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PubMed2003

Atrophy responses to muscle inactivity. I. Cellular markers of protein deficits.

The goal of this study was to use the model of spinal cord isolation (SI), which blocks nearly all neuromuscular activity while leaving the motoneuron muscle-fiber connections intact, to characterize the cellular processes linked to marked muscle atrophy. Rats randomly assigned to normal control and SI groups were studied at 0, 2, 4, 8, and 15 days after SI surgery. The slow soleus muscle atrophied by approximately 50%, with the greatest degree of loss occurring during the first 8 days. Throughout the SI duration, muscle protein concentration was maintained at the control level, whereas myofibrillar protein concentration steadily decreased between 4 and 15 days of SI, and this was associated with a 50% decrease in myosin heavy chain (MHC) normalized to total protein. Actin relative to the total protein was maintained at the control level. Marked reductions occurred in total RNA and DNA content and in total MHC and actin mRNA expressed relative to 18S ribosomal RNA. These findings suggest that two key factors contributing to the muscle atrophy in the SI model are 1). a reduction in ribosomal RNA that is consistent with a reduction in protein translational capacity, and 2). insufficient mRNA substrate for translating key sarcomeric proteins comprising the myofibril fraction, such as MHC and actin. In addition, the marked selective depletion of MHC protein in the muscles of SI rats suggests that this protein is more vulnerable to inactivity than actin protein. This selective MHC loss could be a major contributor for the previously reported loss in the functional integrity of SI muscles. Collectively, these data are consistent with the involvement of pretranslational and translational processes in muscle atrophy due to SI.

Actins↗

PubMed2002

Increased antioxidant capacity does not attenuate muscle atrophy caused by unweighting.

Previous studies have increased antioxidant capacity in skeletal muscle to attenuate oxidative stress and muscle atrophy during limb immobilization (Appell HJ, Duarte JAR, and Soares JMC. Int J Sports Med 18: 157-160, 1997; Kondo H, Miura M, Nakagaki I, Sasaki S, and Itokawa Y. Am J Physiol Endocrinol Metab 262: E583-E590, 1992). The purpose of this study was to determine the level of oxidative stress in muscle during hindlimb unweighting (HLU) and whether antioxidant supplementation can attenuate the atrophy and changes in contractile properties resulting from 14 days of unweighting. Muscle unweighting caused a 44% decrease in soleus (Sol) and a 30% decrease in gastrocnemius (GS) mass, a 7% decrease in body weight, and 28% decrease in tetanic force in the GS. Protein carbonyls increased by 44% in the Sol with HLU. Antioxidant supplementation did not attenuate the GS or Sol atrophy or the decrease in GS force generation during HLU. Sol and GS protein concentration was not different between groups. The GS was also subjected to three different oxidative challenges to determine whether the supplement increased the antioxidant capacity of the muscle. In all cases, muscles exhibited an increased antioxidant capacity. These data indicate that antioxidant supplementation was not an effective countermeasure to the atrophy associated with HLU.

Animal Feed↗

PubMed2005

O-GlcNAc level variations are associated with the development of skeletal muscle atrophy.

O-linked N-acetylglucosaminylation (O-GlcNAc) is a regulatory posttranslational modification of nucleocytoplasmic proteins, which consists of the attachment of N-acetylglucosamine to serine or threonine residues of a protein. This glycosylation is a ubiquitous posttranslational modification, which probably plays important roles in many aspects of protein function. Our laboratory has previously reported that, in skeletal muscle, proteins of the glycolytic pathway and energetic metabolism and contractile proteins were O-GlcNAc modified (Cieniewski-Bernard C, Bastide B, Lefebvre T, Lemoine J, Mounier Y, and Michalski JC. Mol Cell Proteomics 3: 577-585, 2004). O-GlcNAc has been recently demonstrated to play a role in modulating cellular function in response to nutrition and also in stress conditions. Therefore, we have investigated here the implication of the glycosylation/deglycosylation process in the development of atrophy in rat skeletal muscle after hindlimb unloading. The high O-GlcNAc level found in control soleus [compared with control extensor digitorum longus (EDL)] becomes lower in atrophied soleus. On the opposite side, the low rate of O-GlcNAc in control EDL reaches higher levels in EDL, not atrophied after hindlimb unloading. These variations in O-GlcNAc level are correlated with a variation of the O-GlcNAc process enzyme activities and could be associated with a differential expression of heat shock proteins. Our results suggest that O-GlcNAc variations could control the muscle protein homeostasis and be implicated in the regulation of muscular atrophy.

Acetylglucosamine↗

PubMed2005

Ovariectomy prevents the recovery of atrophied gastrocnemius skeletal muscle mass.

The recovery of atrophied muscle mass in animals is thought to be dependent on a number of factors including hormones, cytokines, and/or growth factor expression. The Akt/mammalian target of rapamycin (mTOR) signaling pathway is believed to be activated by these various factors, resulting in skeletal muscle growth through the initiation of protein synthesis. It was hypothesized that surgical removal of the ovaries (Ovx) may alter activation of the Akt/mTOR signaling pathway, a mechanism necessary for muscle regrowth. To test this, 36 Sprague-Dawley rats underwent Ovx or sham surgeries. A portion of the animals were then subjected to hindlimb unloading (HLU) for 28 days. After HLU, one group of Sham and Ovx rats underwent a 14-day recovery period in which the animals were allowed free cage ambulation. The HLU animals demonstrated approximately 21-27% reduction in medial gastrocnemius muscle mass irrespective of whether the ovaries were intact or not. The Sham animals that were reloaded recovered their atrophied muscle mass; however, the Ovx group failed to recover any of the atrophied muscle mass with reloading. The failure to recover muscle mass in the Ovx group was associated with reduced phosphorylation levels of both Akt and p70s6k, whereas in the Sham recovery animals no reductions were found in Akt phosphorylation and significant increases in p70s6k activation were detected. Finally, no differences were detected in mTOR phosphorylation in any of Sham or Ovx groups. These results suggest that ovariectomy surgeries could be detrimental to the recovery of atrophied muscle mass.

Animals↗

PubMed2006

Effect of flywheel-based resistance exercise on processes contributing to muscle atrophy during unloading in adult rats.

Flywheel-based resistance exercise (RE) attenuates muscle atrophy during hindlimb suspension. We have previously shown that protein synthesis is elevated in response to RE, but the effect on protein degradation, cell proliferation, or apoptosis was not investigated. We hypothesized that, in addition to affecting protein synthesis, RE inhibits processes that actively contribute to muscle atrophy during hindlimb suspension. Male rats were housed in regular cages (control), tail suspended for 2 wk (HS), or HS with RE every other day for 2 wk (HSRE). Although RE attenuated soleus muscle atrophy during HS, the observed fivefold elevation in apoptosis and the 53% decrease in cell proliferation observed with HS were unaffected by RE. Expression of genes encoding components of the ubiquitin-proteasome pathway of protein degradation were elevated with HS, including ubiquitin, MAFbx, Murf-1, Nedd4, and XIAP, and proteasome subunits C2 and C9. Total ubiquitinated protein was increased with HS, but proteasome activity was not different from control. RE selectively altered the expression of different components of this pathway: MAFbx, Murf-1, and ubiquitin mRNA abundance were downregulated, whereas C2 and C9 subunits remained elevated. Similarly, Nedd4 and XIAP continued to be upregulated, potentially accounting for the observed augmentation in total ubiquitinated protein with RE. Thus a different constellation of proteins is likely ubiquitinated with RE due to altered ubiquitin ligase composition. In summary, the flywheel-based resistance exercise paradigm used in this study is associated with the inhibition of some mechanisms associated with muscle atrophy, such as the increase in MAFbx and Murf-1, but not with others, such as proteasome subunit remodeling, apoptosis, and decreased proliferation, potentially accounting for the inability to completely restore muscle mass. Identifying specific exercise parameters that affect these latter processes may be useful in designing effective exercise strategies in the elderly or during spaceflight.

Animals↗

PubMed1987

Retrograde effects of target atrophy on submandibular ganglion neurons.

1. To study the retrograde effects of changes in target tissue upon the innervating nerve supply, we have examined the parasympathetic submandibular ganglion of the adult rat. Neurons of this ganglion innervate the submandibular and sublingual salivary glands. 2. Ligating the salivary ducts leads to rapid and prolonged salivary gland cell atrophy. 3. Duct ligations, without direct injury to the glandular nerve supply, initially produced few alterations in the ganglion. After 8 wk, however, neuron number was reduced by 50%. The numbers of presynaptic inputs/neuron and synapses/neuron perimeter were not affected by the cell loss. 4. After 1 wk of duct ligation in which the glandular nerve supply was intentionally damaged, some ganglionic neurons have lost all presynaptic inputs, suggesting synaptic disjunction. This is followed at 3 wk by a 40% decrease in neuron number and an increase in the number of inputs per (remaining) ganglion cell. However, the number of synapses/neuronal profile was unchanged. 5. Thus axotomy plus target atrophy causes synaptic disjunction, neuron cell death, and input rearrangement, presumably due to a combination of direct injury effects and an abrupt loss of peripheral trophic supplies. 6. In contrast, target atrophy alone produced more gradual changes in submandibular ganglion neurons. Only prolonged target atrophy leads to a decrease in the number of ganglionic neurons, perhaps due to the gradual loss of peripheral trophic supplies. However, other features, such as the number of inputs/cell and the number of synapses/neuron perimeter, remain unaltered. Evidently, the gradual loss of trophic support does not result in synaptic disjunction to the degree needed to produce presynaptic input rearrangement.

Animals↗

PubMed1999

Hypertension as an etiopathological factor in the development of cerebral atrophy in hemodialyzed patients.

Twenty-five patients on long-term regular hemodialysis treatment (RDT) at our dialysis unit who underwent diagnostic cerebral computed tomography (CCT) participated in a study aimed at clarifying the pathogenesis of cerebral atrophy occasionally found at their original scan. The upper age limit was 55 years to exclude the physiological involutive brain changes occurring with age. Cerebral atrophy (CA), as defined morphologically (enlargement of cerebral sulci or an increased Evan's Index), was detected in all cases. Seventeen patients underwent magnetic resonance imaging (MRI) to define possible white matter changes more accurately. No significant correlation was found between the degree of atrophy and the following uremia-altered hematoseric parameters: creatinine, hematocrit, cholesterol, triglyceridemia, albumin, PTH, calcium, inorganic phosphate. There was no correlation between degree of atrophy and number of months the patients had been on RDT or time that passed between the finding of a creatinine clearance <30 ml/min and the start of RDT. Very high correlations were found between the degree of CA and predialytic blood pressure values, and between CA and the duration of hypertension (n = 13, r = 0.66, p < 0.013). Thus, hypertension seems to be an early cause of cerebral parenchymal damage in RDT patients, and should be promptly corrected.

Adult↗

PubMedDate not supplied

A comparison of medial and lateral temporal lobe atrophy in dementia with Lewy bodies and Alzheimer's disease: magnetic resonance imaging volumetric study.

OBJECTIVES: To compare medial and lateral temporal lobe atrophy on magnetic resonance imaging (MRI) in dementia with Lewy bodies (DLB) and Alzheimer's disease (AD), and to examine the relationship between volumetric indices and cognitive and non-cognitive symptoms. METHODS: T(1)-weighted 1.0-tesla MRI scans were acquired in elderly subjects with DLB (n = 26; mean age = 75.8 years) and AD (n = 22; 77.3 years) and normal controls (n = 26; 76.2 years). MRI-based volume measurements of the hippocampus, parahippocampus, fusiform gyrus, combined inferior and middle temporal gyri, and superior temporal gyrus were acquired. RESULTS: Hippocampal and parahippocampal volumes were significantly larger in subjects with DLB compared to AD. Differences in hippocampal volumes between DLB and AD were observed across the entire length, and in all subjects with dementia there was a loss of hippocampal asymmetry compared to normal controls. Atrophy of temporal lobe structures correlated with memory impairment in both groups, and with age in DLB. There was no association between atrophy and psychotic symptoms in either group. CONCLUSIONS: Subjects with DLB and AD have a different pattern of temporal lobe atrophy with the most striking differences relating to medial rather than lateral temporal lobe structures. These structural differences could explain the relative preservation of memory function in DLB compared to AD.

Age Factors↗

PubMed2002

Posterior cortical atrophy: clinical characteristics and differences compared to Alzheimer's disease.

BACKGROUND: Predominant and progressive complex visual disorders are often due to posterior cortical atrophy (PCA), a rare early-onset dementing syndrome presenting with visual complaints. In clinicopathological studies, PCA is most commonly considered a form of Alzheimer's disease (AD); no prior study has evaluated clinical differences between PCA and AD. METHODS: This study identified 15 patients who presented with progressive complex visual disorders and predominant occipitoparietal hypoperfusion on SPECT. These patients were retrospectively compared on clinical variables with 30 patients with clinically probable AD matched for gender, age and duration of illness. RESULTS: The PCA patients presented with alexia, elements of Balint's syndrome, apperceptive visual agnosia, dressing apraxia and environmental disorientation along with elements of Gerstmann's syndrome. Compared to the AD patients, the 15 PCA patients (mean age of onset 58 years, range 51-64) had significantly better verbal fluency, less memory difficulty, more depression and greater insight into their illness but similar familial and apolipoprotein E risk factors. In the PCA patients, MRI often showed occipitoparietal atrophy without detectable mesiotemporal atrophy. CONCLUSIONS: PCA is a distinct clinical syndrome and not just AD with prominent visual deficits. Compared to AD controls, PCA patients have better language and memory but more insight and depression and more posterior atrophy on MRI. These results indicate clinical criteria for the diagnosis of PCA and recommend specific interventions such as visual aids and antidepressant medications. Similar risk factors and course suggest that PCA is most commonly an early-onset posteriorly shifted AD variant.

Aged↗

PubMedDate not supplied

Pigmented paravenous retinochoroidal atrophy. A literature review supported by seven cases.

Seven patients (4 men and 3 women, ranging in age from 27 to 64 years) with pigmented paravenous retinochoroidal atrophy, a rare disorder of unknown origin, were studied. The mean follow-up time was 18.5 months. Fundus examinations were performed, and color fundus photographs were taken. In addition to fluorescein angiography, visual field examinations, color vision and electroretinographic tests were performed. All 7 patients were asymptomatic, with visual acuities ranging from 3/10 to 10/10. Both fundi showed patches of retinochoroidal atrophy and pigmentation along the retinal veins in all patients. Fluorescein angiography showed hyperfluorescence due to the pigment epithelial atrophy together with hypofluorescence corresponding to bone spicule pigment clumping. Visual field tests showed scotomas corresponding with areas of atrophy along the retinal veins. The electroretinography showed reduced responses in 2 cases. Color vision was normal in all cases. The patients had no history of trauma or a previous inflammatory process. Serology for syphilis, Toxoplasma and cytomegalovirus as well as a skin test for tuberculosis were negative. When the patients were seen at the end of the follow-up period, no variation of the findings was noted. Although the fundus abnormalities can be mild or severe, retinal function tests indicated that this is a geographic and not a generalized disorder.

Adult↗

PubMed2004

Does the pattern of atrophy of the Corpus callosum differ between patients with frontotemporal dementia and patients with Alzheimer's disease?

The pattern of callosal atrophy might be useful for the differentiation between frontotemporal dementia (FTD) and Alzheimer's disease (AD) in advanced cases. However, it is unclear whether the pattern of callosal atrophy differs between patients with FTD and patients with AD in mild to moderate stages. Volumetric MR images were recorded from 48 probands (12 with FTD, 12 with late-onset AD, and 24 controls). All patients were in a mild or in a moderate stage. The corpus callosum was divided into five segments. A repeated-measures analysis of variance showed that there was no difference in the pattern of callosal atrophy between the groups. We provide evidence that patients with FTD and patients with late-onset AD do not differ in the pattern of callosal atrophy on condition that: (1) FTD patients and AD patients are in a mild to moderate stage and (2) FTD patients and AD patients differ in age.

Aged↗

PubMed2006

Pulmonary function, cognitive impairment and brain atrophy in a middle-aged community sample.

OBJECTIVE: To determine the relationship of lung function to brain anatomical parameters and cognitive function and to examine the mediating factors for any relationships. METHODS: A random sub-sample of 469 persons (men = 252) aged 60-64 years from a larger community sample underwent brain magnetic resonance imaging scans and pulmonary function tests (forced vital capacity, FVC, forced expiratory volume in the first second, FEV(1)). Subjects were assessed for global cognitive function, episodic memory, working memory, information processing speed, fine motor dexterity and grip strength. The magnetic resonance imaging scans were analysed for overall brain atrophy, subcortical atrophy (ventricle-to-brain ratio, VBR), hippocampal volume, and white matter hyperintensity (WMH) volume. RESULTS: FEV(1) had a significant negative correlation with overall brain atrophy and VBR in men. The FEV(1)/FVC ratio had a significant correlation with WMHs in both men and women. In regression models that controlled for sex, age, height, level of activity, smoking, chronic respiratory disease and education, FEV(1) and FVC were significant predictors of VBR but no other structural brain measure. Pulmonary function was also significantly related to information processing speed and fine motor dexterity. Male subjects with chronic respiratory disease had more deep WMHs. Path analyses to examine if structural measures mediated between lung function and cognition, and whether markers of inflammation and oxidative stress or cortisol mediated between lung function and brain measures were negative. CONCLUSIONS: Decreased lung function is related to poorer cognitive function and increased subcortical atrophy in mid-adult life. Presence of chronic respiratory disease may be related to deep WMHs in men.

Atrophy↗

PubMedDate not supplied

Striatonigral degeneration combined with olivopontocerebellar atrophy with subcortical dementia and hallucinatory state.

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.

Autopsy↗

PubMed1983

Unilateral scapulohumeral muscular atrophy.

A peculiar form of chronic spinal muscular atrophy is described, 5 unrelated young males developed muscle wasting of the left shoulder and upper arm region, mainly in the distribution of myotomes C5 and C6. This muscle atrophy remained confined to the primary site for 13-18 years, being followed in 4 cases by a mild muscle atrophy of the right upper arm or or the left forearm and hand and in 1 case by atrophy of the legs and the facial muscles. On EMG examination, muscle involvement was always found to be more widespread than on clinical examination. The repeated and extensive EMG examinations gave results typical of an anterior horn cell disease. Pyramidal signs were absent. During the observation period of 21-40 years the course was benign and at least partial working capacity was retained until retiring age.

Aged↗

PubMed1987

Spindle and EEG sleep alterations in subjects affected by cortical cerebellar atrophy.

All-night polygraphic records (EEG, EOG and ECG) were performed on 9 subjects. Four of them were affected by Familiar Cerebellar Atrophy (FCA) whereas the others were their blood relatives without clinical signs of cerebellar deficit. In the former FCA was diagnosed clinically and the cerebellar atrophy was confirmed by computer tomography (CT). In all the latter except one who showed slight cerebellar atrophy, the CTs were negative. The EEG sleep records of the FCA patients were characterized by slowly changing phases between synchronized and desynchronized sleep, instability of the synchronized sleep with frequent modifications of EEG activity, subnormal measurement of both REM and slow-wave sleep and presence of spindles in REM sleep (only in 2 patients). The spindle activity was reduced in two FCA subjects. The electroencephalographic sleep records of two BRs, one of which with small cerebellar atrophy, showed qualitative and quantitative alterations similar to those of FCA patients, even if marked to a lesser degree. Increased spindle densities were present in the same BRs who showed sleep abnormalities. The EEG alterations observed in the two BR subjects could show small cerebellar injuries which would be insufficient to induce clinical signs.

Adult↗

PubMed1996

Characteristics of renal tubular atrophy in experimental renovascular hypertension: a model of kidney hibernation.

The inability to separate irreversible lesions of tubular epithelia from reversible tubular atrophy constitutes a major problem in histopathology and in decisions for revascularization of shrunken kidneys with renal artery stenosis. In order to characterize reversible tubular atrophy ('kidney hibernation') we studied the physiological and biochemical parameters and morphology including histochemistry in rat kidneys made atrophic by renal artery stenosis and treatment with the angiotensin-converting enzyme inhibitor, enalapril. Renal artery stenosis was induced by a 0.2-mm clip around the left renal artery. Following 7 weeks of clipping and 2 concomitant weeks of enalapril treatment, the kidney length decreased from 17.8 +/- 0.3 to 13.7 +/- 0.7 mm (mean +/- SEM). Renal blood flow and glomerular filtration rate decreased to 39 +/- 3% and to approximately 3% of control values, respectively. The activities of the intracellular proteolytic enzymes cathepsin B and L and of Na-K-ATPase in microdissected proximal tubular segments decreased to values below 50 and 10%, respectively. All changes were significant (p < 0.05). Histochemical staining for ATPase activity in the distal tubule segments remained unchanged. Tubular cells were atrophic but not necrotic. Histochemical staining of alkaline phosphatase in the tubular brush border and of acid phosphatase and peroxidase in lysosomes was greatly reduced. All observed changes were reversible within 2-3 weeks following removal of the clip and withdrawal of enalapril either with or without contralateral nephrectomy. Thus, a form of kidney hibernation with readily reversible tubular atrophy has been described. Based on this description it may be possible in consecutive experiments to differentiate between reversible and irreversible tubular atrophy.

Acid Phosphatase↗

PubMed1989

Correlation between carotid blood flow and brain atrophy in patients with multi-infarct dementia.

The relation between carotid blood flow measured by Doppler spectrum analysis and brain atrophy on computed tomography (CT) was studied in 22 subjects with multiple lacunar cerebral infarctions. The subjects were divided into two groups, 7 patients with multi-infarct dementia (MID) (mean age 73 years) and 15 nondemented lacunar stroke subjects (NDLS) (mean age 66 years), according to DSM III criteria. All subjects had a score of 7 points or more on Hachinski's ischemic score and showed no carotid artery stenosis. Systolic peak frequency of the common carotid artery (CCA) was measured by Doppler spectrum analysis (Angioscan II). Brain atrophy was measured quantitatively on CT images by two-dimensional measurement using a digitizer. Peak frequencies were lower in MID than in NDLS. Brain atrophy was more severe in MID than in NDLS. There was a significant correlation between peak frequencies and brain atrophy in all subjects. These results indicate that CCA blood flow may reflect brain function in patients with multiple lacunar infarctions.

Aged↗

PubMed1998

A population-based study on blood pressure and brain atrophy in 85-year-olds.

In the general population, mean systolic and diastolic blood pressure increases up to age 75 years but decreases thereafter. The brain has a role in blood pressure regulation; it is not clear whether the cerebral changes that occur with aging contribute to the decline in blood pressure in the very elderly. We examined a population-based sample of 484 85-year-old persons (344 nondemented and 140 demented, 61 with Alzheimer's disease, 65 with vascular dementia, and 14 with other types of dementia) with a neuropsychiatric examination and blood pressure measurements. Dementia was diagnosed according to the criteria proposed in the Diagnostic and Statistical Manual of Mental Disorders, edition 3, revised. Brain atrophy was measured by CT of the brain. In the nondemented group, frontal (r=-0.18, P=0.037) and parietal (r=-0.23, P=0.008) cortical atrophy and bifrontal ratio (r=-0.20, P=0.013) were associated with lower systolic blood pressure, and frontal (r=-0.23, P=0.010) and parietal (r=-0.24, P=0.008) cortical atrophy and bifrontal ratio (r=-0.23, P=0.006) with lower diastolic blood pressure. Systolic blood pressure was lower in subjects with Alzheimer's disease and vascular dementia, and diastolic blood pressure was lower in those with vascular dementia compared with the nondemented. Systolic (r=-0.27, P<0.0001) and diastolic (r=-0.10, P=0.020) blood pressure was negatively correlated to dementia severity. In the demented subjects, frontal cortical atrophy was correlated to lower diastolic blood pressure (r=-0.21, P=0.043). Our findings suggest that age-related changes in brain structure may contribute to the decrease in blood pressure in the very elderly and that low blood pressure in dementia disorders is mainly a secondary phenomenon.

Aged↗