Familial Creutzfeldt-Jakob Disease with M232R Mutation Progressed Slowly like Alzheimer's Disease.
Dementia and Neurocognitive Disorders.2017;16(3):91-93. doi:10.12779/dnd.2017.16.3.91
Dementia and Neurocognitive Disorders
2002 to Present ISSN: 1738-1495
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Dementia and Neurocognitive Disorders.2017;16(3):87-90. doi:10.12779/dnd.2017.16.3.87
BACKGROUND: The dot-like hippocampal signal intensity in diffusion-weighted MR images is well-known as a characteristic imaging feature in transient global amnesia, a neurological syndrome in which sudden forward-and-backward memory loss occurs that is slowly recovered within 24 hours. We here report on patients with this dot-like hippocampal hyperintensity who did not present with anterograde amnesia except for headaches. CASE REPORT: Two women without a specific medical history presented with sudden-onset headaches on the same day. Neither had any trauma or infection history before the symptom or any sudden emotional or postural changes. Brain MRI showed tiny hippocampal high signal intensity on diffusion-weighted images (DWI). CONCLUSIONS: Dot-like hippocampal lesions seen on DWI may be present without memory impairment, and more studies are needed to determine whether there is any association with headache as in this case.
Amnesia, Anterograde ; Amnesia, Transient Global* ; Brain ; Diffusion* ; Female ; Headache* ; Hippocampus ; Humans ; Magnetic Resonance Imaging ; Memory ; Memory Disorders
Amnesia, Anterograde ; Amnesia, Transient Global* ; Brain ; Diffusion* ; Female ; Headache* ; Hippocampus ; Humans ; Magnetic Resonance Imaging ; Memory ; Memory Disorders
A Case of Scrub Typhus Related Encephalopathy Presenting as Rapidly Progressive Dementia.
Dementia and Neurocognitive Disorders.2017;16(3):83-86. doi:10.12779/dnd.2017.16.3.83
BACKGROUND: An infection known to be a major cause of mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). Rapidly progressive dementia is a neurological condition in which dementia progresses in a short period of time. CASE REPORT: We report on a 78-year-old woman presenting with a rapid decline in cognitive function resulting from a scrub typhus infection. Diffusion weighted images showed a signal intensity at the splenium, and subcortical white matter of both hemispheres suggesting MERS. On the neuropsychological test, the patient showed frontal executive dysfunction. CONCLUSIONS: This case suggests that diagnosticians should consider the possibility that a MERS patient with a rapidly cognitive decline could have a scrub typhus infection because early diagnosis of scrub typhus is very important in this aspect of the treatment.
Aged ; Brain Diseases* ; Cognition ; Dementia* ; Diffusion ; Early Diagnosis ; Female ; Humans ; Neuropsychological Tests ; Scrub Typhus* ; White Matter
Aged ; Brain Diseases* ; Cognition ; Dementia* ; Diffusion ; Early Diagnosis ; Female ; Humans ; Neuropsychological Tests ; Scrub Typhus* ; White Matter
Hypertension and Neuropsychiatric Symptoms in Patients with Drug-Naïve Alzheimer's Disease.
Dementia and Neurocognitive Disorders.2017;16(3):78-82. doi:10.12779/dnd.2017.16.3.78
BACKGROUND AND PURPOSE: Neuropsychiatric symptoms (NPS) such as anxiety, depression, and delusions affect up to 90% of all patients with Alzheimer's disease (AD). NPS is associated with significant caregiver burden and patient distress. Given the severe burden of NPS in AD, it is critical to know potential modifiable risk factors of NPS in AD. This study explores the association between hypertension and NPS in patients with drug-naïve AD. METHODS: We reviewed medical records of 149 patients with AD with (n=80) and without (n=69) hypertension. NPS were assessed using the Korean version of Neuropsychiatric Inventory (K-NPI). Affective, psychotic, and behavior symptom clusters were assessed separately. RESULTS: The total score of K-NPI was not significantly different between patients with AD with and without hypertension. Among K-NPI domains, scores of depression/dysphoria (p=0.045), anxiety (p=0.022), and apathy/indifference (p=0.037) were significantly higher in patients with AD with hypertension. Systolic blood pressure (BP) was associated with higher total K-NPI and affective symptom cluster scores. Diastolic BP was associated with affective symptom cluster scores. CONCLUSIONS: Results suggest that hypertension increases risk of specific NPS in patients with AD. Among NPS, hypertension was associated with affective symptom cluster.
Affective Symptoms ; Alzheimer Disease* ; Anxiety ; Blood Pressure ; Caregivers ; Delusions ; Depression ; Humans ; Hypertension* ; Medical Records ; Risk Factors
Affective Symptoms ; Alzheimer Disease* ; Anxiety ; Blood Pressure ; Caregivers ; Delusions ; Depression ; Humans ; Hypertension* ; Medical Records ; Risk Factors
Associations between Brain Perfusion and Sleep Disturbance in Patients with Alzheimer's Disease.
Dementia and Neurocognitive Disorders.2017;16(3):72-77. doi:10.12779/dnd.2017.16.3.72
BACKGROUND AND PURPOSE: Although sleep disturbances are common and considered a major burden for patients with Alzheimer's disease (AD), the fundamental mechanisms underlying the development and maintenance of sleep disturbance in AD patients have yet to be elucidated. The aim of this study was to examine the correlation between regional cerebral blood flow (rCBF) and sleep disturbance in AD patients using technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography (SPECT). METHODS: A total of 140 AD patients were included in this cross-sectional study. Seventy patients were assigned to the AD with sleep loss (SL) group and the rest were assigned to the AD without SL group. SL was measured using the sleep subscale of the Neuropsychiatric Inventory. A whole-brain voxel-wise analysis of brain SPECT data was conducted to compare the rCBF between the two groups. RESULTS: The two groups did not differ in demographic characteristics, severity of dementia, general cognitive function, and neuropsychiatric symptoms, with the exception of sleep disturbances. The SPECT imaging analysis displayed decreased perfusion in the bilateral inferior frontal gyrus, bilateral temporal pole, and right precentral gyrus in the AD patients with SL group compared with the AD patients without SL group. It also revealed increased perfusion in the right precuneus, right occipital pole, and left middle occipital gyrus in the AD with SL group compared with the AD without SL group. CONCLUSIONS: The AD patients who experienced sleep disturbance had notably decreased perfusion in the frontal and temporal lobes and increased rCBF in the parietal and occipital regions. The findings of this study suggest that functional alterations in these brain areas may be the underlying neural correlates of sleep disturbance in AD patients.
Alzheimer Disease* ; Brain* ; Cerebrovascular Circulation ; Cognition ; Cross-Sectional Studies ; Dementia ; Frontal Lobe ; Humans ; Occipital Lobe ; Parietal Lobe ; Perfusion* ; Prefrontal Cortex ; Rabeprazole ; Temporal Lobe ; Tomography, Emission-Computed ; Tomography, Emission-Computed, Single-Photon
Alzheimer Disease* ; Brain* ; Cerebrovascular Circulation ; Cognition ; Cross-Sectional Studies ; Dementia ; Frontal Lobe ; Humans ; Occipital Lobe ; Parietal Lobe ; Perfusion* ; Prefrontal Cortex ; Rabeprazole ; Temporal Lobe ; Tomography, Emission-Computed ; Tomography, Emission-Computed, Single-Photon
Dementia and Neurocognitive Disorders.2017;16(3):64-71. doi:10.12779/dnd.2017.16.3.64
BACKGROUND AND PURPOSE: Neurogenesis in the adult brain is important for memory and learning, and the alterations in neural stem cells (NSCs) may be an important aspect of Alzheimer's disease (AD) pathogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway has been suggested to have an important role in neuronal cell survival and is highly involved in adult neurogenesis. Candesartan is an angiotensin II receptor antagonist used for the treatment of hypertension and several studies have reported that it also has some neuroprotective effects. We investigated whether candesartan could restore the amyloid-β(25–35) (Aβ₂₅₋₃₅) oligomer-inhibited proliferation of NSCs by focusing on the PI3K pathway. METHODS: To evaluate the effects of candesartan on the Aβ₂₅₋₃₅ oligomer-inhibited proliferation of NSCs, the NSCs were treated with several concentrations of candesartan and/or Aβ₂₅₋₃₅ oligomers, and MTT assay and trypan blue staining were performed. To evaluate the effect of candesartan on the Aβ-inhibited proliferation of NSCs, we performed a bromodeoxyuridine (BrdU) labeling assay. The levels of p85α PI3K, phosphorylated Akt (pAkt) (Ser473), phosphorylated glycogen sinthase kinase-3β (pGSK-3β) (Ser9), and heat shock transcription factor-1 (HSTF-1) were analyzed by Western blotting. RESULTS: The BrdU assays demonstrated that NSC proliferation decreased with Aβ25-35 oligomer treatment; however, a combined treatment with candesartan restored it. Western blotting displayed that candesartan treatment increased the expression levels of p85α PI3K, pAkt (Ser473), pGSK-3β (Ser9), and HSTF. The NSCs were pretreated with a PI3K inhibitor, LY294002; the effects of candesartan on the proliferation of NSCs inhibited by Aβ₂₅₋₃₅ oligomers were almost completely blocked. CONCLUSIONS: Together, these results suggest that candesartan restores the Aβ₂₅₋₃₅ oligomer-inhibited proliferation of NSCs by activating the PI3K pathway.
Adult ; Alzheimer Disease ; Amyloid* ; Blotting, Western ; Brain ; Bromodeoxyuridine ; Cell Survival ; Glycogen ; Hot Temperature ; Humans ; Hypertension ; Learning ; Memory ; Neural Stem Cells* ; Neurogenesis ; Neurons ; Neuroprotective Agents ; Phosphatidylinositol 3-Kinase* ; Phosphatidylinositols* ; Receptors, Angiotensin ; Shock ; Trypan Blue
Adult ; Alzheimer Disease ; Amyloid* ; Blotting, Western ; Brain ; Bromodeoxyuridine ; Cell Survival ; Glycogen ; Hot Temperature ; Humans ; Hypertension ; Learning ; Memory ; Neural Stem Cells* ; Neurogenesis ; Neurons ; Neuroprotective Agents ; Phosphatidylinositol 3-Kinase* ; Phosphatidylinositols* ; Receptors, Angiotensin ; Shock ; Trypan Blue
Dementia and Neurocognitive Disorders.2017;16(3):57-63. doi:10.12779/dnd.2017.16.3.57
BACKGROUND AND PURPOSE: The aim of this paper was to investigate the utility of 18F-N-(3-fluoropropyl)-2β-carboxymethoxy-3β-(4-iodophenyl) nortropane (FP-CIT) positron emission tomography (PET) for evaluating the severity of Parkinson's disease (PD) according to various clinical stages, and to identify the relationship between the striatal substructure and the Unified Parkinson's Disease Rating Scale (UPDRS) motor score, cognitive symptoms through 18F-FP-CIT PET. METHODS: We retrospectively identified 542 patients with various clinical stages of PD who underwent an 18F-FP-CIT PET at our clinics. The difference between the 18F-FP-CIT PET according to the Hoehn-Yahr stage, correlation between 18F-FP-CIT PET and the UPDRS III grouped motor items, and the Korean Mini-Mental State Examination (K-MMSE) were investigated. RESULTS: As disease progressed, the right caudate and both the anterior putamen and caudate/putamen ratios exhibited a significantly lower uptake. The uptake of all striatal substructures was significantly correlated with the UPDRS total motor score. The right caudate nucleus was significantly related to both the UPDRS tremor items and the right UPDRS akinesia-rigidity items. The left caudate nucleus was related to both the UPDRS tremor items and UPDRS akinesia-rigidity items. The right anterior putamen was related to the axial items, right tremor and akinesia-rigidity items; while the left anterior putamen was related to the right tremor and right akinesia-rigidity items. Both of the posterior putamens were related to the axil items, left tremor and left akinesia rigidity items. K-MMSE was not significantly related to any striatal substructures. CONCLUSIONS: The UPDRS total motor score was significantly correlated with the uptake of all striatal substructures. However, the 18F-FPCIT uptake in specific striatal substructures was rather complexly correlated with the UPDRS motor grouped items and was not significantly related to K-MMSE. These results suggest the possibility of the complex pathophysiology of motor symptoms of PD and limitation of 18F-FPCIT PET for the evaluation of the severity of PD motor and cognitive symptoms.
Caudate Nucleus ; Electrons* ; Humans ; Neurobehavioral Manifestations* ; Parkinson Disease* ; Positron-Emission Tomography* ; Putamen ; Retrospective Studies ; Tremor
Caudate Nucleus ; Electrons* ; Humans ; Neurobehavioral Manifestations* ; Parkinson Disease* ; Positron-Emission Tomography* ; Putamen ; Retrospective Studies ; Tremor
A Case of Familial Creutzfeldt-Jacob Disease (V180I) Initially Presenting with Depression.
Dementia and Neurocognitive Disorders.2012;11(2):74-77. doi:10.12779/dnd.2012.11.2.74
Creutzfeldt-Jakob disease (CJD) is a degenerative neurological disorder that is incurable and invariably fatal. It is characterized by rapidly progressive dementia presenting with memory loss, personality changes and hallucinations. The symptoms of CJD are caused by progressive death of neurons in the central nervous system, which is associated with build-up of the abnormal prion proteins forming amyloids. In human, CJD can be acquired genetically through a mutation of the gene encoding for the prion protein (PRNP). This occurs in only 5-10% of all CJD cases. We report a 64-year old woman with CJD carrying a V180I mutation that features late onset, rapid progression, no periodic sharp wave complexes on electroencephalography, and cortical signal change and edema in bilateral frontotemporoparietal lobes and basal ganglia on MRI.
Amyloid ; Basal Ganglia ; Central Nervous System ; Creutzfeldt-Jakob Syndrome ; Dementia ; Depression ; Edema ; Electroencephalography ; Female ; Hallucinations ; Humans ; Lifting ; Memory Disorders ; Nervous System Diseases ; Neurons ; Prions
Amyloid ; Basal Ganglia ; Central Nervous System ; Creutzfeldt-Jakob Syndrome ; Dementia ; Depression ; Edema ; Electroencephalography ; Female ; Hallucinations ; Humans ; Lifting ; Memory Disorders ; Nervous System Diseases ; Neurons ; Prions
Dementia and Neurocognitive Disorders.2012;11(2):67-73. doi:10.12779/dnd.2012.11.2.67
BACKGROUND: Cerebral white matter lesions (WMLs) and lacunar infarcts (LIs) are mostly caused by small vessel disease (SVD). Whereas the main pathomechanism behind LIs is SVD, a variety of mechanisms could be responsible for WMLs. We tried to investigate the relationship between WMLs and LIs and the impact of subtypes of WMLs on its relationship. METHODS: We assessed 128 subjects with vascular cognitive impairment with subcortical vascular lesion (VCI-S). LI number and WML volume were determined on T1-, T2-weighted images and fluid-attenuated inversion recovery images using a semiquantitative visual scale. Cognitive function and daily functional impairment were assessed with Mini-Mental State Examination (MMSE) and the Seoul-Instrumental Activities of Daily Living (S-IADL). RESULTS: Of the 128 patients, 106 (82.8%) had Alzheimer's disease with WML and 22 (17.2%) had subcortical vascular dementia. Seventy patients (54.7%) had at least one lacune. A univariate Poisson model showed that history of hypertension, history of stroke and WML volume (periventricular and deep subcortical) were associated with LIs. A multivariate Poisson model showed that increased WML volume of both types and history of hypertension were associated with LIs. Neither S-IADL score nor MMSE was significantly associated with WML volume of both types. CONCLUSIONS: We found that LIs were associated with WMLs regardless of their types in patients with VCI-S. These findings may suggest that periventricular and deep subcortical WMLs share the same vascular pathomechanism of SVD as LIs.
Activities of Daily Living ; Alzheimer Disease ; Dementia, Vascular ; Glycosaminoglycans ; Humans ; Hypertension ; Stroke ; Stroke, Lacunar
Activities of Daily Living ; Alzheimer Disease ; Dementia, Vascular ; Glycosaminoglycans ; Humans ; Hypertension ; Stroke ; Stroke, Lacunar
Dementia and Neurocognitive Disorders.2012;11(2):59-66. doi:10.12779/dnd.2012.11.2.59
BACKGROUND: Episodic memory impairment can be subdivided into two subtypes, encoding failure vs. retrieval deficit. We defined two subtypes of amnestic mild cognitive impairment (aMCI) according to recognition performance on the memory test: aMCI with encoding failure or aMCI-E and aMCI with retrieval deficit or aMCI-R. We hypothesized that compared to aMCI-R, subjects with aMCI-E are more likely to convert to Alzheimer's disease, as encoding failure suggests that medial temporal lobes are affected early in the disease process. We also investigated whether aMCI-E can be a predictor for progression to AD. METHODS: Using the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, a total of 397 aMCI subjects were included. APOE genotype, cerebrospinal fluid (CSF) fluid biomarkers, and a set of neuropsychological measures were also collected. Unadjusted and adjusted odds ratios were calculated to predict the conversion to AD dementia. The Spearman's rs test was used to measure the degree of correlation between aMCI subtypes and the prognostic factors for progression to AD. RESULTS: Among the 397 subjects, 209 (52.6%) subjects were classified into aMCI-E and 188 (47.4%) into aMCI-R. One hundred two (48.8%) subjects with aMCI-E and 57 (30.3%) of those with aMCI-R progressed to AD (unadjusted odds ratio=2.19 with 95% confidence interval [CI] 1.45-3.31) over 3 years. However, when adjusted odds ratio by a logistic regression was calculated, probability value of aMCI-E disappeared with the odds of conversion by of 1.47 (95% CI 0.89-2.43). There were statistically significant correlations between aMCI-E subtype and MMSE, CDR Memory, RAVLT delayed recall, CSF biomarkers, and genotypes. CONCLUSIONS: This analysis did not show that aMCI-E is an independent prognostic factor to predict the progression to AD. However, this subtype significantly correlates with other prognostic factors for progression. This may suggest that aMCI-E might be a later stage of aMCI and aMCI-R an earlier stage which might be a better target than aMCI-E for therapeutic intervention. Further studies are needed to validate this conjecture.
Alzheimer Disease ; Apolipoproteins E ; Biomarkers ; Dementia ; Deoxycytidine ; Disease Progression ; Genotype ; Logistic Models ; Memory ; Memory, Episodic ; Mild Cognitive Impairment ; Neuroimaging ; Odds Ratio ; Temporal Lobe
Alzheimer Disease ; Apolipoproteins E ; Biomarkers ; Dementia ; Deoxycytidine ; Disease Progression ; Genotype ; Logistic Models ; Memory ; Memory, Episodic ; Mild Cognitive Impairment ; Neuroimaging ; Odds Ratio ; Temporal Lobe
Country
Republic of Korea
Publisher
Korean Dementia Association
ElectronicLinks
http://dnd.or.kr/Editor-in-chief
Kun-Woo Park
secretkda@thedementia.co.kr
Abbreviation
Dement Neurocognitive Disord
Vernacular Journal Title
ISSN
1738-1495
EISSN
2384-0757
Year Approved
2012
Current Indexing Status
Currently Indexed
Start Year
2002
Description
The Dementia and Neurocognitive Disorders (DND) is the official journal of the Korean Dementia Association and is published quarterly on the last day of March, June, September, and December. Abbreviated title is Dement Neurocog Disord, DND contains manuscripts pertaining to clinical and translational investigations of dementia and neurocognitive disorders that will allow clinician or researcher for dementia or neurocognitive disorders to enrich their knowledge of patient management, education, and clinical or experimental research, and hence their professionalism.
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