andrew S. Blum
Part of the Current Clinical Neurology book series (CCNEU)


Alzheimer’s disease (AD) is a neurodegenerative disorder characterized ­pathologically by large numbers of extracellular neuritic plaques containing a core of amyloid Aβ fibrils as well as intracellular neurofibrillary tangles containing hyperphosphorylated tau protein filaments in the neurons of the cerebral cortex. Other features include reactive gliosis, synaptic loss, neuronal death, and mitochondrial dysfunction. A small percentage of cases are due to genetic mutations of the amyloid precursor gene on chromosome 21 and mutations in presenilin 1 and 2 genes on chromosomes 2 and 14, respectively [1]. These presenilin proteins are inherent to secretase enzymes involved with cleavage of the amyloid Aβ precursor protein into amyloidogenic A fragments, particularly Aβ42 [2]. Apolipoprotein E4 is an important risk factor allele for other cases [3]. The molecular underpinnings for the common form of AD occurring sporadically in older patients remain largely to be elucidated.


Dementia Neuritic plaques Immunotherapy Limbic encephalitis Neuromyotonia 


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Julie L. Roth
    • 1
  • Brian R. Ott
    • 2
  • John N. Gaitanis
    • 3
  • Andrew S. Blum
    • 1
  1. 1.Comprehensive Epilepsy Program, Department of Neurology, Rhode Island HospitalThe Warren Alpert Medical School at Brown UniversityProvidenceUSA
  2. 2.Alzheimer’s Disease & Memory Disorders Center, Department of Neurology, Rhode Island HospitalThe Warren Alpert Medical School at Brown UniversityProvidenceUSA
  3. 3.Department of Clinical NeurosciencesWarren Alpert Medical School at Brown UniversityProvidenceUSA

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