Dementia (Basel, Switzerland)最新文献

We evaluated the relationship between periventricular white matter lesions (PWMLs) and EEG abnormalities in probable Alzheimer's disease (AD). We visually analyzed the EEG of 27 probable AD patients with mild to moderate degree of cognitive impairment participating in a longitudinal study of dementia. Patients had both CT and MRI scans performed at baseline examination, which also included an EEG. PWMLs were rated in CT and MRI films using a semiquantitative method. The EEGs were classified according to the Mayo Clinic Classification System. Abnormal EEGs correlated with PWMLs rating scores were detected on CT, but not on MRI. These data suggest that the presence of PWMLs contribute to the abnormal EEGs observed in AD patients, and that white matter abnormalities in CT correlate better with both the clinical findings and EEG than does the more sensitive but less specific MRI.

The heat shock protein 70 (HSP70) gene is located in chromosome 14, it is now considered as a molecular 'chaperone' and a cell-protective agent. It may be closely related to the pathogenesis of dementia of the Alzheimer type (DAT). To examine the relationship between HSP70 and DAT, HSP70 mRNA expression levels in mononuclear blood cells (MBCs) from patients with DAT were measured by Northern blotting. We found no significant correlation between HSP70 mRNA levels and aging. We found that HSP70 mRNA levels in MBCs from patients with DAT were significantly lower than those from patients with vascular dementia and nondemented controls. These findings suggest that the lower levels of constitutive HSP70 mRNA in DAT play an important role in developing DAT and that the measurement of HSP70 mRNA may be useful for the diagnosis of DAT.

The cumulative risk of Alzheimer-like dementia (AD) was investigated in first-degree relatives (n = 176) of 35 probands with autopsy-confirmed clinical diagnoses of Alzheimer's disease. Seventeen of the 176 first-degree relatives showed evidence of AD. Cumulative morbid risk for the first-degree relatives was estimated to be 28.8%. This result is broadly consistent with previously reported studies, and affirms the presence of substantial disease risk in close relatives of those with Alzheimer's disease.

Brains from 22 patients with Alzheimer's disease (AD) and 20 non-diseased subjects were examined. Intraneuronal lipopigment in 2,440 nucleolated neurons throughout the depth of cortex was identified by fluorescence microscopy. In the AD brains, the mean total area per neuron of the outlines of lipopigment was significantly increased in the region adjacent to the brain surface (sixths 1-3), and analysis of variance showed a significant interaction between depth of cortex (in sixths) and AD for this lipopigment variable (p = 0.012). After relating this lipopigment variable to the size of neuronal bodies, the results indicate that this change occurs in pyramidal neurons, although other neuronal types may also be affected. At least one of three AD-related changes in lipopigment was found in each sixth of the depth of cortex.

Serum and cerebrospinal fluid (CSF) from 44 patients with clinical probable Alzheimer's disease (AD) (subdivided in two groups with 18 early onset, EO, and 26 late onset, LO, cases), 10 patients with vascular dementia (VD) and 24 patients with major depression (MD) were assayed for concentrations of albumin and IgG. The severity of dementia was assessed with the Mini Mental State Examination. The CSF/serum ratio for albumin and IgG as well as the IgG index were used to evaluate blood-CSF barrier function. Various patients showed signs of blood-CSF-barrier (BCB) dysfunction and only few displayed evidence of local IgG synthesis in the central nervous system (CNS) in the AD, VD and in the MD group (IgG index > 0.7). The permeability of the blood-CSF barrier was not correlated to measures of dementia severity. Our data support the hypothesis of a BCB leakage in a subgroup of all investigated patients. Furthermore, we found a small number of patients with increased intrathecal IgG synthesis. Elevated CSF immunoglobulins combined with BCB impairment might be associated or caused by a general immune activation. Our data are in agreement with the assumption that an inflammatory process may play a role in a subgroup of patients with AD but also with MD and less likely in VD. In conclusion BCB impairment and elevated IgG immunoglobulin levels are unspecific either for AD, VD or MD.

Computerized tomographic measures of recurrent cerebral infarctions, atrophy and local perfusion were all prospectively correlated with cognitive testing during treatment of risk factors plus antiplatelet therapy among vascular dementia patients. Neurological and cognitive status were quantified among 22 demented patients with small strokes and compared with 22 age-matched normal volunteers. In vascular dementia, risk factor control plus antiplatelet therapy reduced cerebral infarctions, increased perfusion, and stabilized or improved cognitive test performance, despite age-related, progressive cerebral atrophy.

A fundamental issue in the clinical and neuropathological assessment of Alzheimer's disease patients is quantification of dementia severity progression. Several methods have been advanced for the purpose of staging dementia with various sensitivities at different phases of the disease, but no mathematical function has been developed to link these measures to a physical continuum. Using a dynamic method for quantifying illness severity, change in severity over time was referenced to a cumulative temporal index, a physical dimension. Data from 33 patients with probable Alzheimer's disease with at least 2 successive assessments on three 50-point scales measuring cognitive, behavioral, and daily living skills were used to determine rate of change. 'Fuzzylogic' smoothing of the data, integration over time, and least-squares regression were used to derive a cubic polynomial function to calculate a severity measure in which 'days of illness' was estimated from the severity score. This method can be used to improve the comparability of performance across various mental status tests, and to link measures of very early phases of preclinical dementia and late profound dementia phases. This method also provides a description of an 'average' time course for any population from which the index is derived.

Potassium (K+) channel dysfunction in fibroblasts was recently proposed as a potential diagnostic marker for Alzheimer disease (AD). We utilized a microspectrofluorometric method with Fura-2AM to measure intracellular free calcium ([Ca2+]i) following depolarization with the K+ channel blocker tetraethylammonium (TEA) in seven AD and seven control fibroblast cultures. Contrary to our expectation, 43% of the AD and 36% of the control fibroblast plated coverglasses responded with an increase in [Ca2+]i on addition of 100 mM TEA. The data suggest that the TEA-elicited [Ca2+]i response is not a useful AD screening test.

Intravascular malignant lymphomatosis (IML) is a rare disease characterized by proliferation of neoplastic cells of lymphoid origin within small blood vessels. The median survival of IML patients is only 6 months. Any organ can be affected, with or without clinical expression. Although skin lesions are classic, they are relatively uncommon (28%). Neurological symptomatology (which evolves over a few weeks) is the most common clinical expression (83%). Dementia is the most common neurological symptom that occurs in about half of the patients with central nervous system pathology, and is associated with poorer prognosis. The diagnosis is confirmed by histology but, except for lung, biopsies are not sensitive and are helpful only when performed in the symptomatic organs; furthermore, when associated with anesthesia, they can be followed by dramatic worsening of the patient's condition. Elevated LDH is a good indicator of IML in patients with subacute neurological symptomatology, especially if associated with signs suggestive of other organ involvement.

The case of a patient is reported who suffered from disturbed concentration and memory and constructive apraxia. She had only mild neuropsychological deficits at the first examination. T2-weighted MRI presented extensive focal white matter changes. A brain biopsy showed changes typical for Alzheimer's disease (AD). The extent of the white matter lesions was surprising compared to the mild clinical signs she had. This case confirms that AD may result in prominent white matter disease caused by incomplete infarction or demyelination.