1.Practice Guidelines for the Manegement of Alzheimer's Disease.
Jong Han PARK ; Byoung Hoon OH ; Byeong Kil YEON ; Seol Heui HAN ; Il Woo HAN ; Guk Hee SUH ; SangYun KIM ; Jae Nam BAE ; Jee Hyang CHONG ; Jae Hong LEE
Journal of the Korean Medical Association 2003;46(12):1071-1096
No abstract available.
Alzheimer Disease*
2.A Case of Early Onset Alzheimer's Disease Diagnosed by ¹⁸F Flutemetamol PET Image.
Jeong Hoon KIM ; Eun Jeong LEE ; Sang Soon PARK ; Jae Hyeok HEO
Dementia and Neurocognitive Disorders 2018;17(4):174-175
No abstract available.
Alzheimer Disease*
3.Neuropeptide Y(NPY)-immunoreactive neuronal changes in senile dementia of alzheimer type(SDAT).
Korean Journal of Physical Anthropology 1993;6(2):249-261
No abstract available.
Alzheimer Disease*
;
Neurons*
;
Neuropeptides*
6.Typical Case of Alzheimer's Disease Confirmed by Autopsy.
Eun Joo KIM ; Hyun Woo KIM ; Tae Ho KANG ; Jae Hyeok LEE ; Young Min LEE ; Seong Jang KIM ; Dae Soo JUNG ; Kyu Hyun PARK ; Gi Yeong HUH
Journal of the Korean Neurological Association 2013;31(1):62-65
No abstract available.
Alzheimer Disease
;
Autopsy
7.Significance of Non-Alzheimer Dementia.
Journal of Korean Geriatric Psychiatry 2001;5(1):47-49
Most of the research activities on dementias have been and are focused on Alzheimer's disease. With regard to the treatment possibility and the cause and pathogenesis of cognitive impairment, however, non-Alzheimer dementias are also very important. We should extend our efforts to other dementing diseases than Alzheimer's disease.
Alzheimer Disease
;
Cognition
;
Dementia*
8.A Novel Presenilin Gene 1 Mutation in Early Onset Familial Alzheimer's Disease.
Sangwon YOO ; Seungyoo KIM ; Dae Woong BAE ; Joong Seok KIM ; Jong Won KIM ; Kwang Soo LEE
Journal of the Korean Neurological Association 2014;32(4):323-325
No abstract available.
Alzheimer Disease*
;
Dementia
;
Presenilins*
9.Age, hypertension, and genetic polymorphisms and their relative associations with white matter hyperintensities in Korean patients with Alzheimer’s disease
Heejeong Jeong ; Seungnam Son ; Soo-Kyoung Kim ; Ki-Jong Park ; Nack-Cheon Choi ; Oh-Young Kwon ; Byeonghoon Lim ; Heeyoung Kang
Neurology Asia 2015;20(1):35-41
Objectives: White matter hyperintensities are known to influence dementia in Alzheimer’s disease.
Genetic components are suggested as putative risk factors for vascular pathology and cognitive
decline. This study aimed to determine whether there is an association between candidate genetic
polymorphisms and the severity of white matter hyperintensities in patients with Alzheimer’s disease.
Methods: Seventy-five patients diagnosed with Alzheimer’s disease underwent genetic tests for specific
alleles of apolipoprotein E, angiotensin-converting enzyme, and methylenetetrahydrofolate reductase.
All patients underwent brain magnetic resonance imaging scans and neuropsychological tests. The
severity of white matter hyperintensities was semiquantified using the CREDOS rating scale, and
patients were divided into three groups according to their rating. Results:The severity of white matter
hyperintensities was related to age and hypertension. However, none of the gene polymorphisms we
tested was found to be associated with the severity of white matter hyperintensities.
Conclusion:The genetic polymorphisms found in apolipoprotein E, angiotensin-converting enzyme
and methylenetetrahydrofolate reductase did not contribute to white matter hyperintensities in
Alzheimer’s disease.Only age and hypertension factors were found to be contributory to white matter
hyperintensities.
Alzheimer Disease
;
Dementia
Result Analysis
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