Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause of dementia. Neurons communicate via chemical messages passed between two cells across a small gap called a synapse. In AD, abnormal cellular structures lead to a loss of synapses and neurons, which results in atrophy of the brain.
The pathogenesis is largely unknown, but there are several characteristic abnormalities found in the brain tissue of patients with AD. These features include excessive granulovacuoles, amyloid plaques, and neurofibrillary tangles.
The nucleus basalis of Meynert (nbM) is a basal forebrain structure that houses the brain’s largest collection of cholinergic neurons. In AD the nbM suffers severe neuron loss and decreased production of acetylcholine, a neurotransmitter with an important role in learning and memory.
Granulovacuolar degeneration is found within the cytoplasm of neurons of the hippocampus. An abnormally high number of fluid-filled spaces, called vacuoles, enlarge the cell’s body causing neuronal dysfunction or cell death.
Amyloid plaques form outside of neurons when protein pieces called beta-amyloid clump together. The plaques block cell-to-cell signaling at synapses and may trigger processes that lead to nerve cell death.
Neurofibrillary tangles are abnormal collections of protein threads inside the nerve that twist around each other. The main protein composing neurofibrillary tangles is called tau.