Diffuse Plaques Research Articles

Heparan Sulfate Subdomains that are Degraded by Sulf Accumulate in Cerebral Amyloid ß Plaques of Alzheimer's Disease: Evidence from Mouse Models and Patients

Alzheimer's disease (AD) is characterized by extracellular cerebral accumulation of amyloid β peptide (Aβ). Heparan sulfate (HS) is a glycosaminoglycan that is abundant in the extracellular space. The state of sulfation within the HS chain influences its ability to interact with a variety of proteins. Highly sulfated domains within HS are crucial for Aβ aggregation in vitro. Here, we investigated the expression of the sulfated domains and HS disaccharide composition in the brains of Tg2576, J20, and T41 transgenic AD mouse models, and patients with AD. RB4CD12, a phage display antibody, recognizes highly sulfated domains of HS. The RB4CD12 epitope is abundant in the basement membrane of brain vessels under physiological conditions. In the cortex and hippocampus of the mice and patients with AD, RB4CD12 strongly stained both diffuse and neuritic amyloid plaques. Interestingly, RB4CD12 also stained the intracellular granules of certain hippocampal neurons in AD brains. Disaccharide compositions in vessel-enriched and nonvasculature fractions of Tg2576 mice and AD patients were found to be comparable to those of non-transgenic and non-demented controls, respectively. The RB4CD12 epitope in amyloid plaques was substantially degraded ex vivo by Sulf-1 and Sulf-2, extracellular HS endosulfatases. These results indicate that formation of highly sulfated HS domains may be upregulated in conjunction with AD pathogenesis, and that these domains can be enzymatically remodeled in AD brains.

257 Long Term Asbestos Exposure as a Cause of Eozinophilic Pleural Effusions

BackgroundExposure to asbestos can cause several different types of pleural disease: first diffuse malignant mezothelioma, plural plaques or calcification, loculated pleural abnormality called “rounded atelectasis” and benign pleural effusions (PE).ObjectiveTo determine the frequency of various pleural diseases related to asbestos exposure.MethodsA retrospective analysis of 6 cases of PE related to the occupational asbestos exposure (AE) was made, after exclusion of other possible causes of PE. They were evaluated in the period of 7 years.ResultsAll cases were male and almost all were more than 60 years old. All cases had more then 30 years from the first occupational AE (5 in building construction and sixt in mine). All of them reported pleuritic chest pain, or feeling heavy in their chest. The chest radiographs showed small to moderate-sized PE, which was bilateral by tree patients (pts) by the others with pleural califications in one of them. One of the pts had 3 episodes of PE and evidence of parenhimal asbestosis. PE was serous exudate and serosanguineous in 2 pts, with polymorphonuclear leucocytes, mononuclear cells and eosinophils (EO). We have evaluated the number of EO in the pleural fluid (PF), from the smear of PF colored by May-Grunwald-Giemsa. The PF differential WBC consisted predominately EO and mononuclear cells. At 4 pts more than 30% EO were found in the PF and 21% and 17% in other 2 pts respectively. During the follow up period of 3 years no other cause of PE has been found and there has been no evidence of mesothelioma in all the pts.ConclusionsExposure to asbestos can cause PE with predominant presence of Eo cells.

Medium-Term Survival of Diffuse Coronary Artery Disease Patients following Coronary Artery Reconstruction with the Internal Thoracic Artery

Objective: Diffuse coronary artery disease makes cardiac surgeons hesitant regarding whether coronary artery bypass grafting (CABG) surgery is feasible or not. Coronary artery reconstruction using the internal thoracic artery (ITA) allows bypassing of coronary arteries with diffuse atheromatous plaques without systematically resorting to endarterectomy. The aim of the present study was to evaluate the medium-term results of coronary artery reconstruction. Methods: All patients undergoing coronary artery reconstruction using the ITA between 1999 and 2002 (233 patients) were included in the study. The mean age was 61.9 ± 9.8 years. Two hundred and eighty-one coronary artery reconstructions using the ITA were performed (mean length 3.6 ± 2 cm) for 514 CABGs. Coronary artery reconstruction using the ITA was associated with endarterectomy in 48 cases (17%). Results: In-hospital mortality was 2.6%. Follow-up data were compiled in December 2008. Mean follow-up was 73.4 ± 16.7 months. The actuarial survival rate at 7 years was 89.3 ± 2.1%, and 88% of patients were free of major cardiac events at 7 years. Conclusions: Coronary artery reconstruction gives comparable medium-term results to conventional coronary surgery, even though it is indicated for patients with more severe lesions.

Neuroinflammation, Hyperphosphorylated Tau, Diffuse Amyloid Plaques, and Down-Regulation of the Cellular Prion Protein in Air Pollution Exposed Children and Young Adults

Air pollution exposures have been linked to neuroinflammation and neuropathology. Autopsy samples of the frontal cortex from control (n = 8) and pollution-exposed (n = 35) children and young adults were analyzed by RT-PCR (n = 43) and microarray analysis (n = 12) for gene expression changes in oxidative stress, DNA damage signaling, NFκB signaling, inflammation, and neurodegeneration pathways. The effect of apolipoprotein E (APOE) genotype on the presence of protein aggregates associated with Alzheimer's disease (AD) pathology was also explored. Exposed urbanites displayed differential (>2-fold) regulation of 134 genes. Forty percent exhibited tau hyperphosphorylation with pre-tangle material and 51% had amyloid-β (Aβ) diffuse plaques compared with 0% in controls. APOE4 carriers had greater hyperphosphorylated tau and diffuse Aβ plaques versus E3 carriers (Q = 7.82, p = 0.005). Upregulated gene network clusters included IL1, NFκB, TNF, IFN, and TLRs. A 15-fold frontal down-regulation of the prion-related protein (PrP(C)) was seen in highly exposed subjects. The down-regulation of the PrP(C) is critical given its important roles for neuroprotection, neurodegeneration, and mood disorder states. Elevation of indices of neuroinflammation and oxidative stress, down-regulation of the PrP(C) and AD-associated pathology are present in young megacity residents. The inducible regulation of gene expression suggests they are evolving different mechanisms in an attempt to cope with the constant state of inflammation and oxidative stress related to their environmental exposures. Together, these data support a role for air pollution in CNS damage and its impact upon the developing brain and the potential etiology of AD and mood disorders.

A case of acute coronary syndrome following the use of parenteral penicillin: Kounis syndrome

Kounis syndrome refers to the concurrence of acute coronary events and allergic or hypersensitivity reactions. In this report, we describe the case of a male patient, in whom acute ST-segment elevation and myocardial infarction developed immediately after injection of depot penicillin, and we discuss the Kounis syndrome. A 52-year-old male patient had chest pain, hypotension and ST-elevation on leads DI and aVL of electrocardiography 30 minutes after intramuscular penicillin injection due to cryptic tonsillitis. Kounis syndrome was considered as a possible diagnosis according to the presentation. Histamine and tryptase levels were not studied due to the delay on arrival to the emergency department. The patient promptly underwent coronary angiography, which revealed only diffuse plaques in all main coronary arteries without any obstructive lesion. We found only increased immunoglobulin (Ig) E, which is associated with the syndrome. With this report, we remind clinicians to consider Kounis syndrome in patients who are subjected to allergenic substances and demonstrate acute chest pain.

A Case of Central Retinal Artery Occlusion after Chiropractic Manipulation of the Neck

Here we report a case of central retinal artery occlusion after chiropractic manipulation on the neck. A 49-year old man presented at the hospital because of sudden visual loss in his right eye after chiropractic neck manipulation. He had received chiropractic manipulation of the neck by a chiropractor eight days prior. When he first visited us, his best corrected visual acuity in his right eye was hand motion. A full ophthalmic examination was performed. There was cherry-red spot in the macula in his right eye. We performed a fluorescein angiogram and cervical color Doppler. The arterio-venous transit time in the fluorescein angiogram was delayed, and we detected stenosis of the right internal carotid artery with diffuse atherosclerotic plaques in the right common carotid artery. We prescribed ginko biloba extract (Tanamin). Three years after his first visit, the best corrected visual acuity of his right eye was 20 / 200.

Air Pollution, Socioeconomic Status, and Children's Cognition in Megacities: The Mexico City Scenario

OPINION article Front. Psychol., 09 July 2012Sec. Developmental Psychology https://doi.org/10.3389/fpsyg.2012.00217

ものわすれ外来でフォロー中に軽度認知障害から認知症へ移行した嗜銀顆粒性認知症の1剖検例

An 84-year-old Japanese woman with no family history of dementia visited our memory clinic complaining of memory disturbance. Neurological examination revealed no apparent motor abnormalities, focal cerebral signs, parkinsonism, or cerebellar dysfunction. Hasegawa's Dementia Scale-Revised (HDS-R) and Mini mental state examination (MMSE) scores were 24 and 23 points, respectively. MRI revealed left-side-dominant dilatation of the inferior horn of the lateral ventricle. Although egocentric behavior was remarkable, no disturbance of intelligence was apparent at the first examination, and she was diagnosed as having mild cognitive impairment. Her memory disturbance and disorientation gradually worsened. Atrophy of the cerebrum and dilatation of the lateral ventricle advanced gradually on MRI. Two years later, she required care to perform activities of daily living. HDS-R and MMSE scores had dropped to 13 and 18 points, respectively, and conversion to dementia was diagnosed. Ability to perform 3D cube-copying was well preserved. The patient died due to acute myocardial infarction at the age of 87. The clinical diagnosis was Alzheimer disease. At autopsy, the brain weighed 1,250g, and argyrophilic grains were widely observed in the limbic system, corresponding to Saito's stage III. Neuron loss, gliosis, spongiform change, and tissue rarefaction were recognized in the superficial layer of the parahippocampal gyrus. Ballooned neurons, pretangles, oligodendroglial coiled bodies, and neuropil threads were also observed. Neurofibrillary tangles and senile plaques, mainly consisting of diffuse plaque, were recognized as corresponding to Braak stage III and CERAD stage B, respectively. Neither Lewy nor Pick bodies were observed. Although mild phosphorylated TDP-43 immunoreactivity was observed, it was suspected to be due to secondary degeneration of tau deposition. The patient was diagnosed pathologically as having argyrophilic grain dementia. The clinical findings of the present patient reveal important observations that help to clinically discriminate between various dementias such as Alzheimer disease and argyrophilic grain dementia.

L’amylose bronchopulmonaire : à propos de quatre cas

Amyloidosis limited to bronchopulmonary apparatus is expressed as tracheobronchial deposits in diffuse plaques that can cause stenosis or parenchymal nodules or masses. In this regard, we report four cases of pulmonary amyloidosis and discuss the diagnostic difficulties of this location. These are two women and two men aged 60, 68, 44 and 57 years. They presented a pulmonary parenchymal amyloidosis in all cases associated with bronchial in one case. The diagnosis was confirmed by histology in all cases. The staging was negative in all cases. The evolution was marked by the stabilization of the lesions in all cases. Localized amyloidosis, which may be the only telltale sign of a systemic illness, its diagnosis requires finding other locations to better tailor the treatment strategy.

Cross‐functional E3 ligases Parkin and C‐terminus Hsp70‐interacting protein in neurodegenerative disorders

The study of neurodegenerative disorders has had a major impact on our understanding of more fundamental mechanisms underlying neurobiology. Breakthroughs in the genetics of Alzheimer's (AD) and Parkinson's diseases (PD) has resulted in new knowledge in the areas of axonal transport, energy metabolism, protein trafficking/clearance and synaptic physiology. The major neurodegenerative diseases have in common a regional or network pathology associated with abnormal protein accumulation(s) and various degrees of motor or cognitive decline. In AD, β-amyloids are deposited in extracellular diffuse and compacted plaques as well as intracellularly. There is a major contribution to the disease by the co-existence of an intraneuronal tauopathy. Additionally, PD-like Lewy Bodies (LBs) bearing aggregated α-synuclein is present in 40-60% of all AD cases, especially involving amygdala. Amyloid deposits can be degraded or cleared by several mechanisms, including immune-mediated and transcytosis across the blood-brain barrier. Another avenue for disposal involves the lysosome pathway via autophagy. Enzymatic pathways include insulin degradative enzyme and neprilysin. Finally, the co-operative actions of C-terminus Hsp70 interacting protein (CHIP) and Parkin, components of a multiprotein E3 ubiquitin ligase complex, may be a portal to proteasome-mediated degradation. Mutations in the Parkin gene are the most common genetic link to autosomal recessive Parkinson's disease. Parkin catalyzes the post-translational modification of proteins with polyubiquitin, targeting them to the 26S proteasome. Parkin reduces intracellular Aβ(1-42) peptide levels, counteracts its effects on cell death, and reverses its effect to inhibit the proteasome. Additionally, Parkin has intrinsic cytoprotective activity to promote proteasome function and defend against oxidative stress to mitochondria. Parkin and CHIP are also active in amyloid clearance and cytoprotection in vivo. Parkin has cross-functionality in additional neurodegenerative diseases, for instance, to eliminate polyglutamine-expanded proteins, reducing their aggregation and toxicity and reinstate proteasome function. The dual actions of CHIP (molecular co-chaperone and E3 ligase) and Parkin (as E3-ubiquitin ligase and anti-oxidant) may also play a role in suppressing inflammatory reactions in animal models of neurodegeneration. In this review, we focus on the significance of CHIP and Parkin as inducers of amyloid clearance, as cytoprotectants and in the suppression of reactive inflammation. A case is made for more effort to explore whether neurodegeneration associated with proteinopathies can be arrested at early stages by promoting their mutual action.

Positron Emission Tomography and Neuropathologic Estimates of Fibrillar Amyloid-β in a Patient With Down Syndrome and Alzheimer Disease

Down syndrome appears to be associated with a virtually certain risk of fibrillar amyloid-β (Aβ) pathology by the age of 40 and a very high risk of dementia at older ages. The positron emission tomography (PET) ligand florbetapir F18 has been shown to characterize fibrillar Aβ in the living human brain and to provide a close correlation with subsequent Aβ neuropathology in individuals proximate to and after the end of life. The extent to which the most frequently used PET ligands can be used to detect fibrillar Aβ in patients with Down syndrome remains to be determined. To characterize PET estimates of fibrillar Aβ burden in a Down syndrome patient very close to the end of life and to compare them with neuropathologic assessment made after his death. Design/ With the family's informed consent, florbetapir PET was used to study a 55-year-old Down syndrome patient with Alzheimer disease near the end of life; his brain was donated for neuropathologic assessment when he died 14 days later. Visual ratings of cerebral florbetapir uptake were performed by trained readers who were masked to the patient's diagnosis as part of a larger study, and an automated algorithm was used to characterize regional-to-cerebellar standard uptake value ratios in 6 cerebral regions of interest. Neuropathologic assessments were performed masked to the patient's diagnosis or PET measurements. Visual ratings and automated analyses of the PET image revealed a heavy fibrillar Aβ burden in cortical, striatal, and thalamic regions, similar to that reported for patients with late-onset Alzheimer disease. This matched neuropathologic findings of frequent neuritic and diffuse plaques, as well as frequent amyloid angiopathy, except for neuropathologically demonstrated frequent cerebellar diffuse plaques and amyloid angiopathy that were not detected by the PET scan. Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum. Additional studies are needed to determine the extent to which PET could be used to detect and to track fibrillar Aβ and to evaluate investigational Aβ-modifying treatments in the presymptomatic and symptomatic stages of Alzheimer disease.

Neuropathologic features associated with Alzheimer disease diagnosis

To examine whether the association between clinical Alzheimer disease (AD) diagnosis and neuropathology and the precision by which neuropathology differentiates people with clinical AD from those with normal cognition varies by age. We conducted a cross-sectional analysis of 2,014 older adults (≥70 years at death) from the National Alzheimer's Coordinating Center database with clinical diagnosis of normal cognition (made ≤1 year before death, n = 419) or AD (at ≥65 years, n = 1,595) and a postmortem neuropathologic examination evaluating AD pathology (neurofibrillary tangles, neuritic plaques) and non-AD pathology (diffuse plaques, amyloid angiopathy, Lewy bodies, macrovascular disease, microvascular disease). We used adjusted logistic regression to analyze the relationship between clinical AD diagnosis and neuropathologic features, area under the receiver operating characteristic curve (c statistic) to evaluate how precisely neuropathology differentiates between cognitive diagnoses, and an interaction to identify effect modification by age group. In a model controlling for coexisting neuropathologic features, the relationship between clinical AD diagnosis and neurofibrillary tangles was significantly weaker with increasing age (p < 0.001 for interaction). The aggregate of all neuropathologic features more strongly differentiated people with clinical AD from those without in younger age groups (70-74 years: c statistic, 95% confidence interval: 0.93, 0.89-0.96; 75-84 years: 0.95, 0.87-0.95; ≥85 years: 0.83, 0.80-0.87). Non-AD pathology significantly improved precision of differentiation across all age groups (p < 0.004). Clinical AD diagnosis was more weakly associated with neurofibrillary tangles among the oldest old compared to younger age groups, possibly due to less accurate clinical diagnosis, better neurocompensation, or unaccounted pathology among the oldest old.

Harm Avoidance and Risk of Alzheimer's Disease

To test the hypothesis that harm avoidance, a trait associated with behavioral inhibition, is associated with the risk of developing Alzheimer's disease (AD). A total of 791 adults 55 years and older without dementia completed a standard self-report measure of harm avoidance. They then underwent annual evaluations that included detailed cognitive testing and clinical classification of mild cognitive impairment (MCI), dementia, and AD. In a uniform neuropathologic examination of those who died, counts of neuritic plaques, diffuse plaques, and neurofibrillary tangles were standardized and combined to yield a pathologic measure of disease. The relation of harm avoidance to incidence of AD and related outcomes was estimated in analyses adjusted for age, sex, and education. During a mean of 3.5 years of annual observation, 98 people (12.4%) developed incident AD. A high level of harm avoidance (90th percentile) was associated with a more than two-fold increase in risk of AD compared with a low score (10th percentile). Higher harm avoidance was also associated with increased incidence of MCI and more rapid decline in episodic memory, working memory, and perceptual speed (but not semantic memory or visuospatial ability). In 116 participants who died and underwent brain autopsy, harm avoidance was not related to a composite measure of plaques and tangles. A high level of the harm avoidance trait, indicating a tendency toward behavioral inhibition, is related to the risk of developing AD and its precursor, MCI.

Widespread Tau and Amyloid‐Beta Pathology Many Years After a Single Traumatic Brain Injury in Humans

While a history of a single traumatic brain injury (TBI) is associated with the later development of syndromes of cognitive impairment such as Alzheimer's disease, the long-term pathology evolving after single TBI is poorly understood. However, a progressive tauopathy, chronic traumatic encephalopathy, is described in selected cohorts with a history of repetitive concussive/mild head injury. Here, post-mortem brains from long-term survivors of just a single TBI (1-47 years survival; n=39) vs. uninjured, age-matched controls (n=47) were examined for neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaques using immunohistochemistry and thioflavine-S staining. Detailed maps of findings permitted classification of pathology using semiquantitative scoring systems. NFTs were exceptionally rare in young, uninjured controls, yet were abundant and widely distributed in approximately one-third of TBI cases. In addition, Aβ-plaques were found in a greater density following TBI vs. controls. Moreover, thioflavine-S staining revealed that while all plaque-positive control cases displayed predominantly diffuse plaques, 64% of plaque-positive TBI cases displayed predominantly thioflavine-S-positive plaques or a mixed thioflavine-S-positive/diffuse pattern. These data demonstrate that widespread NFT and Aβ plaque pathologies are present in up to a third of patients following survival of a year or more from a single TBI. This suggests that a single TBI induces long-term neuropathological changes akin to those found in neurodegenerative disease.

Expression of cytokine IL-1α and S100β in different types of plaques in Alzheimer's disease

To study the significance of cytokine IL-1α and S100β expression in formation and evolution of different types of plaques in Alzheimer's disease. Thirty-four autopsy cases of Alzheimer's disease encountered during the period from 1982 to 2008 were retrieved from the archival files of Department of Pathology, Beijing Hospital. Tissue blocks were taken from hippocampus for dual immunostaining for IL-1α/Aβ and S100β/Aβ. Immunohistochemical studied for IL-1α/Aβ and S100β/Aβ delineated four different types of senile plaques: diffuse non-neuritic plaques, diffuse neuritic plaques, dense-core neuritic plaques and dense-core non-neuritic plaques. The numbers of IL-1α-positive microglias and S100β-positive astrocytes associated with diffuse neuritic plaques were (7.29 ± 3.04) per mm(2) and (6.49 ± 2.20) per mm(2), respectively. In contrast, the numbers of IL-1α-positive microglias and S100β-positive astrocytes associated with diffuse non-neuritic plaques, dense-core neuritic plaques and dense-core non-neuritic plaques were (3.24 ± 1.53) per mm(2) and (4.14 ± 1.77) per mm(2), (2.09 ± 1.37) per mm(2) and (2.25 ± 0.83) per mm(2), and (1.38 ± 0.90) per mm(2) and (0.58 ± 0.36) per mm(2), respectively. The numbers of IL-1α-positive microglias and S100β-positive astrocytes associated with diffuse neuritic plaques were significantly higher than those of the other three types of plaques (P < 0.05). The IL-1α-positive microglias and S100β-positive astrocytes may be of certain significance in transformation of diffuse non-neuritic plaques to diffuse neuritic plaques in Alzheimer's disease.

A Retrospective Study of Chest Pain in Benign Asbestos Pleural Disease

The aims of this review were to ascertain the incidence of asbestos-related chest pain at presentation in two groups of patients referred with asbestos diseases and the demographics, comorbidities, and chest computed tomography findings associated with chest pain. Medical charts of patients presenting 1995-2008, audited for quality assurance, were chosen at random by data managers. Patients with mesothelioma, lung cancer, and angina were excluded. Rigorous attempts had been taken by the authors to exclude other causes of chest pain. There were 167 patients who were medicolegal referrals (Group 1) and 115 clinical referrals (Group 2). Although the patients in Group 1 had more severe disease generally than Group 2, the proportion with pain was not significantly different (45.5% and 55.7%, mean duration 4.8 years, range 1-22 years). Group 1 had more severe disease as a rule. However, the proportion with pain in Groups 1 and 2, respectively, was as follows: diffuse pleural thickening (50.8% and 67.6%, P=0.072), pleural plaques (47.0% and 59.7%, P=0.076), folded atelectasis (70.6% and 83.3%, P=1.000), and asbestosis (43.6% and 53.3%, P=0.346). Of all those with folded atelectasis, 73.9% had pain. Chest pain appears to be much more common in patients with benign asbestos diseases than is currently recognized, particularly in those with folded atelectasis and is not restricted to litigants. Improved recognition of this entity is needed along with practical management guidelines for the general practitioner. Further studies are envisaged by the authors.

Caso familiar de nevo branco esponjoso oral: uma rara condição hereditária

White sponge nevus (WSN) is an autosomal dominant skin disorder characterized by white, corrugated and diffuse plaques mainly affecting the oral mucosa. The condition has a high penetrance and variable expressivity, but familial reports are uncommon. This report presents a familial case of WSN in which two sisters are affected by the disorder.

MyD88 Deficiency Ameliorates β-Amyloidosis in an Animal Model of Alzheimer's Disease

The accumulation of β-amyloid protein (Aβ) in the brain is thought to be a primary etiologic event in Alzheimer's disease (AD). Fibrillar Aβ plaques, a hallmark of AD abnormality, are closely associated with activated microglia. Activated microglia have contradictory roles in the pathogenesis of AD, being either neuroprotective (by clearing harmful Aβ and repairing damaged tissues) or neurotoxic (by producing proinflammatory cytokines and reactive oxygen species). Aβ aggregates can activate microglia by interacting with multiple toll-like receptors (TLRs), the pattern-recognition receptors of the innate immune system. Because the adapter protein MyD88 is essential for the downstream signaling of all TLRs, except TLR3, we investigated the effects of MyD88 deficiency (MyD88(-/-)) on Aβ accumulation and microglial activation in an AD mouse model. MyD88 deficiency decreased Aβ load and microglial activation in the brain. The decrease in Aβ load in an MyD88(-/-) AD mouse model was associated with increased and decreased protein expression of apolipoprotein E (apoE) and CX3CR1, respectively, compared with that in an MyD88 wild-type AD mouse model. These results suggest that MyD88 deficiency may reduce Aβ load by enhancing the phagocytic capability of microglia through fractalkine (the ligand of CX3CR1) signaling and by promoting apoE-mediated clearance of Aβ from the brain. These findings also suggest that chronic inflammatory responses induced by Aβ accumulation via the MyD88-dependent signaling pathway exacerbate β-amyloidosis in AD.

Diffuse hyperpigmented plaques as cutaneous manifestation of multicentric Castleman disease and treatment with thalidomide: Report of three cases

Diffuse hyperpigmented plaques as cutaneous manifestation of multicentric Castleman disease and treatment with thalidomide: Report of three cases

Lack of detectable diffuse or neuritic plaques and neurofibrillary tangles in the brains of aged hamsters

Syrian golden hamsters (Mesocricetus auratus) are facultative hibernators with a life expectancy of approximately 2 years. Previous investigations showed a hyperphosphorylation of the tau protein during hibernation and aging and raised hopes that Syrian hamsters might represent a useful animal model to study pathogenetic mechanisms of Alzheimer's disease. Brain and spinal cord transversal sections of 190 hamsters 1–36 months of age were investigated using histology and immunohistochemistry to detect neurofibrillary tangles and/or diffuse as well as neuritic plaques. Summarized, amyloid deposition, neurofibrillary tangles, and diffuse as well as neuritic plaques were absent indicating that the Syrian golden hamster does not develop changes characteristic of Alzheimer's disease even at advanced age and does not represent an appropriate animal model for this disease.