Affiliations: [a] Department of Anatomy, Touro College of Osteopathic Medicine, New York, NY, USA
| [b] Professor of Pathology and Dean for Research, Touro College of Osteopathic Medicine, New York, NY, USA
| [c] Associate Professor of Pharmacology and Pre-Clinical Dean, Touro College of Osteopathic Medicine, New York, NY, USA
| [d] Department of Basic Biomedical Sciences, Touro College of Osteopathic Medicine, New York, NY, USA
Correspondence:
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Correspondence to: Christine M. Lomiguen, MD, Clinical Instructor of Pathology, Department of Anatomy, Touro College of Osteopathic Medicine, 230 West 125th Street, New York, NY 10027, USA. Tel.: +1 646 981 4747; Fax: +1 212 678 1782; E-mail: [email protected].
Abstract: Chitin is a β-linked straight chain carbohydrate matrix monopolymer prominent in invertebrates, from fungi to arthropods. Surprisingly, chitin is now documented in vertebrates, including humans, a component of vertebrate physiology that has been neglected until now. Chitin levels are elevated in Alzheimer’s disease (AD) patients, not only in the central nervous system but also in the cerebrospinal fluid and plasma. Elevated levels of chitin lectin have been reported in patients with AD. Chitinase activity varies widely in the human population. Chitin levels can increase in individuals with intrinsically low chitinase activity. Elevated amounts of chitin can reflect accumulation of the small chitin fragments that remain wherever rapid hyaluronan synthesis occurs. Another source of chitin may be from remote fungal infections. Chitin can be toxic for neurons, and its accumulation may lead to the development of AD. We present new suggestions for animal models and treatment modalities that could prove useful in future research endeavors. An unexpected connection with Gaucher’s disease patients and their heterozygote relatives is also identified. These chitin-related mechanisms are novel approaches to AD whose etiology until now has defied explication.
