Cerebral Blood Flow in White Matter Is Correlated with Systolic Blood Pressure and EEG in Senile Dementia of the Alzheimer Type

1997 ◽  
Vol 9 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Arkadiusz Siennicki-Lantz ◽  
Bo Lilja ◽  
Ingmar Rosén ◽  
Sölve Elmståhl
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Systolic Blood Pressure ◽  
Senile Dementia ◽  
Alzheimer Type ◽  
Senile Dementia Of The

scholarly journals Selective neuronal damage and blood pressure in atherosclerotic major cerebral artery disease

2019 ◽  
Vol 90 (9) ◽  
pp. 975-980 ◽  
Author(s):  
Hiroshi Yamauchi ◽  
Shinya Kagawa ◽  
Masaaki Takahashi ◽  
Kuninori Kusano ◽  
Chio Okuyama
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systolic Blood Pressure ◽  
Cerebral Artery ◽  
Neuronal Damage ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Artery Disease

ObjectiveIn patients with atherosclerotic major cerebral artery disease, low blood pressure might impair cerebral perfusion, thereby exacerbate the risk of selective neuronal damage. The purpose of this retrospective study was to determine whether low blood pressure at follow-up is associated with increased selective neuronal damage.MethodsWe retrospectively analysed data from 76 medically treated patients with atherosclerotic internal carotid artery or middle cerebral artery disease with no ischaemic episodes on a follow-up of 6 months or more. All patients had measurements of the distribution of central benzodiazepine receptors twice using positron emission tomography and 11C-flumazenil. Using three-dimensional stereotactic surface projections, we quantified abnormal decreases in the benzodiazepine receptors of the cerebral cortex within the middle cerebral artery distribution and correlated these changes in the benzodiazepine receptors index with blood pressure values at follow-up examinations.ResultsThe changes in the benzodiazepine receptor index during follow-up (mean 27±21 months) were negatively correlated with systolic blood pressure at follow-up. The relationship between changes in benzodiazepine receptor index and systolic blood pressure was different among patients with and without decreased cerebral blood flow at baseline (interaction, p<0.005). Larger increases in benzodiazepine receptor index (neuronal damage) were observed at lower systolic blood pressure levels in patients with decreased cerebral blood flow than in patients without such decreases.ConclusionIn patients without ischaemic stroke episodes at follow-up but with decreased cerebral blood flow due to arterial disease, low systolic blood pressure at follow-up may be associated with increased selective neuronal damage.

Periventricular white matter lucencies in senile dementia of the Alzheimer type and in normal aging

Neurology ◽  
1987 ◽  
Vol 37 (8) ◽  
pp. 1365-1365 ◽  
Author(s):  
D. L. Rezek ◽  
J. C. Morris ◽  
K. H. Fulling ◽  
M. H. Gado
Keyword(s):  
White Matter ◽  
Senile Dementia ◽  
Normal Aging ◽  
Periventricular White Matter ◽  
Alzheimer Type ◽  
Senile Dementia Of The

Membrane Components Separate Early-Onset Alzheimer's Disease From Senile Dementia of the Alzheimer Type

1996 ◽  
Vol 8 (3) ◽  
pp. 365-372 ◽  
Author(s):  
Carl-Gerhard Gottfries ◽  
Ingvar Karlsson ◽  
Lars Svennerholm
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Brain Tissue ◽  
Membrane Lipids ◽  
Senile Dementia ◽  
Alzheimer Type ◽  
Synapse Degeneration ◽  
Membrane Components ◽  
Senile Dementia Of The

Brain tissue from 12 subjects with pure Alzheimer's disease (AD) and 21 subjects with senile dementia of the Alzheimer type (SDAT) was investigated for membrane lipids and compared with that in age-matched controls. In brain tissue from the patients with AD, phospholipids were significantly decreased compared with that from SDAT patients and controls, cholesterol was reduced compared with that in controls, and gangliosides were significantly reduced in all gray-matter areas investigated compared with those in both SDAT subjects and controls. A reduction in gangliosides also occurred in the SDAT group, but it was smaller. In the white matter, the pattern of changes was the opposite. Phospholipids, cholesterol, cerebroside, and sulfatide were significantly reduced in the frontal-lobe white matter in the SDAT group compared with that in age-matched controls and AD patients. Gangliosides in the cerebrospinal fluid also separated AD from SDAT and controls. The findings indicate synapse degeneration as an important pathogenetic factor in AD. This disorder should be separated from SDAT, in which white-matter degeneration appears to be more prominent.

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