Alzheimer's disease, autoimmunity and inflammation. The good, the bad and the ugly

Autoimmun Rev. 2011 Dec;11(2):149-53. doi: 10.1016/j.autrev.2011.09.005. Epub 2011 Oct 5.

Abstract

Alzheimer's disease (AD) has been recognized as the most common cause of sporadic dementia. It represents both a medical and social problem, as it affects 10% of over-65 population. Even if the elderly are the most involved population, aging alone cannot be considered as the only cause of this disease. In this review we wanted to focus on the last hypotheses on the possible causes of this neuronal affection. We focused in particular on the role of inflammation and alteration of the inflammatory status that is typical of the elderly and may lead to chronic inflammation. The inflammation seems to be a cause of neuronal impairment and loss. Some studies have proposed a protective role of antiinflammatory drugs. Then we analyzed the role of genetic polymorphisms of some pro-inflammatory substances that seem to be linked to some cases of dementia. The complement system seems to have a role too, as some factors have been found in senile plaques, representing a possible involvement of classical complement pathway. One of the latest hypotheses is about the role of blood-brain barrier (BBB), as its loss of integrity may lead to a passage of proteins in cerebro spinal fluid (CSF), causing a compromised role of BBB in preserving the brain as an "immune sanctuary".

Publication types

  • Review

MeSH terms

  • Aged
  • Alzheimer Disease / complications
  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / genetics
  • Alzheimer Disease / immunology*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Anti-Inflammatory Agents, Non-Steroidal / administration & dosage
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Apolipoproteins E / genetics
  • Apolipoproteins E / immunology
  • Autoimmunity / drug effects
  • Autoimmunity / immunology
  • Blood-Brain Barrier / immunology*
  • Blood-Brain Barrier / metabolism
  • Blood-Brain Barrier / pathology
  • Brain / drug effects
  • Brain / immunology*
  • Brain / metabolism
  • Brain / pathology
  • Complement System Proteins / immunology
  • Complement System Proteins / metabolism*
  • Humans
  • Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent / genetics
  • Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent / immunology
  • Immunologic Memory
  • Inflammation / complications
  • Inflammation / drug therapy
  • Inflammation / genetics
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Inflammation / pathology
  • Interleukin-10 / genetics
  • Interleukin-10 / immunology
  • Interleukin-1beta / genetics
  • Interleukin-1beta / immunology
  • Neurons / drug effects
  • Neurons / immunology*
  • Neurons / metabolism
  • Neurons / pathology
  • Plaque, Amyloid / immunology
  • Plaque, Amyloid / metabolism*
  • Polymorphism, Genetic
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / immunology
  • alpha 1-Antichymotrypsin / genetics
  • alpha 1-Antichymotrypsin / immunology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Apolipoproteins E
  • IL10 protein, human
  • Interleukin-1beta
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • alpha 1-Antichymotrypsin
  • Interleukin-10
  • Complement System Proteins
  • Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent