title: Alzheimer's disease, autoimmunity and inflammation. The good, the bad and the ugly.
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".
authors: Department of Internal Medicine and Therapeutics, Geriatric Section, University of Pavia, ASP, IDR S. Margherita, via Emilia 12, Pavia, Italy.
authors: F
authors: F
authors: Sardi
authors: L
authors: L
authors: Fassina
authors: L
authors: L
authors: Venturini
authors: M
authors: M
authors: Inguscio
authors: F
authors: F
authors: Guerriero
authors: E
authors: E
authors: Rolfo
authors: G
authors: G
authors: Ricevuti
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000627:therapeutic use; D001057:Apolipoproteins E / Q000235:genetics / Q000276:immunology; D015551:Autoimmunity / Q000187:drug effects / Q000276:immunology; D001812:Blood-Brain Barrier / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent / Q000235:genetics / Q000276:immunology; D007156:Immunologic Memory; D007249:Inflammation / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000235:genetics / Q000276:immunology; D009474:Neurons / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D058225:Plaque, Amyloid / Q000276:immunology / Q000378:metabolism*; D011110:Polymorphism, Genetic; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000276:immunology; D000514:alpha 1-Antichymotrypsin / Q000235:genetics / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001057:Apolipoproteins E; C508609:IL10 protein, human; D053583:Interleukin-1beta; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000514:alpha 1-Antichymotrypsin; D016753:Interleukin-10; D003165:Complement System Proteins; D025782:Hydroxymethylglutaryl-CoA-Reductases, NADP-dependent