| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3341840 | Autoimmunity Reviews | 2011 | 5 Pages |
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”.
► Aging alone cannot be the only cause of Alzheimer's disease. ► Chronic inflammation may lead to neurotoxicity. ► Polymorphisms in proinflammatory substances can lead to AD development. ► A new diagnostic and therapeutic target could be represented by antibodies anti Aβ peptide. ► Both autoimmunity and inflammation have a role in developing AD.
