Morphological alterations of mitochondria may be related to metabolic and energy deficiency in neurons in Alzheimer's disease (AD) and other neurodegenerative disorders. In previous studies on the morphological and morphometric estimation of mitochondria in AD electron microscopy revealed substantial morphological and morphometric changes in the hippocampus, the acoustic cortex, the frontal cortex, and the cerebellum. This study extends this observation to subcortical centers, namely the thalamus, the globus pallidus, the red nucleus, and the locus caeruleus in 10 brains of patients who suffered from AD. The morphological alterations consisted of very obvious changes of the mitochondrial cristae, accumulation of osmiophilic material and decrease of their size, in comparison with the normal controls. Mitochondrial alterations were particularly prominent in neurons, which showed loss of dendritic spines and abbreviation of the dendritic arborization. The ultrastructural study of a large number of neurons in the thalamus and the red nucleus revealed that the mitochondrial alterations did not coexist with cytoskeletal pathology and accumulation of amyloid deposits. However, they were prominent in neurons, which demonstrated fragmentation of the cisternae of the Golgi apparatus. The morphological alterations of the mitochondria presumably suggest oxidative damage in neurons in AD brains.

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Multiple sclerosis (MS) is a progressive demyelinating and degenerative disease of the CNS with symptoms dependent on the type of the disease and the site of lesions. During the progression of the disease, symptoms become more permanent and progressive disability ensues. MS is a disease characterized by wide variations between patients, thus making categorization difficult. The aim of the current study was to review the existing epidemiological data of MS in Europe published during the last decade (2000-2009), using PubMed. Findings revealed an increasing incidence of MS during the last decade. Recent data indicate that latitude does not play a key role in determining the onset of the disease. MS has a significant impact on the quality of life for most patients over many years. The disease is twice as common inwomen than in men, and is at its peak in the most economically productive years of life. Pregnancy, postpartum status and vaccines may influence the onset and the course of the disease. Only one of the reviewed papers provides a view of progression from onset to death.

The levels of interleukin 1beta, interleukin 6, and interleukin 10 were elevated in the serum of patients with dementia. No statistically significant correlation was recorded in the interleukin levels among patients with Alzheimer's disease and vascular dementia. Also, no significant correlation was observed in the interleukin levels in the serum and the severity of dementia. However, a significant correlation was found between IL-6 and tumor necrosis factor-alpha (TNF-alpha) levels and age. The levels of IL-1beta and IL-6 were positively correlated with hypertension, and IL-2 levels were negatively correlated. No correlation was found between depressive symptoms and levels of cytokines in the serum.

Alzheimer's disease is a neurodegenerative disorder, characterized by progressive decline in memory and in social performance. The morphological hallmarks of the disease are neuronal loss, loss of dendritic spines, neurofibrillary degeneration and neuritic plaques mainly in the hippocampus and the cortex of the cerebral hemispheres. This study is based on the morphological analysis of the cerebellar cortices of eight brains, 4 patients suffered from Alzheimer's disease and 4 normal controls, by Golgi method, as well as Nissl, Gallyas', Bielschowsky's, Methenamine Silver staining and Congo red methods. Although typical neuritic plaques were not seen in the cerebellar cortex and the diffuse plaques found in the cerebellum in far smaller proportion than plaques in the prefrontal and parietal cortices of the same cases, Golgi impregnation technique revealed a loss of Purkinje cells and a marked decrease in the density of dendritic arborization.

Alzheimer's disease is a neurodegenerative disorder characterized by progressive decline in memory, loss of professional skills, impairment of judgement and behavior, and decline in social performances. In terms of neuropathology, the morphological hallmarks of the disease are the accumulation of alpha-beta peptide and the neurofibrillary degeneration, associated with synaptic alterations, involving mostly the dendritic spines. This study is based on the morphological analysis of 10 brains, 5 of which were obtained from patients who suffered from Alzheimer's disease and 5 from nondemented senile individuals used as control group. The segments taken in major from the occipital lobe were studied with the use of Golgi method, as well as Gallyas' and Bielschowski' s staining methods. In most of the pyramidal cells in the affected brains, there seems to be important spine loss and extensive dendrite pathology. Apical dendrites are distorted and tortuous. Horizontal dendritic arborization is severely decreased leading to an amputated, bell-shaped cell soma. Senile plaques have been often revealed, and neurofibrillary changes have also been noticed.

The morphological and morphometric estimation of the acoustic cortex revealed loss of Cajal-Retzius cells in layer I, as well as an impressive abbreviation of the dendritic fields associated with loss of dendritic spines in all layers of the cortex. Numerous distorted, dystrophic and degenerated dendritic spines were also seen, which were intermixed with a considerable number of giant spines. The dendritic and spinal alterations were closely associated with mitochondrial alterations.

Anosognosia is a common symptom of dementia. The aim of this study was to evaluate the contribution of different regions of the brain to anosognosia in Alzheimer's disease (AD) brains using single photon emission computed tomography (SPECT). Forty-two patients with AD were included in this study. After clinical interviews with the patients and their relatives, the patients were divided into two groups: Anosognosia and No-anosognosia. The patients were studied regarding the severity of dementia. They underwent SPECT with HMPAO and regional cerebral blood flow (rCBF) was measured. Regional CBF significantly differed between Anosognosia and No-anosognosia groups in right prefrontal (P < or = 0.02), right inferior parietal (P < or = 0.00), and right (P < or = 0.01) and left (P < or = 0.01) medial temporal cortex. There was a significant correlation between the severity of dementia and rCBF in medial temporal regions. When comparisons were made between mild and moderate stages separately, the 'right inferior parietal region' was the common region which showed hypoperfusion in both anosognosia subgroups. We conclude that anosognosia may be a reflection of functional impairment in right prefrontal, right frontal and especially right inferior parietal regions in AD.