Motor cortex excitability in Alzheimer's disease and in subcortical ischemic vascular dementia.

Twenty Alzheimer's disease (AD) patients, 20 subcortical ischemic vascular dementia (SIVD) patients and 20 neurologically and cognitively normal subjects underwent transcranial magnetic stimulation to study motor cortex excitability changes. Motor threshold (MT), amplitude of motor evoked potentials, silent period and the H/M ratio (amplitude of maximal Hoffman reflex vs. that of maximal motor response) were considered. MT was lower in SIVD patients when compared with AD patients (P = 0.003) and the control group (P < 0.001) and lower in AD patients when compared with the control group (P < 0.001). The increment of motor cortex excitability in AD and SIVD did not lead us to distinguish clearly the two types of dementia. It is likely that the electrophysiological similarity between AD and SIVD could represent another common mechanism shared from these forms of dementia.

Helicobacter pylori and Alzheimer's disease: a possible link.

BACKGROUND: Although serological findings indicate the presence of a relationship between Helicobacter pylori (HP) and vascular disease, no data have been reported about a possible association of HP with dementia. The aim of the present study was to determine whether chronic HP infection might play a role in Alzheimer's disease (AD). METHODS: Plasma homocysteine level, serum folate and vitamin B(12) concentrations, plasma pyridoxal phosphate level, IgG and IgA antibodies to HP, and C-reactive protein (CRP) were determined in 30 AD patients, 30 patients affected by vascular dementia (VaD), and 30 control subjects. All patients and control subjects were matched for age, educational level, and nutritional and socioeconomic status. None of the subjects had a history of chronic gastritis, peptic ulcer, gastric cancer, or major abdominal surgery. RESULTS: HP-IgG level was significantly increased in VaD patients as compared to controls and AD patients, while AD patients had HP-IgG levels higher than those of normal controls. HP-IgA levels were equally increased in both VaD and AD patients. CRP was higher in AD patients than in VaD patients and controls, although CRP levels in VaD patients were also significantly increased. CONCLUSIONS: The present study found an association between HP infection and AD. The question remains as to whether this association is due to the ubiquity of HP, or whether it contributes to the neuroinflammatory process in AD. The relationship between HP and AD, if confirmed by additional studies with a greater number of patients, may have important clinical and therapeutic implications.

Homocysteine, vitamin B12 and folate in vascular dementia and in Alzheimer disease.

The association between elevated plasma levels of homocysteine (Hcy) and nutritional status has been shown in Alzheimer disease (AD) patients and also in vascular dementia (VaD). Moreover, a previous study provided evidence that the relation between a high Hcy level and low vitamin B12 and folate levels in AD patients is due to biochemical damage, rather than a nutritional deficit. The purpose of this study was to investigate the relationship between plasma Hcy levels and vitamins involved in its metabolism in AD and VaD. Twenty-two VaD patients, 22 AD patients and 24 healthy subjects were studied for Hcy, vitamin B12, vitamin B6 and folate. All patients and control subjects were comparable for age, educational level, nutritional and socioeconomic status. None of them showed macrocytic anemia or impaired renal function. Hcy was significantly increased in VaD patients (26.0 +/- 6.58 micromol/l) as compared to controls (10.7 +/- 3.0 micromol/l) and AD patients (22.3 +/- 4.51 micromol/l; p<0.001); however, AD patients also showed increased levels of Hcy. Folates were significantly reduced in both VaD (10.8 +/- 2.81 nmol/l) and AD (10.0 +/- 2.72 nmol/l; p<0.001) patients, while vitamin B12 showed significantly reduced levels only in AD patients (392.1 +/- 65.32 pmol/l; p=0.02). Vitamin B6 was not significantly different in the three groups. Increased levels of Hcy associated with low vitamin B12 plasma levels were found only in AD patients. This observation led us to consider that vitamin B12 metabolism does not represent the direct consequence of the nutritional status and suggests that neuronal damage results in a functional vitamin B12 deficiency, as emphasized by recent reports. New therapeutic strategies are necessary, considering that available pharmaceutical forms of vitamin B12 are not utilized by neurons in oxidative stress conditions.