1.A Case of Fainiliai Amyloid Neuropathy presenting as Autonomic Failure.
Youngchul YOON ; Seihee CHANG ; Dongsuk HAM ; Kangkon LEE ; Byungchul AN ; Ohsang KWON ; Eunsub PARK
Journal of the Korean Neurological Association 1995;13(2):341-346
No abstract available.
Amyloid Neuropathies*
;
Amyloid*
3.Tafamidis for a Transplant Patient with Transthyretin Amyloid Polyneuropathy.
Jesús ROMERO-IMBRODA ; Teresa SAGRARIO-FUSTERO ; Clementina DEL CANTO-PÉREZ
Journal of Clinical Neurology 2017;13(4):444-446
No abstract available.
Amyloid Neuropathies*
;
Amyloid*
;
Humans
;
Prealbumin*
4.Magnetic Resonance Image Findings of Cerebral Amyloid Angiopathy Related Inflammation
Byeol A YOON ; Kyung Won PARK ; Sang Myung CHEON
Journal of the Korean Neurological Association 2019;37(4):438-439
No abstract available.
Cerebral Amyloid Angiopathy
;
Inflammation
6.Association between QRS voltages and amyloid burden in patients with cardiac amyloidosis.
Jing-Hui LI ; Changcheng LI ; Yucong ZHENG ; Kai YANG ; Yan HUANG ; Huixin ZHANG ; Xianmei LI ; Xiuyu CHEN ; Linlin DAI ; Tian LAN ; Yang SUN ; Minjie LU ; Shihua ZHAO
Chinese Medical Journal 2024;137(3):365-367
7.Drug Development for Alzheimer's Disease: Recent Progress.
Experimental Neurobiology 2010;19(3):120-131
Alzheimer's disease, the most common cause of dementia, is characterized by two major pathological hallmarks: amyloid plaques and neurofibrillary tangles. Based on these two indicators, an amyloid cascade hypothesis was proposed, and accordingly, most current therapeutic approaches are now focused on the removal of beta-amyloid peptides (Abeta from the brain. Additionally, strategies for blocking tau hyperphosphorylation and aggregation have been suggested, including the development of drugs that can block the formation of tangles. However, there are no true disease-modifying drugs in the current market, though many drugs based on theories other than Abeta and tau pathology are under development. The purpose of this review was to provide information on the current development of AD drugs and to discuss the issues related to drug development.
Alzheimer Disease
;
Amyloid
;
Brain
;
Dementia
;
Neurofibrillary Tangles
;
Peptides
;
Plaque, Amyloid
8.Amyloid Deposit in Malignant Cutaneous Epithelial Tumors.
Kwang Hyun CHO ; Kyu Han KIM ; Seung Ho CHANG ; Eui Keun HAM
Korean Journal of Dermatology 1990;28(6):715-721
We examined the amyloid deposit in various malignant cutaneous epithelial tumors by using Dylon stain. Histochemically identifiable amyloid deposits associated with basal cell epitheliomas(BCEs), squamous cell carcinomas(SCCs) and Bowens diseases were studied with monoclonal cytokeratin antibodies and anti-amyloid P antibodies. The results were as follaws, l. Amyloid deposits were detected in 5 of 12 BCEs, 4 of 11 SCCs, 3 of 9 Bowens diseases and 1 of 8 actinic keratoses. Amyloid deposits were not detected in o keratoacanthomas, 2 verrucous carcinomas, 1. Pagets disease and 3 extramammary Pagets diseases. 2. Anti-keratin antibody 34BE12 and anti-amyloid P antibody reacted with amyloid deposits in 3 of 5 BCEs which showed abundant amyloid deposits by Dylon stain. 3. Of 4 SCCs which showed amyloid deposits by Dylon stain, anti-keratin ant.ibody 34pE12 reacted with amyloid deposits in 2 cases and anti-amyloid P antibody reacted with amyloid deposits in 3 cases. 4. Anti-amyloid P antibody reacted with arnyloid deposits in 3 of 3 Bowens diseases which showed arnyloid deposits by Dylon stain. Anti-keratin antibody 34pE12 reacted with amyloid deposits only 1 of them. These findings suggest that epidermal keratins are the percursor substance of amyloid in malignant cutaneous epithelial tumors. The difference of antikeratin staining pattern between BCE-associated amyloid and SCC or Bowens disease-associated amyloid may be the results of difference in development stage of cutaneous amyloids.
Amyloid*
;
Antibodies
;
Carcinoma, Verrucous
;
Keratins
;
Keratoacanthoma
;
Keratosis, Actinic
;
Plaque, Amyloid*
9.Prospect of Geriatric Psychiatric Research: Research on Alzheimer's Disease.
Seung Hyun KIM ; Heon Jeong LEE
Journal of Korean Neuropsychiatric Association 2002;41(5):767-777
Alzheimer's disease(AD) is a progressive dementia characterized by global cognitive decline and is defined pathologically by amyloid plaques and neurofibrillary tangles. In the past 10 years, important progress has been made in the understanding of the pathogenic mechanism of AD, and new therapeutic targets have become available that should allow the underlying disease process to be tackled directly. In this respect, the 'amyloid hypothesis' has been become the dominant theory in the cause of AD. New strategies for conquering the AD include attempts to stop the production of beta-amyloid protein(Abeta), increasing Abeta clearance, or interfere with Abeta aggregation and precipitation into fibril or plaques. This review summarizes recent advances in research on AD and inspects the perspective of research in potential therapies of AD.
Aged
;
Alzheimer Disease*
;
Amyloid
;
Dementia
;
Humans
;
Neurofibrillary Tangles
;
Plaque, Amyloid
10.Secondary Localized Cutaneous Amyloidosis in Seborrheic Keratosis.
Jong Hee LEE ; He Tae AHN ; Dong Yoon LEE ; Kwang Hyun CHO
Korean Journal of Dermatology 2001;39(3):370-372
We examined the amyloid deposits in seborrheic keratosis by using Dylon stain. Histochemically identified amyloid deposits in seborrheic keratosis were studied with monoclonal cytokeratin antibodies. Amyloid deposits were detected in 2 of 22 seborrheic keratosis. Anti-keratin antibody 34E12 reacted with amyloid deposits shown by Dylon stain in 2 of 22 seborrheic keratosis. Anti-keratin antibody 34B4 did not react with amyloid deposits
Amyloid
;
Amyloidosis*
;
Antibodies
;
Keratins
;
Keratosis, Seborrheic*
;
Plaque, Amyloid