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Article type: Short Communication
Authors: Siedlak, Sandra L.a | Jiang, Yinfeia | Huntley, Mikayla L.a | Wang, Luwena | Gao, Jua | Xie, Feia | Liu, Jingyia | Su, Bob | Perry, Georgec | Wang, Xinglonga; *
Affiliations: [a] Department of Pathology, Case Western Reserve University, Cleveland, OH, USA | [b] Department of Neurobiology, Shandong University, Shandong Sheng, China | [c] College of Sciences, University of Texas at San Antonio, San Antonio, TX, USA
Correspondence: [*] Correspondence to: Xinglong Wang, Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. Tel.: +1 216 368 2957; Fax: +1 216 368 8964; E-mail: xinglong.wang@case.edu.
Abstract: Transmembrane Protein 230 (TMEM230) is a newly identified protein associated with Parkinson’s disease (PD) found in Lewy bodies and Lewy neurites of patients with PD or dementia with Lewy body disease. However, TMEM230 has not yet been investigated in the most common neurodegenerative disorder, Alzheimer’s disease (AD). Here, we demonstrate that the expression of TMEM230 is specifically increased in neurons in AD patients. Importantly, both granulovacuolar degeneration (GVD) and dystrophic neurites (DNs), two prominent characteristic pathological structures associated with AD, contain TMEM230 aggregates. TMEM230 immunoreactivity can be detected in neurofibrillary tangles-containing neurons and hyperphosphorylated tau positive DNs. TMEM230 accumulation is also noted around senile plaques. These findings identifying TMEM230 as a component of GVD and DNs suggest TMEM230 dysregulation as a likely mechanism playing an important role in the pathogenesis of AD.
Keywords: Alzheimer’s disease, dystrophic neurites, granulovacuolar degeneration, neurofibrillary tangles, senile plaques, TMEM230
DOI: 10.3233/JAD-170190
Journal: Journal of Alzheimer's Disease, vol. 58, no. 4, pp. 1027-1033, 2017
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