Advertisement was diagnosed based on medical history, clinical symptoms, physical examination (including nervous system), neuropsychological assessment, laboratory examination, and imaging examination in the Department of Neurology (6/25, 60

Advertisement was diagnosed based on medical history, clinical symptoms, physical examination (including nervous system), neuropsychological assessment, laboratory examination, and imaging examination in the Department of Neurology (6/25, 60.9% 24.0%; P 0.05) and older patients (74.0 72.2 years; P 0.01), suggesting that elderly male patients with AD may be more likely to exhibit an autoimmune anti-BP180 serum response. Discussion BP180 is expressed not only in basal keratinocytes but also in the nucleus basalis and hippocampus of the brain (6). protein from the human brain extract, but none of the controls sera recognized the corresponding protein band. The majority of the patients in the anti-BP180-positive AD group were men (14/23, 60.9%) who were older (74.0 NU7026 years) compared with those in the control group (6/25, 24.0%; P 0.05) (72.2 years; P 0.01). Conclusions Anti-BP180 autoantibodies are present in AD and recognize human recombinant full-length BP180 and a 180-kDa protein from the human brain extract, suggesting that BP180 is a shared autoantigen in AD and BP and may help clarify the mechanism to explain why a high risk of BP exists in AD. Elderly male patients with AD are significantly more likely to develop BP180 serum autoreactivity compared with other patients with AD. (17) found that 73.8% (76/103) of patients with BP had a history of at least one pre-existing ND, among which only dementia was statistically significant (P 0.05). In a systematic review, patients with BP had an increased risk of dementia [odds ratio (OR): 5.48 (95% CI: 3.26C9.23); P 0.001] and ND preceded BP in the majority of cases with a mean time interval of 6.7 years (18). According to our study and others, the development of BP autoantibodies against both the skin and neuronal forms of antigens in BP with ND might be related to cutaneous- and neuronal-subtype BP antigens that have different locations, epitopes, and natural conformations (19-22). In this study, we randomly enrolled 48 patients with AD and 50 sex- and age-matched healthy controls to detect the level of anti-BP180/BP230 IgG autoantibodies in sera. We sought to determine whether these antibodies have reactivity against the BP180 protein of the human brain and skin, which may help reveal the mechanism of high BP incidence in AD. S1PR4 We present the following article in accordance with the MDAR reporting checklist (available at http://dx.doi.org/10.21037/atm-20-5343). Methods Patient samples Forty-eight patients with AD were recruited from the Neurology Clinics of Peking Union Medical College Hospital. AD was diagnosed based on medical history, clinical symptoms, physical examination (including nervous system), neuropsychological assessment, laboratory examination, and imaging examination in the Department of Neurology (6/25, 60.9% 24.0%; P 0.05) and older patients (74.0 72.2 years; P 0.01), suggesting that elderly male patients with AD may be more likely to exhibit an autoimmune anti-BP180 serum response. Discussion BP180 is expressed not only in basal keratinocytes but also in the nucleus basalis and hippocampus of the brain (6). Coincidentally, the nucleus basalis of Meynert and the hippocampal region, which exhibit strong BP180 expression, are well-recognized predilection areas for AD-related lesions (5). Specifically, BP180 is located in lipofuscin granules, which are also associated with AD and ageing processes (23,24). Our data demonstrated that anti-BP180 autoantibodies are more frequent in AD. In a study by Kokkonen (25), 18.0% (20/115) of patients with AD were positive for BP180, which was close to our current result (9/48, 18.8%). Furthermore, we found that 18.8% (9/48) of AD samples reacted with BP180-NC16A, the major epitope of dermal BP180, which revealed that these autoantibodies found in patients with AD could also react with BP180-NC16A similar to in patients with BP. Moreover, different ELISA results have NU7026 been reported in several studies. For example, Foureur (26) tested BP180 antibodies in 138 patients aged over 69 years with no signs of BP (69 patients with dementia and 60 nondementia controls) and found BP180 autoantibodies in 7% (9/138) of dementia patients, which was obviously lower than the proportion in our study. In Messinghams study (27), only one of 26 (3.8%) patients with different types of dementia had detectable autoantibodies against NC16A. The differing results of these studies may be explained by methodological differences, different inclusion criteria, different sample sizes, or different average ages (25). In the present study, we observed that the serum samples of anti-BP180 antibody-positive patients with AD recognized a 180-kDa protein of the human brain extract as well as human cutaneous BP180 and BP180-NC16A, which increases the likelihood that BP180 indeed serves as a common autoantigen NU7026 in AD and BP. Low titers of anti-BP180 autoantibodies may be biomarkers for BP at a later stage. In a previous study, we found that the 180-kDa proteins of mouse and human brains can be recognized by the serum samples of patients with.