- Email: [email protected]
Randomized evaluation of mmse and npi in patients using rivastigmine in Alzheimer’s disease
P788
Poster Presentations: P4
primary site of pathology. Genetic testing for known mutations of hereditary leukodystrophy with axonal spheroids was negative. Conclusions: This case describes a new pathologic correlate of Primary Progressive Aphasia, and further shows that the common denominator of diseases causing this syndrome is the asymmetric predilection for the language-dominant hemisphere rather than the cellular nature of the pathology. The patient-specific factors that determine the selective vulnerability of the language-dominant hemisphere in Primary Progressive Aphasia remain to be identified.
ease modifying variables underlying the clinical variability in lvPPA progression is an important target for future research.
P4-058
RANDOMIZED EVALUATION OF MMSE AND NPI IN PATIENTS USING RIVASTIGMINE IN ALZHEIMER’S DISEASE
Gustavo A.A. Santos, Paulo Celso Pardi, Anhanguera, Sao Paulo, Brazil. Contact e-mail: [email protected] Background: Evaluation by the Mini - Mental State Examination
P4-057
SLOWLY PROGRESSING LOGOPENIC APHASIA IN A PATIENT WITH A TREM2 (P.T96K) MUTATION
Klaus Fliessbach1,2, Ingo Frommann3,4, Alfredo Ramirez5, Alexander Drzezga6, Frank Jessen4,6, 1University of Bonn, Bonn, Germany; 2 German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; 3 University Hospital Bonn, Bonn, Germany; 4German Center for Neurodegenerative Diseases, Bonn, Germany; 5Human Genetics, University of Bonn, Bonn, Germany; 6University of Cologne, Cologne, Germany. Contact e-mail: [email protected] Background: The logopenic variant of Primary Progressive Aphasia
(lvPPA) is frequently associated with Alzheimer’s pathology. There is conflicting data on the natural course of the syndrome. Most sources claim a rapid progression to generalized dementia especially in the case of underlying Alzheimer’s pathology. Methods: We present a single case of a patient with lvPPA and biomarker evidence for underlying Alzheimer’s pathology (CSF and PiB-PET). Longitudinal clinical, neuropsychological and MR-imaging investigations were performed over more than three years. Genetic testing for APOE-status and TREM2-mutations was performed. Results: More than five years after symptom onset the patient is capable of highly functional independent living. Neuropsychological test results were widely stable over the observation period of three years. Deficits are restricted to the core deficits of lvPPA (language and working memory). At last follow-up the patient scored 28 out of 30 points in the Mini-Mental-Status-Test. Genetic testing showed APOE-3/3 status and a probably pathogenic variant in the TREM2 gene (p.T96K) which has recently been reported to be overrepresented in focal neurodegenerative disease. Conclusions: The case is an example of an extreme benign clinical course in lvPPA. We suggest that the investigation of genetics and other dis-
(MMSE) and through the neuropsychiatric inventory (NPI) of the effects of rivastigmine tartrate administration of oral and transdermal form as a stabilization or decline in Alzheimer’s disease frames. Methods: We assessed 40 individuals, volunteers, of both sexes, with Alzheimer ’s disease. The volunteers were divided in this experiment according to the clinical characteristics evaluated by the members of the study physicians and are already in use Rivastigmine at the initiation of the study. It is divided into 2 groups : Oral Group (GO) - 20 patients using the drug in capsules. Group Patch ( GP ) - 20 patients with patch use. Both were subjected to neurocognitive surveys over a period of 180 days: MMSE and NPI. The patients in the GO and GP already used Rivastigmine when the first interview. Results: We conclude that statisticall, the Rivastigmine tartrate present in the experiment course a difference between the MMSE score and the NPI. Shows a slight improvement in neurocognition of the patch group patients, even with decline on the MMSE, which is evident in the case of dementia of the Alzheimer’s type. Thus we obtained final scores of the mini- mental state examination of 27,1+/- 12.3 for the oral group and 29.3 +/18.0 for the patch group. In relation to the neuropsychiatric inventory at the end of the experiment an average of 14,1+/-7.0 for oral group and 16,2+/- 6.8 to patch group, indicating in both cases that the patch shape differences were observed in the Rivastigmine tartrate administration in patch form. Conclusions: Both the oral form such as transdermal form of Rivastigmine tartrate drug were similar statistically with respect cognition patients after 180 days of treatment. It was important to note these small oscillations demonstrated by test MMSE and the NPI, despite not having been presented interesting cognitive differences.
Poster Presentations: P4 P4-059
P789 RIVASTIGMINE AND CITALOPRAM TREATMENT FOR ALZHEIMER’S DISEASE (AD) WITH DEPRESSION
Krishna Prasad Pathak, Macedonia University, Thessaloniki, Greece. Contact e-mail: [email protected] Background: AD and Depression diagnosis still depends on clinical
criteria (patient’s history, physical and neurological examination, blood laboratory tests and neuroimaging). Pharmacological treatments for AD and depression in AD are few and of limited efficacy, serving mostly to delay progression and not to cure the disease. Methods: A longitudinal clinical prospective study in 3rd Department of Aristotle University of Thessaloniki, Greece with AD diagnosed patients on rivastigmine 9,5mg/patch and citalopram 20-40 mg/day over 48 months. A total of 1278 patients with mild to moderately severe probable Alzheimer’s disease diagnosed according to DSM-IV and NINCDS-ADRDA criteria. Neuropsychological tests such as MMSE, FRSSD, GDS, HRS-D, were used for the baseline and follow up of the patients. Results: Four years after the baseline assessment, there were no significant differences in MMSE between patients treated with rivastigmine alone or combined rivastigmine with citalopram with or without depression (p>0.05). The FRSSD Activities of Daily Living) of patients with AD and depression treated with rivastigmine was significantly worse than patients treated with rivastigmine and no depression (p¼0.027). There was no difference in GDS and HRS-D between patients with depression treated with rivastigmine alone or combined with citalopram (p>0.05). Conclusions: The results indicate that there is no better effect of the combination of rivastigmine and citalopram than risvastigmine alone. The combined treatment with rivastigmine and citalopram has been shown to be unable to manage dementia and depression as successfully as rivastigmine alone. This is the first study to show evidence of no efficacy of combination therapy in a Greek population with dementia and depression.
P4-060
OLFACTORY FMRI REVEALED THE RELATIONSHIP OF AD DEFICITS IN OLFACTION AND COGNITION
Prasanna Karunanayaka1, Jianli Wang2, Megha Vasavada3, Paul J. Eslinger2, Bing Zhang4, Bin Zhu4, Xin Zhang4, Qing X. Yang2, 1The Pennsylvania State University, College of Medicine, Hershey, PA, USA; 2 The Pennsylvania State University, College of Medicine, Hershey, PA, USA; 3UCLA, Los Angeles, CA, USA; 4Department of Radiology, The Drum Tower Hospital of Nanjing University Medical School, Nanjing, China. Contact e-mail: [email protected] Background: Olfactory deficits in early AD precede clinicallydetectable declines in cognition. However, there is a large gap in understanding the relationship between AD deficits in olfaction and cognition. In this study, we use independent component analysis (ICA) of olfactory fMRI data to investigate the relationship between primary olfactory network (PON) and the default mode network (DMN): a well-known resting state network implicated in AD. Methods: Twelve AD (73.7 yrs), 19 aMCI (72.8 yrs) and 36 cognitive normal (69.5 years) were tested behaviorally using the University of Pennsylvania Smell Identification Test (UPSIT) along with olfactory fMRI paradigm consisted of the visual cue “smell?” synchronized with interleaved odor and no-odor conditions (Fig. 1). The group ICA was performed by combining all three groups. The responsiveness (average correlation) of each network to the odor stimulation events was calculated over the olfactory
Poster Presentations: P4
primary site of pathology. Genetic testing for known mutations of hereditary leukodystrophy with axonal spheroids was negative. Conclusions: This case describes a new pathologic correlate of Primary Progressive Aphasia, and further shows that the common denominator of diseases causing this syndrome is the asymmetric predilection for the language-dominant hemisphere rather than the cellular nature of the pathology. The patient-specific factors that determine the selective vulnerability of the language-dominant hemisphere in Primary Progressive Aphasia remain to be identified.
ease modifying variables underlying the clinical variability in lvPPA progression is an important target for future research.
P4-058
RANDOMIZED EVALUATION OF MMSE AND NPI IN PATIENTS USING RIVASTIGMINE IN ALZHEIMER’S DISEASE
Gustavo A.A. Santos, Paulo Celso Pardi, Anhanguera, Sao Paulo, Brazil. Contact e-mail: [email protected] Background: Evaluation by the Mini - Mental State Examination
P4-057
SLOWLY PROGRESSING LOGOPENIC APHASIA IN A PATIENT WITH A TREM2 (P.T96K) MUTATION
Klaus Fliessbach1,2, Ingo Frommann3,4, Alfredo Ramirez5, Alexander Drzezga6, Frank Jessen4,6, 1University of Bonn, Bonn, Germany; 2 German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; 3 University Hospital Bonn, Bonn, Germany; 4German Center for Neurodegenerative Diseases, Bonn, Germany; 5Human Genetics, University of Bonn, Bonn, Germany; 6University of Cologne, Cologne, Germany. Contact e-mail: [email protected] Background: The logopenic variant of Primary Progressive Aphasia
(lvPPA) is frequently associated with Alzheimer’s pathology. There is conflicting data on the natural course of the syndrome. Most sources claim a rapid progression to generalized dementia especially in the case of underlying Alzheimer’s pathology. Methods: We present a single case of a patient with lvPPA and biomarker evidence for underlying Alzheimer’s pathology (CSF and PiB-PET). Longitudinal clinical, neuropsychological and MR-imaging investigations were performed over more than three years. Genetic testing for APOE-status and TREM2-mutations was performed. Results: More than five years after symptom onset the patient is capable of highly functional independent living. Neuropsychological test results were widely stable over the observation period of three years. Deficits are restricted to the core deficits of lvPPA (language and working memory). At last follow-up the patient scored 28 out of 30 points in the Mini-Mental-Status-Test. Genetic testing showed APOE-3/3 status and a probably pathogenic variant in the TREM2 gene (p.T96K) which has recently been reported to be overrepresented in focal neurodegenerative disease. Conclusions: The case is an example of an extreme benign clinical course in lvPPA. We suggest that the investigation of genetics and other dis-
(MMSE) and through the neuropsychiatric inventory (NPI) of the effects of rivastigmine tartrate administration of oral and transdermal form as a stabilization or decline in Alzheimer’s disease frames. Methods: We assessed 40 individuals, volunteers, of both sexes, with Alzheimer ’s disease. The volunteers were divided in this experiment according to the clinical characteristics evaluated by the members of the study physicians and are already in use Rivastigmine at the initiation of the study. It is divided into 2 groups : Oral Group (GO) - 20 patients using the drug in capsules. Group Patch ( GP ) - 20 patients with patch use. Both were subjected to neurocognitive surveys over a period of 180 days: MMSE and NPI. The patients in the GO and GP already used Rivastigmine when the first interview. Results: We conclude that statisticall, the Rivastigmine tartrate present in the experiment course a difference between the MMSE score and the NPI. Shows a slight improvement in neurocognition of the patch group patients, even with decline on the MMSE, which is evident in the case of dementia of the Alzheimer’s type. Thus we obtained final scores of the mini- mental state examination of 27,1+/- 12.3 for the oral group and 29.3 +/18.0 for the patch group. In relation to the neuropsychiatric inventory at the end of the experiment an average of 14,1+/-7.0 for oral group and 16,2+/- 6.8 to patch group, indicating in both cases that the patch shape differences were observed in the Rivastigmine tartrate administration in patch form. Conclusions: Both the oral form such as transdermal form of Rivastigmine tartrate drug were similar statistically with respect cognition patients after 180 days of treatment. It was important to note these small oscillations demonstrated by test MMSE and the NPI, despite not having been presented interesting cognitive differences.
Poster Presentations: P4 P4-059
P789 RIVASTIGMINE AND CITALOPRAM TREATMENT FOR ALZHEIMER’S DISEASE (AD) WITH DEPRESSION
Krishna Prasad Pathak, Macedonia University, Thessaloniki, Greece. Contact e-mail: [email protected] Background: AD and Depression diagnosis still depends on clinical
criteria (patient’s history, physical and neurological examination, blood laboratory tests and neuroimaging). Pharmacological treatments for AD and depression in AD are few and of limited efficacy, serving mostly to delay progression and not to cure the disease. Methods: A longitudinal clinical prospective study in 3rd Department of Aristotle University of Thessaloniki, Greece with AD diagnosed patients on rivastigmine 9,5mg/patch and citalopram 20-40 mg/day over 48 months. A total of 1278 patients with mild to moderately severe probable Alzheimer’s disease diagnosed according to DSM-IV and NINCDS-ADRDA criteria. Neuropsychological tests such as MMSE, FRSSD, GDS, HRS-D, were used for the baseline and follow up of the patients. Results: Four years after the baseline assessment, there were no significant differences in MMSE between patients treated with rivastigmine alone or combined rivastigmine with citalopram with or without depression (p>0.05). The FRSSD Activities of Daily Living) of patients with AD and depression treated with rivastigmine was significantly worse than patients treated with rivastigmine and no depression (p¼0.027). There was no difference in GDS and HRS-D between patients with depression treated with rivastigmine alone or combined with citalopram (p>0.05). Conclusions: The results indicate that there is no better effect of the combination of rivastigmine and citalopram than risvastigmine alone. The combined treatment with rivastigmine and citalopram has been shown to be unable to manage dementia and depression as successfully as rivastigmine alone. This is the first study to show evidence of no efficacy of combination therapy in a Greek population with dementia and depression.
P4-060
OLFACTORY FMRI REVEALED THE RELATIONSHIP OF AD DEFICITS IN OLFACTION AND COGNITION
Prasanna Karunanayaka1, Jianli Wang2, Megha Vasavada3, Paul J. Eslinger2, Bing Zhang4, Bin Zhu4, Xin Zhang4, Qing X. Yang2, 1The Pennsylvania State University, College of Medicine, Hershey, PA, USA; 2 The Pennsylvania State University, College of Medicine, Hershey, PA, USA; 3UCLA, Los Angeles, CA, USA; 4Department of Radiology, The Drum Tower Hospital of Nanjing University Medical School, Nanjing, China. Contact e-mail: [email protected] Background: Olfactory deficits in early AD precede clinicallydetectable declines in cognition. However, there is a large gap in understanding the relationship between AD deficits in olfaction and cognition. In this study, we use independent component analysis (ICA) of olfactory fMRI data to investigate the relationship between primary olfactory network (PON) and the default mode network (DMN): a well-known resting state network implicated in AD. Methods: Twelve AD (73.7 yrs), 19 aMCI (72.8 yrs) and 36 cognitive normal (69.5 years) were tested behaviorally using the University of Pennsylvania Smell Identification Test (UPSIT) along with olfactory fMRI paradigm consisted of the visual cue “smell?” synchronized with interleaved odor and no-odor conditions (Fig. 1). The group ICA was performed by combining all three groups. The responsiveness (average correlation) of each network to the odor stimulation events was calculated over the olfactory