L Minthon, K Nilsson, L Edvinsson, P E Wendt, L Gustafson
{"title":"Long-term effects of tacrine on regional cerebral blood flow changes in Alzheimer's disease.","authors":"L Minthon, K Nilsson, L Edvinsson, P E Wendt, L Gustafson","doi":"10.1159/000106954","DOIUrl":"https://doi.org/10.1159/000106954","url":null,"abstract":"<p><strong>Unlabelled: </strong>Regional cerebral blood flow (rCBF) was studied in patients with Alzheimer's disease (AD) before and after 14 months of tacrine treatment. The treated group was compared with an identical reference group of untreated AD patients. At baseline the two groups showed an identical rCBF and mean hemispheric blood flow. After 14 months the tacrine-treated patients showed a stable rCBF level and a significant increase in rCBF in the central-parietal regions, compared to the untreated reference group, who showed typical AD reductions in rCBF in these regions.</p><p><strong>Clinical outcome: </strong>7 of 9 patients in the tacrine group were clinically unchanged or slightly improved during the study time. In the untreated group 8 of 11 patients had deteriorated in clinical assessments and none had improved. Long-term tacrine treatment in Alzheimer's disease may delay the progression of symptoms.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 5","pages":"245-51"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106954","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19510569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of seizures on progression of dementia of the Alzheimer type.","authors":"L Volicer, S Smith, B J Volicer","doi":"10.1159/000106956","DOIUrl":"https://doi.org/10.1159/000106956","url":null,"abstract":"<p><p>A survey of institutionalized patients with clinical diagnosis of probable dementia of the Alzheimer type (DAT) indicated that 21% of patients developed seizures after the onset of DAT. Of the total of 27 patients, 11 developed seizures at home and 16 after institutionalization. In 9 of 11 patients (82%), who suffered the initial seizure at home, the patients' condition suddenly worsened and required long-term care admission within 6 months of the seizure onset. Language function declined significantly more rapidly in 5 patients with seizures than in controls matched by age and duration of DAT.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 5","pages":"258-63"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106956","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19508618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Changes of the relative severity of naming, fluency and recall impairment in the course of dementia of the Alzheimer type.","authors":"S Pollman, M Haupt, A Kurz","doi":"10.1159/000106955","DOIUrl":"https://doi.org/10.1159/000106955","url":null,"abstract":"<p><p>In a longitudinal study of 90 patients with mild to moderate dementia of the Alzheimer type (DAT) we investigated the relative severity of impairment in a confrontation naming, a categorical word fluency and a word list recall task. Severity of impairment was assessed in comparison to a healthy age-matched control group. At baseline, confrontation naming and fluency deficits were about equally often the most severe deficit. The number of patients with most severe naming deficits increased from mild to moderate dementia and from baseline to 1-year follow-up. Word recall was the most severe deficit only in a minority of patients. An addition of lexical-semantic and visual-perceptive dysfunctions is discussed as a possible cause for the shift towards naming deficits in the course of the disease.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 5","pages":"252-7"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106955","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19508624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Changes in a CSF antigen associated with dementia.","authors":"M T Carretero, C R Harrington, C M Wischik","doi":"10.1159/000106959","DOIUrl":"https://doi.org/10.1159/000106959","url":null,"abstract":"<p><p>An 85-kDa antigen was detected in cerebrospinal fluid (CSF) using a monoclonal antibody, 11.57, raised against a fraction of paired helical filaments extracted from Alzheimer's disease (AD) brain tissues. The antigen is a thermostable protein that is unrelated either to tau or amyloid beta-protein precursor. Its level was measured in lumbar and post-mortem CSF samples and found to be decreased significantly in patients with dementia as compared with non-demented controls. There was no difference in its level between patients with AD and those with non-Alzheimer type dementia. In AD, however, there was a significant relationship between disease progression and the amount of the 85-kDa antigen.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 5","pages":"281-5"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106959","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19509113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Eye movement dysfunction in dementia of the Alzheimer type.","authors":"A Moser, D Kömpf, J Olschinka","doi":"10.1159/000106957","DOIUrl":"https://doi.org/10.1159/000106957","url":null,"abstract":"<p><p>Patients with dementia of the Alzheimer type (DAT) are described to have disturbances in basic visual, complex visual and oculomotor functions. In order to study and quantify dysfunction of eye movements under several paradigms, they were measured with infrared photoelectric techniques and analyzed by a digital computer. The study included 12 normal subjects and 10 patients with mild to moderate DAT (DSM-III-R criteria). The authors' results could demonstrate both an attentional deficit to externally triggered, unpredictable targets and an impaired systematic, voluntary, internally organized scanning of the environment due to motivational and perceptional deficits.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 5","pages":"264-8"},"PeriodicalIF":0.0,"publicationDate":"1995-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106957","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19508617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Synaptophysin immunoreactivity is stable 36 h postmortem.","authors":"X Liu, A Brun","doi":"10.1159/000106949","DOIUrl":"https://doi.org/10.1159/000106949","url":null,"abstract":"<p><p>The effects of postmortem time, age and tissue storage time on synaptic density were investigated in the prefrontal cortex of human brains. Thirty normal cases and 10 patients with a variety of neurologic diseases were studied, using quantitative immunohistochemistry with a monoclonal antibody to synaptophysin. Synaptophysin immunoreactivity was stable during the first 36 h after death, showing no significant change at 1, 8, 12, 24 and 36 h postmortem in normals. However, at 48 and 72 h postmortem, synaptophysin immunoreactivity decreased significantly. A similar pattern of postmortem changes was found in the disease group. In 14 normal cases with a wide range of ages, a significant reduction in synaptic density with age was observed while the time of tissue storage as paraffin-embedded blocks had no significant effect on the synaptophysin immunoreactivity. These results support the validity of using synaptophysin immunohistochemistry as a measure of synaptic density in human brain autopsied within 36 h of death and stored as paraffin-embedded blocks for a long time.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"211-7"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106949","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18557911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Y Fukutani, N Takeuchi, K Kobayashi, K Miyazu, N Yamaguchi, T Terada, I Nakamura, K Isaki
{"title":"Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state.","authors":"Y Fukutani, N Takeuchi, K Kobayashi, K Miyazu, N Yamaguchi, T Terada, I Nakamura, K Isaki","doi":"10.1159/000106952","DOIUrl":"https://doi.org/10.1159/000106952","url":null,"abstract":"<p><p>We present an autopsied case of striatonigral degeneration (SND) combined with olivopontocerebellar atrophy (OPCA) with subcortical dementia and hallucinatory state. A Japanese woman without a remarkable family history showed hand tremor at the age of 35 years, followed by bradykinesia, muscle rigidity, orthostatic hypotension, neurogenic bladder and pyramidal signs. No obvious cerebellar symptoms were found. Various antiparkinsonian drugs were administered, but were not markedly effective for the parkinsonism. She developed a mild dementia characterized by mild memory disturbance with preservation of orientation, slowing of thought processes, emotional lability toward sadness, impaired ability to manipulate acquired knowledge and poor calculating, and by the absence of aphasia, apraxia and agnosia. The features in this patient were consistent with those seen in subcortical dementia. She also had auditory hallucinations. MRI revealed hypointense T2 signals in the putamina and substantia nigra. T1-weighted MRI demonstrated atrophy of both the pons and cerebellum in addition to atrophy of the putamina and substantia nigra. EEG showed slowing of background activity. She died of cardiac failure at the age of 47. Autopsy disclosed brain stem tegmental atrophy, SND, OPCA and many glial cytoplasmic inclusions in the central nervous system, but well-preserved cerebrum. We discuss the relationship between the psychiatric symptoms and pathologic findings of brain stem tegmentum.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"235-40"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106952","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18557746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
B L Miller, A L Darby, J R Swartz, G G Yener, I Mena
{"title":"Dietary changes, compulsions and sexual behavior in frontotemporal degeneration.","authors":"B L Miller, A L Darby, J R Swartz, G G Yener, I Mena","doi":"10.1159/000106946","DOIUrl":"https://doi.org/10.1159/000106946","url":null,"abstract":"<p><p>The occurrence of weight gain, sweet and carbohydrate craving, hyposexuality, and compulsions in frontal lobe dementia (FLD) compared to Alzheimer's disease (AD) was evaluated. FLD is a progressive dementia with a high rate of misdiagnosis and therefore better diagnostic criteria for FLD are needed. Fourteen patients meeting research criteria for AD were compared to 14 with suspected FLD. All had cerebral perfusion measured with xenon-133 and imaged with HMPAO using brain-dedicated SPECT. The FLD group showed frontotemporal and AD posterior temporoparietal hypoperfusion. The primary caregivers were queried regarding weight gain, sweet/carbohydrate preference, sexual drive, and compulsions. Differences were compared with Fisher's exact test. The following was found in FLD versus AD: Weight gain in FLD patients amounted to 64% (AD 7%), carbohydrate craving was 79% (vs. 0%) and compulsive behavior 64% (vs. 14%). The differences for these symptoms were statistically significant, whereas for the symptoms increased sexual drive (8 vs. 8%) and reduced sexual drive (54 vs. 23%) no significant difference could be found. In FLD the first symptoms were often dietary changes or hyposexuality. Compulsions were more bizarre and severely disabling in FLD than in AD. Dietary changes, hyposexuality, and disabling compulsions are prominent early symptoms in FLD but not AD. The cause of these symptoms may be due to both frontal and subcortical serotonin loss and dysfunction of the anterior temporal lobes.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"195-9"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106946","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18556568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
C F Lippa, T W Smith, L Nee, Y Robitaille, B Crain, D Dickson, D Pulaski-Salo, D A Pollen
{"title":"Familial Alzheimer's disease and cortical Lewy bodies: is there a genetic susceptibility factor?","authors":"C F Lippa, T W Smith, L Nee, Y Robitaille, B Crain, D Dickson, D Pulaski-Salo, D A Pollen","doi":"10.1159/000106945","DOIUrl":"https://doi.org/10.1159/000106945","url":null,"abstract":"<p><p>The reason for the occurrence of Lewy body disease (LBD) in Alzheimer's disease (AD) patients is unknown. If brains from etiologically different AD groups differ in their tendency to develop cortical Lewy bodies, the concurrence of LBD in AD patients may be a manifestation of the AD process in specific AD subsets. To address this issue, we counted cortical Lewy bodies in AD patients with genetic abnormalities on chromosome 14 (n = 19), and chromosome 21 (n = 3), sporadic AD (n = 27), Down's syndrome (n = 1) and control (n = 26) patients. Cortical Lewy bodies were occasionally present in AD patients with long-duration disease in most of the above AD subgroups, but were not present in any of our age-matched control cases. We suggest that cortical Lewy body formation may be an intrinsic part of the late pathologic changes of AD regardless of etiology and that it is not specific to any of the AD subtypes studied.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"191-4"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106945","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18557912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A decrease in neural sialyltransferase activity in Alzheimer's disease.","authors":"T M Maguire, K C Breen","doi":"10.1159/000106944","DOIUrl":"https://doi.org/10.1159/000106944","url":null,"abstract":"<p><p>The activities of both a particulate and soluble form of the sialyltransferase enzyme have been examined in post-mortem brain samples from Alzheimer's disease patients and age-matched controls. There was a considerable decrease in the activity of both the soluble and membrane-bound forms of the enzyme in the frontal and temporal cortical lobes, although no change was observed in the hippocampus. There was, however, no change in activity of the Golgi marker enzyme thiamine pyrophosphatase. Therefore, it is suggested that the decrease in sialyltransferase enzyme activity may be a specific biochemical event associated with the AD-like neurodegeneration.</p>","PeriodicalId":79336,"journal":{"name":"Dementia (Basel, Switzerland)","volume":"6 4","pages":"185-90"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000106944","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18557907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}