In Alzheimer's disease, an inflammatory cascade begins in response to beta-amyloid. The inflammatory response, involving cytokines and prostaglandins, occurs around beta-amyloid in the neuron. This inflammatory process continues and accelerates the loss of neurons.
Inflammation is a protective response of the body that occurs during the process of repair. The four cardinal signs of inflammation are redness, swelling, heat, and pain. The Russian biologist Elie Metchnikoff proposed that the purpose of inflammation was to bring phagocytotic cells to the injured area in order to engulf invading bacteria. Both Metchnikoff and Paul Ehrlich (who developed the humoral theory of immunity) shared the Nobel Prize in 1908.
Alterations in blood flow occur with inflammation, primarily to increase local circulation and speed repair. The blood vessels become more permeable, which allows protein-rich fluid (exudate) to collect between cells. This excess extravascular fluid is called edema.
The mechanism of inflammation is a complex interaction of chemical messengers. Arachadonic acid, via 5-lipoxygenase, forms leukotrienes that cause vasoconstriction, bronchospasm (i.e., asthma), and increased permeability. Alternatively, arachadonic acid can form, via cyclooxygenase, prostaglandins, which have similar actions and cause pain. Aspirin and indomethican inhibit cyclooxygenase which results in pain relief, but does not address the underlying cause of the inflammation or stop the actions of the leukotrienes.
Inflammation can be acute, as occurs after a physical injury, or chronic. There are several causes of chronic inflammation, including:
- Persistent infections
- Prolonged exposure to toxic elements
- Autoimmune disease
Inflammation is considered to be an underlying cause of Alzheimer's disease, primarily because beta-amyloid is an inflammatory protein (Hull 1996; McGeer et al. 1999).
C-reactive protein is a marker of inflammation that is associated with Alzheimer's disease (Iwamoto et al. 1994).