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At least 451 records · Page 25Linked to original sources

PubMed2005

Blood pressure, white matter lesions and medial temporal lobe atrophy: closing the gap between vascular pathology and Alzheimer's disease?

BACKGROUND: Vascular factors are recognized as important risk factors for Alzheimer's disease, although it is unknown whether these factors directly lead to the typical degenerative pathology such as medial temporal lobe atrophy. We set out to investigate the relation between blood pressure and medial temporal lobe atrophy in patients with senile and presenile Alzheimer's disease with or without white matter lesions. METHODS: We determined the relation between blood pressure and pulse pressure and medial temporal lobe atrophy on MRI in 159 patients with Alzheimer's disease, stratified on white matter lesions and age at onset of dementia. RESULTS: There was a linear relation between systolic blood pressure and pulse pressure (both in tertiles) and the severity of medial temporal lobe atrophy (p(trend) = 0.05 and p(trend) 0.03, respectively). A significant relation was found between pulse pressure [beta = 0.08 (95% CI: 0.00-0.15; p = 0.05) per 10 mm Hg] and (borderline significant) systolic blood pressure [beta = 0.05 (95% CI: -0.01 to 0.11; p = 0.1) per 10 mm Hg] and medial temporal lobe atrophy. White matter lesions and age-stratified analysis revealed a significant association between systolic blood pressure and pulse pressure and medial temporal lobe atrophy, only in the subsample with white matter lesions and in the subsample with a senile onset of dementia. The relations were independent of severity of dementia and diabetes mellitus. CONCLUSIONS: Systolic blood pressure and pulse pressure are associated with medial temporal lobe atrophy in Alzheimer's disease, especially in the presence of white matter lesions and in patients with a late onset of dementia. Our finding may be another step in providing a rationale on how vascular factors could ultimately result in Alzheimer's disease.

Age of Onset↗

PubMed2006

The brain reserve hypothesis, brain atrophy and aging.

BACKGROUND: Researchers have used the concept of brain reserve to explain the dissociation between pathological brain damage and cognitive and functional performance. A variety of brain reserve hypotheses exist, and different empirical strategies have been employed to investigate these variants. OBJECTIVE: The study investigates (i) the relationship between measures of brain burden (atrophy, white matter hyperintensities (WMH)) and measures of reserve (education, creativity, and intelligence); (ii) the relationship between cognitive decline and reserve; (iii) whether measures of reserve mediate the effect of atrophy on estimated cognitive change, and (iv) the association between brain risk factors, education and atrophy. METHODS: A cross-sectional study of a sample of 446 individuals 60-64 years of age who underwent MRI scans as part of a large epidemiological study. Measures were taken of education, intelligence, creativity, cognitive speed, brain volume, WMH, estimated cognitive decline from earlier in life and brain atrophy. RESULTS: No association was found between estimated cognitive decline and brain burden (atrophy, WMH). Risk factors for brain insult were not associated with greater brain atrophy in the less well educated. Neither education, nor any other measure including intelligence or creativity, provided a buffer for cognitive decline in individuals with high levels of brain atrophy. CONCLUSION: Little support was found for the brain reserve hypothesis.

Aging↗

PubMedDate not supplied

Regional brain atrophy in idiopathic parkinson's disease and diffuse Lewy body disease.

This study measured brain atrophy in patients with idiopathic Parkinson's disease and diffuse Lewy body disease, all of whom had equivalent loss of midbrain dopammergic neurons and absence of Alzheimer's disease. Characteristic patterns of volume loss were found throughout the brain, depending on the age of onset and clinical signs. An equivalent loss of medial temporal lobe structures occurred in all parkinsonian patients. This atrophy was similar in magnitude to that seen in Alzheimer's disease and is likely to be the anatomical substrate for the memory deficits found in each of these patients groups. Frontal lobe atrophy was a feature of both late-onset Parkinson's disease (mild atrophy) and diffuse Lewy body disease (significant atrophy) groups, with all cases analyzed having dementia. Atrophy of frontal lobes correlated with the duration of motor symptoms in these patients and may suggest an association between dopammergic deafferentation, frontal atrophy and dementia.

Aged↗

PubMed1993

Radiologic correlates of reaction time measurements in olivopontocerebellar atrophy.

We measured simple visual and auditory reaction time (RT) and movement time (MT) in 32 patients with olivopontocerebellar atrophy (OPCA) in comparison to 32 control subjects. In addition, we followed 2 approaches to radiologic assessment by computed tomographic scans: subjective (by inspection of films) and objective (by measurement of 4 radiologic ratios at the level of the posterior fossa and 1 ratio at the supratentorial level). All OPCA patients had various degrees of cerebellar atrophy and lengthened RT and MT in comparison to their controls. There were no significant differences in RT and MT performances in patients with mild-moderate versus those with severe cerebellar atrophy as assessed by inspection of their films. OPCA patients with severe versus mild-moderate atrophy evaluated by 3 measures, i.e., brainstem, brachium pontis and fourth ventricle ratios, presented few significantly lengthened RT and MT performances. In contrast, patients with severe atrophy revealed by the midbrain ratio had significantly lengthened RT and MT performances compared to those with mild-moderate atrophy assessed by this ratio on 7 of 8 measures; the 8th measure showed a borderline significant difference. This could be explained by the fact that atrophy at the midbrain level is the only one which involves dopaminergic, noradrenergic and glutamatergic structures and pathways.

Adult↗

PubMed1992

Cerebral atrophy precedes the change in cerebral blood flow in patients with ischemic cerebrovascular disease: a short-term follow-up study.

Cerebral atrophy and the decrease in cerebral blood flow (CBF) progress with advancing age. Which of them takes first place, the changes in CBF or cerebral atrophy? We investigated longitudinal changes in CBF and cerebral atrophy in 14 patients with ischemic cerebrovascular disease (CVD): 11 patients with supratentorial lacunar infarction and 3 with carotid transient ischemia attack who were neurologically stable during the 1-3 years of observation. Cerebral atrophy was estimated by the brain atrophy index (BAI): one of the CT area measurement methods, and CBF was measured using the 133Xe inhalation technique. While significant progression of cerebral atrophy was observed, there was no significant change in CBF. Cerebral atrophy precedes the change in CBF and CVD.

Aged↗

PubMed2005

Transgenic overexpression of locally acting insulin-like growth factor-1 inhibits ubiquitin-mediated muscle atrophy in chronic left-ventricular dysfunction.

Metabolic abnormalities develop in various chronic diseases and lead to progressive catabolism with decrements in the skeletal musculature that result in muscle atrophy. We investigated pathways of skeletal muscle proteolysis using an experimental model of chronic left-ventricular dysfunction. Skeletal muscle atrophy developed in wild-type mice 12 weeks following myocardial infarction accompanied by an increase in total protein ubiquitination and enhanced proteasome activity, activation of Foxo transcription factors, and robust induction of the ubiquitin-protein ligase atrogin-1/MAFbx. Further studies identified skeletal muscle myosin as a specific target of ubiquitin-mediated degradation in muscle atrophy. In contrast, transgenic overexpression of a local isoform of insulin-like growth factor-1 prevented muscle atrophy and increased proteasome activity, inhibited skeletal muscle activation primarily of Foxo4, and blocked the expression of atrogin-1/MAFbx. These results suggest that skeletal muscle atrophy occurs through increased activity of the ubiquitin-proteasome pathway. The inhibition of muscle atrophy by local insulin-like growth factor-1 provides a promising therapeutic avenue for the prevention of skeletal muscle wasting in chronic heart failure and potentially other chronic diseases associated with skeletal muscle atrophy.

Animals↗

PubMedDate not supplied

Infraspinatus muscle atrophy in professional baseball players.

BACKGROUND: Infraspinatus muscle atrophy has been observed in athletes who stress their upper extremities in an overhead fashion. The majority of such case reports have been in volleyball players, with far fewer cases reported in baseball players. HYPOTHESIS: Infraspinatus muscle atrophy occurs to a notable degree in professional baseball players. STUDY DESIGN: Retrospective cohort study. METHODS: At the end of the 1999 baseball season, data were collected from all Major League Baseball teams in regards to players affected with infraspinatus muscle atrophy. RESULTS: Twelve of the 1491 major league professional baseball players were identified as having appreciable infraspinatus muscle atrophy. There was an increased prevalence of the muscle atrophy in professional pitchers (10 of 494, 4%) compared to position players (2 of 997, 0.2%) (P <0.001). Among affected pitchers, the atrophy was identified more frequently in starting pitchers (8 of 10) compared to relief pitchers (2 of 10) (P = 0.036), pitchers who had played for more years at the major league level (8.7 +/- 4.9 versus 5.2 +/- 4.0) (P = 0.017), and pitchers who had thrown for more innings at the major league level (971.4 +/- 784.4 versus 485.0 +/- 594.6) (P <0.001). CONCLUSION: Infraspinatus atrophy was identified in 4.4% of major league starting pitchers and occurred in those pitchers who pitched for more years and innings during their major league career.

Adult↗

PubMed2005

Quadriceps weakness, atrophy, and activation failure in predicted noncopers after anterior cruciate ligament injury.

BACKGROUND: Quadriceps weakness is common after anterior cruciate ligament injury, especially in those who do not compensate well for the injury ("noncopers"). Both atrophy and activation failure have been demonstrated in this population but have not been directly related to quadriceps weakness. HYPOTHESES: (1) Quadriceps strength, volumes, and cross-sectional areas of the noncopers would be smaller than those of the contralateral muscles, whereas other muscles would not demonstrate atrophy. (2) Quadriceps muscle activation deficits would be observed. (3) Atrophy and activation failure would account for the quadriceps weakness in these patients. STUDY DESIGN: Cross-sectional study, Level of evidence, 3. METHODS: Seventeen noncopers with isolated anterior cruciate ligament injury underwent burst-superimposition strength and activation testing of the quadriceps and magnetic resonance imaging of 12 muscles an average of 2 months after injury. Morphological characteristics was described by digitally reconstructing each muscle from the axial images and calculating muscle volume and peak cross-sectional area. RESULTS: The quadriceps muscles of the anterior cruciate ligament-deficient limb were significantly weaker (average 25%) than those of the uninjured side; activation failure (8%-10%) was observed for the quadriceps muscles of both limbs. The total quadriceps, vastus lateralis, and vastus intermedius volume and cross-sectional area were significantly smaller in the anterior cruciate ligament-deficient limb. There was no significant atrophy of any other muscle or muscle group. Atrophy and activation failure explained more than 60% of the variance in quadriceps weakness (P = .004). CONCLUSION: The quadriceps femoris weakens soon after acute anterior cruciate ligament injury. Activation deficits and atrophy occur and affect quadriceps strength. Rehabilitation techniques that address activation deficits as well as atrophy may be necessary to restore quadriceps strength.

Adolescent↗

PubMed2004

Impact of disease-modifying therapies on brain and spinal cord atrophy in multiple sclerosis.

Brain and spinal cord atrophy occur early in the course of multiple sclerosis (MS) and continue throughout this lifelong illness, resulting in substantial parenchymal tissue loss at later disease stages. Treatments that slow or prevent atrophy may reduce disability progression in the long term. Disease-modifying agents (DMAs) such as interferon beta-1b (IFNbeta-1b), IFNbeta-1a, and glatiramer acetate inhibit inflammatory events believed to initiate and perpetuate the disease process. DMAs have been shown to inhibit aspects of MS related to brain inflammation such as relapses and gadolinium-enhanced lesions. Because brain inflammation has been linked to irreversible brain tissue injury, DMAs should be effective in reducing the rate of brain atrophy progression. Weekly IFNbeta-1a (Avonex or Rebif) has been shown to slow the rate of brain atrophy; a large study of a frequent injection regimen with IFNbeta-1a (Rebif) showed continued atrophy progression despite IFNbeta-1a at a rate similar to placebo-treated patients. It is not clear why weekly treatment regimens with lower total doses of IFNbeta-1a would show beneficial effects on brain atrophy compared with frequent injections with larger weekly doses. This article reviews results of clinical trials that have examined the effects of DMAs on brain and spinal cord atrophy in patients with MS. Some of these agents have demonstrated positive effects in well-controlled studies, suggesting that anti-inflammatory therapy can delay or prevent the emergence of irreversible central nervous system pathology.

Adjuvants, Immunologic↗

PubMed2006

Little effects of insulin-like Growth Factor-I on testicular atrophy induced by hypoxia.

BACKGROUND: Insulin-like Growth Factor-I (IGF-I) supplementation restores testicular atrophy associated with advanced liver cirrhosis that is a condition of IGF-I deficiency. The aim of this work was to evaluate the effect of IGF-I in rats with ischemia-induced testicular atrophy (AT) without liver disease and consequently with normal serum level of IGF-I. METHODS: Testicular atrophy was induced by epinephrine (1, 2 mg/Kg intra-scrotal injection five times per week) during 11 weeks. Then, rats with testicular atrophy (AT) were divided into two groups (n = 10 each): untreated rats (AT) receiving saline sc, and AT+IGF, which were treated with IGF-I (2 microg.100 g b.w.(-1).day(-1), sc.) for 28 d. Healthy controls (CO, n = 10) were studied in parallel. Animals were sacrificed on day 29th. Hypophyso-gonadal axis, IGF-I and IGFBPs levels, testicular morphometry and histopathology, immuno-histochemical studies and antioxidant enzyme activity phospholipid hydroperoxide glutathione peroxidase (PHGPx) were assessed. RESULTS: Compared to controls, AT rats displayed a reduction in testicular size and weight, with histological testicular atrophy, decreased cellular proliferation and transferrin expression, and all of these alterations were slightly improved by IGF-I at low doses. IGF-I therapy increased significantly steroidogenesis and PHGPx activity (p < 0.05). Interestingly, plasma IGF-I did not augment in rats with testicular atrophy treated with IGF-I, while IGFBP3 levels, that reduces IGF-I availability, was increased in this group (p < 0.05). CONCLUSION: In testicular atrophy by hypoxia, condition without IGF-I deficiency, IGF-treatment induces only partial effects. These findings suggest that IGF-I therapy appears as an appropriate treatment in hypogonadism only when this is associated to conditions of IGF-I deficiency (such as Laron Syndrome or liver cirrhosis).

Animals↗

PubMed2004

Frontal parenchymal atrophy measures in multiple sclerosis.

The aim of this study was to establish whether, in a cross-sectional study, the normalized measures of whole and regional brain atrophy correlate better with tests assessing the cognitive function than the absolute brain atrophy measures. The neuropsychological performances and disability have been assessed in 39 patients with relapsing-remitting multiple sclerosis (MS). T1- and T2-lesion load (LL) of total brain and frontal lobes (FLs) were measured using a reproducible semiautomated technique. The whole brain volume and the regional brain parenchymal volume (RBPV) of FLs were obtained using a computerized interactive program, which incorporates semiautomated and automated segmentation processes. Normalized measures of brain atrophy, i.e., brain parenchymal fraction (BPF) and regional brain parenchymal fraction (RBPF) of FLs, were calculated. The scan-rescan, inter- and intrarater coefficient of variation (COV) and intraclass correlation coefficient (ICC) have been estimated. The RBPF of FLs showed an acceptable level of reproducibility which ranged from 1.7% for intrarater variability to 3.2% for scan-rescan variability. The mean ICC was 0.88 (CI 0.82-0.93). The RBPF of FLs demonstrated stronger magnitudes of correlation with neuropsychological functioning, disability and quantitative MRI lesion measures than RBPV. These differences were statistically significant: P<0.001 for Stroop Color Word Interference test, P<0.001 for Paced Auditory Serial Addition Test, P=0.04 for Standard Raven Progressive Matrices, P=0.049 for Expanded Disability Status Scale, P=0.01 for T2-LL of FLs and P<0.001 for T1-LL of FLs. BPF demonstrated significant correlations with tests assessing cognitive functions, whereas BPAV did not. The correlation analysis results were supported by the results of multiple regression analysis which showed that only the normalized brain atrophy measures were associated with tests exploring the cognitive functions. These data suggest that RBPF is a reproducible and sensitive method for measuring frontal parenchymal atrophy. The normalized measures of whole and regional brain parenchymal atrophy should be preferred to absolute measures in future studies that correlate neuropsychological performances and brain atrophy measures in patients with MS.

Adult↗

PubMed2005

Brain atrophy and lesion load in a large population of patients with multiple sclerosis.

OBJECTIVE: To measure white matter (WM) and gray matter (GM) atrophy and lesion load in a large population of patients with multiple sclerosis (MS) using a fully automated, operator-independent, multiparametric segmentation method. METHODS: The study population consisted of 597 patients with MS and 104 control subjects. The MRI parameters were abnormal WM fraction (AWM-f), global WM-f (gWM-f), and GM fraction (GM-f). RESULTS: Significant differences between patients with MS and control subjects included higher AWM-f and reduced gWM-f and GM-f. MRI data showed significant differences between patients with relapsing-remitting and secondary progressive forms of MS. Significant correlations between MRI parameters and between MRI and clinical data were found. CONCLUSIONS: Patients with multiple sclerosis have significant atrophy of both white matter (WM) and gray matter (GM); secondary progressive patients have significantly more atrophy of both WM and GM than do relapsing-remitting patients and a significantly higher lesion load (abnormal WM fraction); lesion load is related to both WM and even more to GM atrophy; lesion load and WM and GM atrophy are significantly related to Expanded Disability Status Scale score and age at onset (suggesting that the younger the age at disease onset, the worse the lesion load and brain atrophy); and GM atrophy is the most significant MRI variable in determining the final disability.

Adolescent↗

PubMed1981

Cognitive correlates of diffuse cerebral atrophy determined by computed tomography.

The relationship between severity of diffuse cerebral atrophy determined by computed tomography (CT) and severity of cognitive impairment was examined in 55 men, 50 to 77 years old. Partial correlations, controlling for the effects of age and education, indicated that increased cerebral atrophy was associated with decline in orientation, recent memory, and general level of intellectual functioning. Correlations between degree of atrophy and decline in immediate and remote memory were not significant. Despite significant associations between cerebral atrophy and some aspects of intellectual functioning, considerable variance in performance on cognitive tasks was not explained by cerebral atrophy. Therefore, the degree of diffuse cortical and central atrophy observed on CT scan did not closely predict the degree of cognitive dysfunction, nor did the observation of cerebral atrophy necessarily indicate the presence of dementia.

Aged↗

PubMed1998

Amygdala atrophy and seizure outcome after temporal lobe epilepsy surgery.

Surgical outcome in hippocampal atrophy (n = 44) and amygdalohippocampal atrophy (n = 14) were compared. Hippocampal atrophy had better seizure-free outcome than amygdalohippocampal atrophy (80% versus 50%, p = 0.043). Severity of hippocampal atrophy correlated with duration of epilepsy in patients with hippocampal atrophy (r = 0.4, p = 0.007), but not in those with amygdalohippocampal atrophy, suggesting that these two groups may have a different pathogenesis.

Amygdala↗

PubMed1999

Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS. Multiple Sclerosis Collaborative Research Group.

BACKGROUND: Episodic inflammation in the CNS during the early stages of MS results in progressive disability years later, presumably due to myelin and axonal injury. MRI demonstrates ongoing disease activity during the early disease stage, even in some patients who are stable clinically. The optimal MRI measure for the destructive pathologic process is uncertain, however. METHODS: In this post-hoc study, MRI scans were analyzed from patients with relapsing MS participating in a placebo-controlled trial of interferon beta-1a. The brain parenchymal fraction, defined as the ratio of brain parenchymal volume to the total volume within the brain surface contour, was used to measure whole brain atrophy. The relationship between disease features and brain atrophy and effect of interferon beta-1a were determined. RESULTS: MS patients had significant brain atrophy that worsened during each of 2 years of observation. In many patients, brain atrophy worsened without clinical disease activity. Baseline clinical and MRI abnormalities were not strongly related to the rate of brain atrophy during the subsequent 2 years. Treatment with interferon beta-1a resulted in a reduction in brain atrophy progression during the second year of the clinical trial. CONCLUSIONS: Patients with relapsing-remitting MS have measurable amounts of whole brain atrophy that worsens yearly, in most cases without clinical manifestations. The brain parenchymal fraction is a marker for destructive pathologic processes ongoing in relapsing MS patients, and appears useful in demonstrating treatment effects in controlled clinical trials.

Adjuvants, Immunologic↗

PubMed2001

Differing patterns of temporal atrophy in Alzheimer's disease and semantic dementia.

OBJECTIVE: To characterize and quantify the patterns of temporal lobe atrophy in AD vs semantic dementia and to relate the findings to the cognitive profiles. Medial temporal lobe atrophy is well described in AD. In temporal variant frontotemporal dementia (semantic dementia), clinical studies suggest polar and inferolateral temporal atrophy with hippocampal sparing, but quantification is largely lacking. METHODS: A volumetric method for quantifying multiple temporal structures was applied to 26 patients with probable AD, 18 patients with semantic dementia, and 21 matched control subjects. RESULTS: The authors confirmed the expected bilateral hippocampal atrophy in AD relative to controls, with involvement of the amygdala bilaterally and the right parahippocampal gyrus. Contrary to expectations, patients with semantic dementia had asymmetric hippocampal atrophy, more extensive than AD on the left. As predicted, the semantic dementia group showed more severe involvement of the temporal pole bilaterally and the left amygdala, parahippocampal gyrus (including the entorhinal cortex), fusiform gyrus, and the inferior and middle temporal gyri. Performance on semantic association tasks correlated with the size of the left fusiform gyrus, whereas naming appeared to depend upon a wider left temporal network. Episodic memory measures, with the exception of recognition memory for faces, did not correlate with temporal measures. CONCLUSIONS: Hippocampal atrophy is not specific for AD but is also seen in semantic dementia. Distinguishing the patients with semantic dementia was the severe global but asymmetric (left > right) atrophy of the amygdala, temporal pole, and fusiform and inferolateral temporal gyri. These findings have implications for diagnosis and understanding of the cognitive deficits in AD and semantic dementia.

Aged↗

PubMed2006

Alpha-methylacyl coenzyme A racemase immunoreactivity in partial atrophy of the prostate.

It was reported that 15 of 19 consultation cases of prostatic partial atrophy were a-methylacyl coenzyme A racemase (AMACR)-positive. We investigated partial atrophy cases from a single institution using a standard AMACR immunostaining method. Immunohistochemical analysis was performed using an antibody cocktail containing p63, high-molecular-weight keratin (34bE12), and AMACR antibodies on 122 foci of partial atrophy. AMACR staining was analyzed in partial atrophy (n = 122) and compared with adjacent benign glands (n = 122) and prostatic carcinomas (n = 28). Of 122 foci of partial atrophy, 38 (31.1%) showed AMACR immunoreactivity. Typically, AMACR staining was weak or moderate. In addition, 82 (67.2%) showed patchy to negative distribution of basal cells. Partial atrophy may show AMACR immunoreactivity when using a 34bE12, p63, and AMACR antibody cocktail staining method. Compounding this problem, focal lack of basal cells may be seen. However, the AMACR staining pattern of partial atrophy is usually comparable to that of adjacent benign glands and substantially different from adenocarcinoma.

Adenocarcinoma↗

PubMed2004

[A neuroradiological study on the influence of cerebral atrophy and white matter lesion on cognitive function in the elderly].

We investigated the influence of brain atrophy and white matter lesions on cognitive function in elderly people. We selected 33 subjects (mean age, 79.2 +/- 5.1yrs) with a MMSE score from 14 to 30 who had no previous history of stroke from the outpatients in the Memory Clinic of our hospital. These subjects were divided into four groups on the basis of their MMSE score as follows: 14-20; moderate dementia (Moderate-D, n = 9), 21-23; mild dementia (Mild-D, n = 9), 24-27; mild cognitive impairment (MCI, n = 10), 28-30; normal (Normal, n = 5). Among these four groups, we compared the frequency of the associated risk factors for cerebral infarction (hypertension, diabetes mellitus, hyperlipidemia, heart disease), and the severity of brain atrophy and cerebral white matter lesion which were visually evaluated by MRI technique. Brain atrophy and white matter lesions were assessed by reviewing the cerebral cortex and hippocampus, and deep white matter lesion (DWML) and periventricular hyperintensity (PVH), respectively. Brain atrophy was divided into three grades (mild, moderate, severe) and white matter lesions were classified into four grades (0-3) using Fazekas's criteria. We performed statistical analysis to detect t parameters which correlate with and influence MMSE scores from among the MRI findings. The cases with dementia were all diagnosed as Alzheimer's disease. There were no significant differences among the four groups in mean age, the incidence of individual associated risk factors, the severity of cortical atrophy, or the grade of DWML (< or = 2) and PVH (< or = 2). However, the frequency of hippocampal atrophic change greater than a moderate grade increased in parallel with the exacerbation of reduced cognitive function (Normal; 20%, MCI: 40%, Mild-D; 56%, Moderate-D 89%), and approximately 76% with such a change were AD cases. Statistical analysis showed a significant negative correlation between the grade of hippocampal atrophy and MMSE score (r = -0.518, p < 0.005) and a great influence of hippocampal atrophy on that score (step-wise regression analysis: r = 0.518, p < 0.005). From the above results, it was suggested that more than moderate atrophic change in the hippocampus might possibly be related with cognitive impairment and that both DWML and PVH less than the second grade had little influence on the decline of brain function.

Aged↗