Hirano bodies are intracellular aggregates of actin and actin-associated proteins first observed in neurons (nerve cells) by Asao Hirano in 1965. The eponym âÂÂHirano bodiesâ was not introduced until 1968, by Schochet et al., three years after Hirano first observed the proteins.
Hirano bodies are found in the nerve cells of individuals afflicted with certain neurodegenerative disorders, such as Alzheimer's disease and CreutzfeldtâÂÂJakob disease.
Hirano bodies were first described in the CA1 in patients with amyotrophic lateral sclerosis and parkinsonism-dementia complex (ALS-PDC). Hirano bodies (Hb) are found mostly in the neuronal processes in the pyramidal layer in the SommerâÂÂs sector (CA1) of the hippocampus, mostly arising from age related changes in the microfilament system. Hirano bodies are often described as rod-shaped, crystal-like, and eosinophilic (pink after staining with haematoxylin and eosin). They are frequently seen in hippocampal pyramidal cells. An experimental model of Hirano body formation has been reported, using a genetically altered strain of the slime mold Dictyostelium discoideum.
Hirano bodies have been noted as a function of age without obvious underlying neurodegeneration.
The SommerâÂÂs sector (CA1) of the hippocampus has been described to be influential in the formation of new memories, as well as, containing inclusion bodies that contribute to a hallmark of AlzheimerâÂÂs disease (AD), intellectual deficit. AlzheimerâÂÂs neurofibrillary tangles show a preference to form in the CA1, which is one of the major areas in which HbâÂÂs have been observed. There are a larger number of HbâÂÂs found in people with AlzheimerâÂÂs disease than those without the disease. Additionally many processes of AlzheimerâÂÂs neurofibrillary tangles have been observed to contain Hirano bodies.
Hirano bodies are described as cytoplasmic paracrystalline lattices, which are a main form of a pathological feature seen in a broad spectrum of neurodegenerative diseases, such as AlzheimerâÂÂs disease (AD). There is an upregulation of a macroautophagic pathway related to AD that can be related to an actin aggregate thought to be an intermediate in the formation of Hirano bodies. More specifically the actin and actin binding proteins seen in Hirano bodies are a significant feature of an AlzheimerâÂÂs disease brain. Additionally, variations in the locational characteristics of ò-amyloid precursor proteins seen in AlzheimerâÂÂs disease are connected to Hirano bodies. It was observed that Hirano bodies are a specific site of a C-terminal fragment of ò-amyloid precursor proteins.