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PubMed1993

Nerve growth factor reverses neuronal atrophy in a Down syndrome model of age-related neurodegeneration.

Atrophy and dysfunction of certain neurons, including cholinergic neurons in the basal forebrain, are key features of the neuropathology of Alzheimer's disease (AD). Since all individuals with Down syndrome (DS) develop AD neuropathology by the 4th decade, we reasoned that a genetic model of DS, the trisomy 16 (Ts 16) mouse, may provide an animal model to study the neurodegeneration in AD. Ts 16 mice fail to survive birth; to evaluate neurons for long periods in vivo required transplantation of fetal tissue. We previously demonstrated that Ts 16 basal forebrain cholinergic neurons (BFCNs) undergo age-related atrophy similar to DS and AD, and now show that a specific neurotrophic factor, nerve growth factor (NGF), acts to reverse Ts 16-induced atrophy of BFCNs and stimulates hypertrophy of these cells. As NGF levels were not decreased in the host, abnormalities intrinsic to Ts 16 BFCNs presumably caused the atrophy. Our results suggest that NGF may be useful in reversing cholinergic neurodegeneration in DS and AD.

Aging↗

PubMed1996

Low body weight in Alzheimer's disease is associated with mesial temporal cortex atrophy.

There are reports of weight loss and low body mass index (BMI) in patients with AD. The mesial temporal cortex (MTC) is involved in feeding behavior and memory and is preferentially involved in AD. We studied 74 subjects, including 58 AD patients and 16 control subjects, to determine whether BMI is associated with atrophy of the MTC or other brain regions. We used MRI morphometric analysis to provide measures of regional brain atrophy. AD patients had significant brain atrophy in all measured brain regions, except the white matter, compared with normal control subjects. The MTC was the only brain region significantly associated with BMI in AD patients (r = 0.39, p = 0.003). Multiple-regression analysis indicated that addition of brain regions other than the MTC to the model did not significantly add to the prediction of BMI. We conclude that low BMI correlates best and specifically with MTC atrophy. This finding supports a connection between limbic system damage and low body weight in AD.

Aged↗

PubMed1996

Striatal efferent involvement and its correlation to levodopa efficacy in patients with multiple system atrophy.

We report an immunohistochemical investigation of the striatal efferents in the striatum, globus pallidus, and substantia nigra of five patients with multiple system atrophy (MSA): olivopontocerebellar atrophy (2), striatonigral degeneration (2), and Shy-Drager syndrome (1). All patients manifested parkinsonism during the clinical course of their illness. The administration of levodopa improved the symptoms of two patients, but not of the other three. Brain tissues from five age-matched neurologically normal subjects served as controls. Immunohistochemical assays were carried with antibodies against met-enkephalin, substance P, and calbindin-D28k. Irrespective of the clinical form of multiple system atrophy, the immunoreactivity with the antibodies was reduced at the dorsolateral portion of the striatum and the ventrolateral portions of the globus pallidus and of the substantia nigra. The woolly fiber arrangement of reaction product deposits seen in both segments of the globus pallidus of normal individuals was totally absent in the ventrolateral portions of the three patients who did not have a response to levodopa. By contrast, there were positively stained woolly fibers in globus pallidum segments of the two levodopa-responsive patients, even though their number and size were decreased in comparison with controls. These results indicate that the three clinical forms of multiple system atrophy share common topographic alterations of the striatal efferent system and that the severity of the involvement correlates with the clinically observed effect of levodopa on the parkinsonism.

Aged↗

PubMed1998

Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer's disease.

OBJECTIVE: To determine whether the hypometabolism observed in PET images of patients with Alzheimer's disease (AD) is due entirely to brain atrophy. BACKGROUND: Reduced brain glucose metabolism in AD patients measured using PET has been reported by numerous authors. Actual glucose metabolic values in AD may be reduced artificially because of brain atrophy, which accentuates the partial volume effect (PVE) on data collected by PET. METHODS: Using segmented MR images, we corrected regional cerebral metabolic rates for glucose for PVEs to evaluate the effect of atrophy on uncorrected values for brain metabolism in AD patients and healthy control subjects. RESULTS: Global glucose metabolism was reduced significantly before and after correction in AD patients compared with controls. Before PVE correction, glucose metabolic values in patients were lower than in control subjects in the inferior parietal, frontal, and lateral temporal cortex; in the posterior cingulate; and in the precuneus. These reductions remained significantly lower after PVE correction, although in the posterior cingulate the difference in metabolism between AD patients and control subjects lessened. Regional glucose metabolism of these areas with PVE correction was lower in moderately-severely demented patients than in mildly demented patients. CONCLUSION: Reduced glucose metabolism measured by PET in AD is not simply an artifact due to an increase in CSF space induced by atrophy, but reflects a true metabolic reduction per gram of tissue.

Aged↗

PubMed2002

Hippocampal, amygdalar, and global brain atrophy in different apolipoprotein E genotypes.

The epsilon4 allele of the APOE gene increases the risk for AD, whereas the epsilon2 allele may be protective. The authors assessed the impact of APOE genotype on hippocampal, amygdalar, and global brain atrophy as putative markers of preclinical AD in a nondemented population. Carriers of epsilon4 had significantly more hippocampal and amygdalar atrophy than epsilon3epsilon3 subjects, but not more global brain atrophy. Carriers of epsilon2 did not have less brain atrophy than epsilon3epsilon3 subjects.

Aged↗

PubMed2003

Hippocampal atrophy and T2-weighted signal changes in familial mesial temporal lobe epilepsy.

OBJECTIVE: To correlate the clinical phenotype with hippocampal volumes (HcVs) and signal changes in patients with familial mesial temporal lobe epilepsy (FMTLE). METHODS: FMTLE was defined when at least two first-degree relatives in a family had a clinical-EEG diagnosis of MTLE. Hippocampal formation measurements were performed using 1- to 3-mm coronal T1-weighted MRIs. The presence of hyperintense T2 signal was evaluated by visual analysis. For statistical analyses, analysis of variance, chi(2) test, and regression analysis were used. RESULTS: A total of 142 patients from 45 unrelated families were studied: 113 individuals with MTLE (80 with good seizure control) and 29 family members with other seizure types. There were 99 patients (69.7%) with hippocampal atrophy (HA). Sixty-seven of the 99 patients with HA also had a hyperintense T2 signal. Hyperintense T2 signal was associated with more severe HA (p = 0.04). Patients with refractory FMTLE had more frequent HA (p = 0.03) and hyperintense T2 signal (p = 0.004) and more severe atrophy (p < 0.0001). Duration of epilepsy correlated with HcV asymmetry index (r(2) = 0.12, p = 0.00008) and with the more atrophic hippocampi but not with contralateral hippocampi. CONCLUSION: In familial mesial temporal lobe epilepsy, seizure severity is variable in affected individuals. Hippocampal atrophy was present in 70% of these patients and 69% of these had an associated hyperintense T2 signal. Although hippocampal atrophy associated with abnormal T2 signal was more frequent and more severe in patients with poor seizure control, it was also frequent in affected individuals across families. These observations suggest that one or more genes resulting in familial mesial temporal lobe epilepsy predisposes both to the clinical features of mesial temporal lobe epilepsy and to the development of hippocampal sclerosis.

Adolescent↗

PubMed1984

Hormonal control of muscle atrophy and degeneration in the moth Antheraea polyphemus.

The intersegmental muscles of the giant silkmoth Antheraea polyphemus (Cramer) can undergo two forms of degenerative changes: a wasting atrophy that lasts about 6 days or rapid dissolution that is completed within 30 h. Muscle atrophy is induced by a dramatic decline in the endogenous titres of the steroid moulting hormone 20-hydroxyecdysone. 20-Hydroxyecdysone appears to act as a trophic factor for the muscles as infusion or injection of this steroid blocks further atrophy of the muscle. The normal decline of 20-hydroxyecdysone also allows the muscles to become competent to respond to the peptide eclosion hormone. Eclosion hormone is then released and acts directly on these muscles to induce rapid cell death which is morphologically and physiologically distinct from steroid-regulated atrophy.

Animals↗

PubMed1999

Relationship between brain atrophy estimated by a longitudinal computed tomography study and blood pressure control in patients with essential hypertension.

To evaluate the relationship between blood pressure control and the progression of brain atrophy in the elderly, patients with essential hypertension and brain atrophy were longitudinally evaluated using computerized tomography (CT). The study evaluated 48 patients with essential hypertension aged 46-78 years, and 30 sex- and age-matched normotensive control subjects. The extent of brain atrophy as determined by caudate head index (CHI), the inverse cella media index (iCMI), and Evans' ratio (ER) was estimated twice at an interval of 5-9 years (mean, 6.9 years). The mean annual increases in CHI (deltaCHI), iCMI (delta iCMI), and ER (deltaER) were evaluated. Mean blood volume in the common carotid artery (BF) and the decrease in BF per year (deltaBF) were also determined. The deltaCHI, delta iCMI, and deltaER increased with age in the hypertensive subjects as well as the control group across all age groups evaluated. The deltaCHI, delta iCMI, and deltaER were significantly greater in the patients with essential hypertension in their 50 s as compared with the controls. In patients with essential hypertension aged 65 years or older, the deltaCHI, delta iCMI, and deltaER were significantly lower in the group in whom the blood pressure was controlled within the range of borderline hypertension than the groups in which it was controlled in the range of normal or mild hypertension. In the younger patients under the age of 65 with essential hypertension, blood pressure control did not affect the deltaCHI, delta iCMI, and deltaER. The deltaCHI, delta iCMI, and deltaER were significantly correlated with deltaBF in both groups. These findings indicate that control of systolic blood pressure within the range of borderline hypertension may delay the progression of brain atrophy in elderly patients with essential hypertension.

Aged↗

PubMed2002

Solid-pseudopapillary tumor of the pancreatic head causing marked distal atrophy: a tumor originated posterior to the main pancreatic duct.

We report the case of a solid-pseudopapillary tumor (SPT) of the head of the pancreas causing occlusion of the main pancreatic duct (MPD) and marked pancreatic atrophy distal to the tumor disproportionate to the tumor size. A 15-yr-old girl was diagnosed with 5-cm solid-pseudopapillary tumor of the pancreatic head with marked distal pancreatic atrophy. Endoscopic retrograde cholangiopancreatography demonstrated obstruction of the MPD in the pancreatic head. We performed a duodenum-preserving pancreatic head resection to avoid postoperative exocrine and endocrine insufficiency. The surgical specimen showed the typical gross appearance of a SPT, with only a thin rim of pancreas anterior to the tumor. We believe that this presentation results when a tumor originates posterior to the MPD. Thus, whether or not pancreatic atrophy occurs depends strongly on the anterior/posterior relationship between the enlarging tumor and the MPD. The risk of SPT causing severe pancreatic atrophy should be kept in mind to avoid irreversible pancreatic insufficiency in young females.

Adolescent↗

PubMed2004

Spinal muscular atrophy: molecular genetics and diagnostics.

Spinal muscular atrophy is one of the most common autosomal recessive diseases, affecting approximately one in 10,000 live births and with a carrier frequency of approximately one in 50. Spinal muscular atrophy is caused by a deficiency of the ubiquitous protein survival of motor neuron (SMN), which is encoded by the SMN genes, SMN1 and SMN2. Due to a single nucleotide polymorphism (840C>T), SMN2 produces less full-length transcript than SMN1 and cannot entirely prevent neuronal cell death at physiologic gene dosages. The 38-kDa SMN protein comprises 294 amino acids and is involved in the biogenesis of uridine-rich small nuclear ribonucleoproteins, facilitating their cytoplasmic assembly into the spliceosome. Various animal models have been developed to study the pathogenesis of spinal muscular atrophy, as well as to test novel therapeutics. Common PCR-restriction fragment length polymorphism assays can detect the homozygous absence of SMN1 in approximately 94% of patients with clinically typical spinal muscular atrophy. SMN gene dosage analysis can determine the copy number of SMN1 to detect carriers and patients heterozygous for the absence of SMN1. Due to the genetic complexity and the high carrier frequency, accurate risk assessment and genetic counseling are particularly important. Comprehensive SMA genetic testing, combined with appropriate genetic counseling and risk assessment, provides the most complete evaluation of patients and their families at this time. New technologies, such as monosomal analysis techniques, may be widely available in the future.

Animals↗

PubMed2001

Urogenital atrophy: prevention and treatment.

Fifteen percent of premenopausal women, 10-40% of postmenopausal women, and 10-25% of women receiving systemic hormone therapy experience urogenital atrophy. The most common symptoms are dryness, burning, pruritus, irritation, and dyspareunia. Estrogen loss, drugs, and chemical sensitivities are causes. Estrogen or hormone replacement therapy (ERT-HRT) is the treatment of choice in postmenopausal women. Dosages prescribed for menopause symptoms or to prevent osteoporosis (and, potentially, other conditions) can restore the vagina to premenopausal physiology and relieve symptoms. Concomitant progestins are necessary for women with an intact uterus to minimize or eliminate estrogen-induced endometrial cancer. Low-dosage oral and vaginal ERT can relieve urogenital atrophy but might not produce systemic effects. Progestins are not necessary with vaginal rings and vaginal tablets. If ERT is given only to treat urogenital atrophy, estrogen creams 1 or 2 times/week may prevent recurrence after symptoms are resolved. Progestins are not required for occasional estrogen cream use. Vaginal moisturizers provide longer relief by changing the fluid content of endothelium and lowering vaginal pH. Vaginal lubricants provide short-term relief. Women with contraindications to ERT-HRT could use lubricants for intercourse-related dryness or moisturizers for more continuous relief. The lay press promotes agrimony, black cohosh, chaste tree, dong quai, witch hazel, and phytoestrogens for vaginal dryness and dyspareunia; however, no evidence exists to support these specific claims. Pharmacists should be actively involved in identifying, preventing, and treating urogenital atrophy.

Aged↗

PubMed2006

Inflammation and atrophy precede prostatic neoplasia in a PhIP-induced rat model.

2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) has been implicated as a major mutagenic heterocyclic amine in the human diet and is carcinogenic in the rat prostate. To validate PhIP-induced rat prostatic neoplasia as a model of human prostate cancer progression, we sought to study the earliest histologic and morphologic changes in the prostate and to follow progressive changes over time. We fed sixty-seven 5-week-old male Fischer F344 rats with PhIP (400 ppm) or control diets for 20 weeks, and then sacrificed animals for histomorphologic examination at the ages of 25, 45, and 65 weeks. Animals treated with PhIP showed significantly more inflammation (P = .002, > .001, and .016 for 25, 45, and 65 weeks, respectively) and atrophy (P = .003, > .001, and .006 for 25, 45, and 65 weeks, respectively) in their prostate glands relative to controls. Prostatic intraepithelial neoplasia (PIN) occurred only in PhIP-treated rats. PIN lesions arose in areas of glandular atrophy, most often in the ventral prostate. Atypical cells in areas of atrophy show loss of glutathione S-transferase pi immunostaining preceding the development of PIN. None of the animals in this study developed invasive carcinomas, differing from those in previous reports. Overall, these findings suggest that the pathogenesis of prostatic neoplasia in the PhIP-treated rat prostate proceeds from inflammation to postinflammatory proliferative atrophy to PIN.

Animals↗

PubMed1984

Measurement of brain atrophy of aging using X-ray computed tomography: sex difference in 1045 normal cases.

We measured brain volume of 1,045 subjects with no brain damage using x-ray computed tomography and investigated brain atrophy of aging. Severity of brain atrophy was estimated by brain atrophy index (BAI): BAI (%) = 100 (%) X (cerebrospinal fluid space volume/cranial cavity volume). Atrophy of the brain began with statistical significance in the forties in both sexes. In males 40-49 years of age the mean BAI was 1.0% greater (p less than 0.001) and the S.D. of BAI was 1.1% greater (p less than 0.001) than those in their thirties. In females of 40-49 years the mean BAI was 0.5% greater (p less than 0.001) than that in their thirties, but there was no statistical significance between the two S.D.'s of both decades. The BAI increased exponentially with the increasing age from thirties in both sexes. Correlation coefficients were 0.702 (p less than 0.001, n = 471) in males and 0.721 (p less than 0.001, n = 480) in females. From the regression coefficients it was calculated that the BAI was doubled in 19.4 years in males and 17.4 years in females after thirties.

Adolescent↗

PubMed1987

Age-related brain atrophy enhanced by smoking: a quantitative study with computed tomography.

We examined the chronic effect of smoking on brain atrophy quantitatively with computed tomography (CT). Study was performed on 159 smokers and 194 non-smokers from 40 to 69 years old with neither neurological nor focal abnormality in brain CT. Brain atrophy index (BAI) which was a quantitative marker of brain atrophy reported previously, was calculated from each pixel of brain CT. There was a significant age dependent increase of BAI in both non-smokers and smokers. Smokers showed a significant increase in BAI (atrophic) compared to non-smokers in three age groups, 50-54, 55-59 (p less than 0.01, both) and 65-69 (p less than 0.05). In the male, the mean BAI became high when the smoking index increased (p less than 0.01). The systolic blood pressure and serum triglycerides of smokers were significantly higher than the non-smokers (p less than 0.05 and p less than 0.01). It was suggested that age-related brain atrophy was increased by chronic smoking through advanced atherosclerosis.

Adult↗

PubMed1990

Atrophy of lymph node compartments lacking lymph-carried lymphocytes in athymic rats.

This paper reports on a form of atrophy of lymph node compartments occurring in mesenteric nodes of athymic nude rats whose perinodal tissue had become unusually rich in mast cells and fibrotic. The subcapsular sinus of an affected compartment was depleted of lymphocytes, while the medullary sinuses were loaded with macrophages. A progressive expansion of medullary sinuses into the medullary cords, the extrafollicular zone, the deep cortex unit and, finally, the folliculo-nodules of the compartment was accompanied by a gradual atrophy of the usual lymphoid cell populations of these nodal components. The occurrence of such a mode of atrophy of a compartment, associated with a lack of lymphocytes in the afferent lymph, agrees with our previous proposal that lymphocytes of the afferent lymph provide the stimuli for the development and maintenance of the structures of the node. The involvement of mast cells and fibrosis in the emergence of the present form of nodal atrophy, which further weakens the immune system of an immunodeficient animal, is considered.

Animals↗

PubMed2005

Early quadriceps strength loss after total knee arthroplasty. The contributions of muscle atrophy and failure of voluntary muscle activation.

BACKGROUND: While total knee arthroplasty reduces pain and provides a functional range of motion of the knee, quadriceps weakness and reduced functional capacity typically are still present one year after surgery. The purpose of the present investigation was to determine the role of failure of voluntary muscle activation and muscle atrophy in the early loss of quadriceps strength after surgery. METHODS: Twenty patients with unilateral knee osteoarthritis were tested an average of ten days before and twenty-seven days after primary total knee arthroplasty. Quadriceps strength and voluntary muscle activation were measured with use of a burst-superimposition technique in which a supramaximal burst of electrical stimulation is superimposed on a maximum voluntary isometric contraction. Maximal quadriceps cross-sectional area was assessed with use of magnetic resonance imaging. RESULTS: Postoperatively, quadriceps strength was decreased by 62%, voluntary activation was decreased by 17%, and maximal cross-sectional area was decreased by 10% in comparison with the preoperative values; these differences were significant (p < 0.01). Collectively, failure of voluntary muscle activation and atrophy explained 85% of the loss of quadriceps strength (p < 0.001). Multiple linear regression analysis revealed that failure of voluntary activation contributed nearly twice as much as atrophy did to the loss of quadriceps strength. The severity of knee pain with muscle contraction did not change significantly compared with the preoperative level (p = 0.31). Changes in knee pain during strength-testing did not account for a significant amount of the change in voluntary activation (p = 0.14). CONCLUSIONS: Patients who are managed with total knee arthroplasty have profound impairment of quadriceps strength one month after surgery. This impairment is predominantly due to failure of voluntary muscle activation, and it is also influenced, to a lesser degree, by muscle atrophy. Knee pain with muscle contraction played a surprisingly small role in the reduction of muscle activation.

Aged↗

PubMed2003

Interventions for the prevention of brain atrophy in multiple sclerosis : current status.

The assessment of brain volume changes on serial magnetic resonance imaging (MRI) scans can provide an objective measure of the neurodegenerative component of multiple sclerosis (MS) pathology. Results from placebo-controlled and crossover clinical trials indicate that immunomodulating (e.g. recombinant interferon-beta [IFNbeta]-1a [Rebif] and IFNbeta-1b [Betaferon] and glatiramer acetate [Copaxone]) and immunosuppressive (e.g. cladribine and alemtuzumab) treatments for relapsing-remitting (RR) and secondary progressive MS lack substantial efficacy in preventing the development of brain atrophy, despite the marked effects of these treatments on clinical and MRI outcomes of disease activity. A modest but significant treatment effect on brain atrophy has been reported for patients with RRMS only in one trial of IFNbeta-1a (Avonex) and in another study of long-term corticosteroid therapy.Failure to find a significant treatment benefit in preventing brain atrophy might be the result of inadequate trial designs, including their relatively short durations, which may not be adequate to reveal beneficial effects in a chronic disease like MS. Alternatively, such a failure might indicate that treatments proven to be effective in reducing MS-related inflammation are unable to act with the same efficacy on the most severe and disabling pathological substrates of the disease. The modest correlation between MRI enhancement frequency and brain atrophy observed in the placebo groups of several trials also fits with the concept that the suppression of inflammatory activity in MS is not fully and rapidly associated with a similar effect on the global neurodegenerative process of the disease.

Adjuvants, Immunologic↗

PubMed2003

Beta adrenoceptor agonists, clenbuterol, and isoproterenol retard denervation atrophy in rat gastrocnemius muscle: use of 3-methylhistidine as a marker of myofibrillar degeneration.

The effects of beta adrenergic agonists, clenbuterol (2 mg/kg body weight/d) and isoproterenol (12 mg/kg body weight/d), in normal innervated and denervated rat gastrocnemius muscle were investigated. The daily administration of beta adrenergic agonists to normal innervated rats for a short period (7 d) resulted in the hypertrophy of gastrocnemius as confirmed from the measurement of total tissue protein contents. The development of denervation atrophy witnessed a stimulation in the expression of acid and alkaline phosphatases, pointing to an enhanced myofibrillar degeneration. An administration of beta adrenergic agonists inhibited the expression of raised levels of these enzymes in denervated muscle. A measurement of 3-methylhistidine in muscle revealed a loss of amino acid with the progress in the development of denervation atrophy. Serum and urine samples from denervated rats showed a progressive accumulation of 3-methylhistidine. Clenbuterol and isoproterenol treatment to these rats resulted in an inhibition of 3-methylhistidine accumulation. When 3-methylhistidine was used as a marker of myofibrillar degeneration, the results seemed to suggest that the degeneration of cyto-contractile apparatus accompanying denervation atrophy is attenuated in the presence of beta adrenergic agonists, implying that these sympathomimetic drugs are capable of reversing denervation atrophy in rat gastrocnemius.

Acid Phosphatase↗