University of California Los Angeles (UCLA) Alzheimers Disease Research Center is one of leading Southern California Alzheimers Disease Research Centers(ADRC). Learn about early signs and symptoms on memory loss and last stages of Alzheimers disease and other dementias through one of the best Alzheimers Neurologists; how to delay the early onset Alzheimers disease and treatments on non-alzheimers dementias such as dementia with Lewy Bodies (DLB), vascular or multi-infarct dementia or frontotemporal dementia (FTD) which is also called Picks disease.
que es el Alzheimer? Alzheimers Disease Research Center at University of California, Los Angles (UCLA) also enrolls patients and subjects in clinical and pre-clinical research program. Alzheimers Disease NeuroImaging Initiative (ADNI) is a brain imaging and biomarkers, and longitudinal studies. We have bilingual staff that speaks Spanish and English. UCLA Alzheimers Disease Research Center is located in Los Angeles, California.
UCLA Alzheimers Disease Research Center at UCLA, Los Angeles, California is looking for clinical trial participants in medication and non-medication research studies for potential drugs to treat Alzheimers disease. Learn the causes, symptoms, risk factors, early onset, progression, treatments, stages related dementias and latest Alzheimers research break-through at the UCLA Alzheimers Disease Research Center.
University of California Los Angeles (UCLA) Alzheimers Disease Research Center is one of the leading Southern California Alzheimers Disease Research Centers(ADRC). Learn about early signs and symptoms on memory loss and Alzheimers disease and other dementias through one of the best Alzheimers Research Centers; how to delay the early onset Alzheimers diesease and treatments on non-alzheimers dementias such as dementia with Lewy Bodies (DLB), vascular or multi-infarct dementia or frontotemporal dementia (FTD) which is also called Picks disease.
These findings suggest that the functional neuroanatomical alterations underlying explicit memory changes in mild Alzheimers disease differ from those seen with normal aging. Particularly striking was the fact that the regions showing the greatest decreases in activation in the patients with mild Alzheimers disease compared with the elderly controls were in the hippocampal formation. We hypothesise that this is the result of the extensive neuronal loss (in conjunction with neuritic plaques and neurofibrillary tangles) that develops early in the course of Alzheimers disease.3 It is likely that regional atrophy is also at least partially responsible for the decreased hippocampal activation in Alzheimers disease.16 However, this is unlikely to be the entire explanation for our findings, as we saw little evidence of paradigm linked activation in the hippocampus in six of the seven Alzheimer patients when the MR signal was sampled within a small section of the hippocampus, guided by each ...
HealthDay News) -- Alzheimers patients given sedatives such as Valium or Xanax may have an increased risk for pneumonia, a new study warns.. People with Alzheimers disease are often given these drugs, called benzodiazepines, over the long term, the researchers said.. Examples of benzodiazepines include alprazolam (Xanax), clonazepam (Klonopin), diazepam (Valium), and lorazepam (Ativan).. An increased risk of pneumonia is an important finding to consider in treatment of patients with Alzheimer disease. Pneumonia often leads to admission to hospital, and patients with dementia are at increased risk of death related to pneumonia, Dr. Heidi Taipale, of Kuopio Research Center of Geriatric Care at the University of Eastern Finland, and co-authors wrote.. For the study, the researchers reviewed data from nearly 50,000 Alzheimers patients in Finland. The patients average age was 80 and about two-thirds were women.. The study found that people with Alzheimers who took benzodiazepines were 30 ...
Dental health problems in Alzheimers patients can lead to pain, unmanageable behavior and extensive dental treatment. Yet, the dental needs of Alzheimers patients are often overlooked, usually for very understandable reasons: the patients forgetfulness results in unintentional dental neglect; medications may cause chronic "dry mouth" (reduction in the healthy flow of saliva) that can lead to tooth decay; patients and their families lose contact with their dentist because they are focused on other health issues.. Good dental health can make eating and digesting food easier for an Alzheimers patient, improving the overall quality of life. If you are a caregiver for someone suffering from Alzheimers, here are some tips and techniques from the Alzheimers Association to assist your loved one in maintaining good oral health.. ...
The cognitive profile of Alzheimer patients without (AD E-, n=17) and with (AD, E+, n=15) extrapyramidal signs (rigidity or bradykinesia), at the time of diagnosis, was examined in a 3-year follow-up
A study involving 159 older adults (average age 76) has confirmed that the amount of brain tissue in specific regions is a predictor of Alzheimers disease development. Of the 159 people, 19 were classified as at high risk on the basis of the smaller size of nine small regions previously shown to be vulnerable to Alzheimers), and 24 as low risk. The regions, in order of importance, are the medial temporal, inferior temporal, temporal pole, angular gyrus, superior parietal, superior frontal, inferior frontal cortex, supramarginal gyrus, precuneus.. There was no difference between the three risk groups at the beginning of the study on global cognitive measures (MMSE; Alzheimers Disease Assessment Scale-cognitive subscale; Clinical Dementia Rating-sum of boxes), or in episodic memory. The high-risk group did perform significantly more slowly on the Trail-making test part B, with similar trends on the Digit Symbol and Verbal Fluency tests.. After three years, 125 participants were re-tested. Nine ...
The Alzheimers Disease Research Center (ADRC) at the Icahn School of Medicine at Mount Sinai is a comprehensive research facility and clinical program dedicated to the study and treatment of normal aging and Alzheimers disease.
The identification of mutations in the APP, PS1, and PS2 genes that cause early-onset familial Alzheimers disease (AD), the demonstration that these mutations all increase Abeta42, and the discovery of an association between Apolipoprotein E4 and late-onset Alzheimers disease have dramatically improved our understanding of Alzheimers disease. It is clear, however, that much of the genetic risk in late onset Alzheimers disease remains unexplained. Current strategies to identify other genes that affect late-onset Alzheimers disease have met with limited success often because of the difficulty associated with obtaining late-onset families with sufficient power for reliable linkage analysis. Genetic studies using large numbers of small families or sib-pairs, to increase the power of the analysis, are also currently being performed by several groups however difficulties with the non-replication of positive loci, identified by different studies, has continued. It will also be difficult to ...
The Alzheimers Disease Neuroimaging Initiative (ADNI) unites researchers with study data as they work to define the progression of Alzheimers disease. ADNI researchers collect, validate and utilize data such as MRI and PET images, genetics, cognitive tests, CSF and blood biomarkers as predictors for the disease. Data from the North American ADNIs study participants, including Alzheimers disease patients, mild cognitive impairment subjects and elderly controls, are available from this site.. ...
Calcium: A proven target in the war on Alzheimers disease Alzheimers disease is practically a household word these days, as the number of individuals dia
In this study, we have evaluated the levels of blood histamine, serum interleukin-1 beta (IL-1 beta), and plasma tumor necrosis factor-alpha (TNF-alpha) in 20 patients with mild to moderate Alzheimer disease (AD; 13 early onset and 7 late-onset AD subjects) and in 20 age-matched control subjects (C) …
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The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for preclinical detection, and discover novel treatment strategies, in affiliation with the UW Memory and Brain Wellness Center.
The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for preclinical detection, and discover novel treatment strategies, in affiliation with the UW Memory and Brain Wellness Center.
The overall goal of the proposed renewal of the Wisconsin Alzheimers Disease Research Center (Wisconsin ADRC) is to support cutting-edge and innovative researc...
Obstructive sleep apnea (OSA) is much more common in the elderly than in the young; the latest studies show prevalence between 45% and 62% in individuals over 60. It is even higher in patients with dementia such as Alzheimer patients.. Several trials in elderly patients showed modified cognitive functions, particularly executive and attentional functions, in patients with respiratory sleep disorder. However the benefit of CPAP (Continuous Positive Airway Pressure) ventilation for Alzheimer patients is still controversial, as there are few studies documenting its effects on dementia patients cognitive abilities, and clinicians appear reluctant to prescribe this type of treatment.. The investigators must keep in mind that Alzheimer patients suffer significant sleep disorders; advanced- stage patients spend 40% of the night awake and are drowsy a large part of the day. In dementia patients, sleep disorder is a major cause of hospitalization and institutionalization. The prevalence of obstructive ...
Obstructive sleep apnea (OSA) is much more common in the elderly than in the young; the latest studies show prevalence between 45% and 62% in individuals over 60. It is even higher in patients with dementia such as Alzheimer patients.. Several trials in elderly patients showed modified cognitive functions, particularly executive and attentional functions, in patients with respiratory sleep disorder. However the benefit of CPAP (Continuous Positive Airway Pressure) ventilation for Alzheimer patients is still controversial, as there are few studies documenting its effects on dementia patients cognitive abilities, and clinicians appear reluctant to prescribe this type of treatment.. The investigators must keep in mind that Alzheimer patients suffer significant sleep disorders; advanced- stage patients spend 40% of the night awake and are drowsy a large part of the day. In dementia patients, sleep disorder is a major cause of hospitalization and institutionalization. The prevalence of obstructive ...
A bit of peanut butter and a ruler may be an easy way confirm a diagnosis of early-stage Alzheimers disease, U.S. researchers say.
Brussels, Belgium, 19 July 2017 - Today, the Innovative Medicines Initiative (IMI) is launching two new Calls for proposals with topics on Alzheimers disease, big data, vaccines, autoimmune disease, the blood-brain barrier, drug development, and the exploitation of IMI project results. The total budget for the two Calls stands at just over EUR 130 million. Around half of this comes from the European Commissions Horizon 2020 programme. The other half comes from EFPIA companies as well as IMI Associated Partners.
The ε4 allele of apolipoprotein E (ApoE) accounts for an estimated 45-60% of the genetic risk for late onset sporadic Alzheimers disease, suggesting that it may be possible to identify other genetic loci that could account for the remaining risk associated with this disease. Recently, a biallelic polymorphism (G/A) in the 3′ untranslated region (UTR) of the transcription factor LBP-1c/CP2/LSF (for brevity, CP2) has been implicated in Alzheimers disease susceptibility, with the 3′-UTR A allele being associated with a reduction in the risk of sporadic Alzheimers disease.1-3 The CP2 gene is a plausible candidate for influencing Alzheimers disease risk: it is located near the LDL receptor related protein gene within the Alzheimers disease linkage region on chromosome 12; it controls the expression of several genes (α2 macroglobulin, glycogen synthase kinase-3β); and it interacts with different proteins (serum amyloid A3, interleukin 1α, tumour necrosis factor α, and Fe65 protein) and ...
TY - JOUR. T1 - Deleterious ABCA7 mutations and transcript rescue mechanisms in early onset Alzheimers disease. AU - De Roeck, Arne. AU - Van den Bossche, Tobi. AU - van der Zee, Julie. AU - Verheijen, Jan. AU - De Coster, Wouter. AU - Van Dongen, Jasper. AU - Dillen, Lubina. AU - Baradaran-Heravi, Yalda. AU - Heeman, Bavo. AU - Sanchez-Valle, Raquel. AU - Lladó, Albert. AU - Nacmias, Benedetta. AU - Sorbi, Sandro. AU - Gelpi, Ellen. AU - Grau-Rivera, Oriol. AU - Gómez-Tortosa, Estrella. AU - Pastor, Pau. AU - Ortega-Cubero, Sara. AU - Pastor, Maria A. AU - Graff, Caroline. AU - Thonberg, Håkan. AU - Benussi, Luisa. AU - Ghidoni, Roberta. AU - Binetti, Giuliano. AU - de Mendonça, Alexandre. AU - Martins, Madalena. AU - Borroni, Barbara. AU - Padovani, Alessandro. AU - Almeida, Maria Rosário. AU - Santana, Isabel. AU - Diehl-Schmid, Janine. AU - Alexopoulos, Panagiotis. AU - Clarimon, Jordi. AU - Lleó, Alberto. AU - Fortea, Juan. AU - Tsolaki, Magda. AU - Koutroumani, Maria. AU - Matěj, ...
Eventbrite - Alzheimers Association, Hudson Valley Chapter presents Alzheimers Disease & Related Disorders Association, Inc. Hudson Valley Chapters 2015 Year End Appeal - Monday, December 7, 2015 | Monday, February 29, 2016 - Find event and ticket information.
Many patients currently diagnosed with very mild or mild Alzheimer disease dementia could potentially be reclassified as having mild cognitive impairment (MCI) under revised criteria for that condition, according to a report published Online First by Archives of Neurology, one of the JAMA/Archives journals.. The National Institute on Aging and the Alzheimers Association convened a work group to update criteria for MCI, and the revised criteria allow "considerable latitude" as to what represents functional independence, writes the studys sole author, John C. Morris, M.D., of Washington University School of Medicine in St. Louis. For example, "mild problems" performing daily activities such as shopping, paying bills and cooking are permissible, as is dependency on aids or assistance to complete those tasks.. In this study, the functional ratings of patients enrolled at federally funded Alzheimers Disease Centers with clinical and cognitive data maintained by the National Alzheimers ...
This new book presents a summary of Alzheimers disease-related ischemic protein changes and gene expression as risk factors for the late-onset of sporadic Alzheimers disease, and their role in Alzheimers disease ischemic etiology. Ischemic brain changes were noted in the staining of different parts of an amyloid protein precursor, presenilin 1 and 2, tau protein, alfa-synuclein, and apolipoproteins A1, E and J.. Current advances in understanding the ischemic etiology of Alzheimers disease has revealed dysregulation of Alzheimers disease-associated genes including presenilin 1 and 2, β-secretase, amyloid protein precursor, apoptosis, autophagy, mitophagy, and tau protein. This book presents the relationship between these genes, dysregulated by cerebral ischemia, and the cellular and tissue neuropathology characteristic of Alzheimers disease. This book draws attention to the latest research confirming the theory that Alzheimers disease-related proteins and genes play an important role in ...
The presence of Abeta(pE3) (N-terminal truncated Abeta starting with pyroglutamate) in Alzheimers disease (AD) has received considerable attention since the discovery that this peptide represents a dominant fraction of Abeta peptides in senile plaques of AD brains. This was later confirmed by other reports investigating AD and Downs syndrome postmortem brain tissue. Importantly, Abeta(pE3) has a higher aggregation propensity, and stability, and shows an increased toxicity compared to full-length Abeta. We have recently shown that intraneuronal accumulation of Abeta(pE3) peptides induces a severe neuron loss and an associated neurological phenotype in the TBA2 mouse model for AD. Given the increasing interest in Abeta(pE3), we have generated two novel monoclonal antibodies which were characterized as highly specific for Abeta(pE3) peptides and herein used to analyze plaque deposition in APP/PS1KI mice, an AD model with severe neuron loss and learning deficits. This was compared with the plaque ...
Alzheimers Disease is a progressive neurodegenerative illness characterized by short-term memory loss, disorientation, and impairments in socialization, self-care and behavioral regulation. It is primarily a disease of old age and affects over 5,000,000 Americans. Medications are often prescribed to manage its symptoms, but no medication has been shown to halt or delay the progression of the disease.. Given the enormous personal, social, and economic consequences of this illness, researchers are actively seeking novel ways to slow and forestall its devastating effects.. In a randomized clinical trial, Quintana-Hernández et al. [Journal of Alzheimers Disease] compared the effectiveness of a Mindfulness-Based Alzheimers Stimulation (MBAS) program in maintaining cognitive functioning in Alzheimers patients to that of two current non-pharmacological interventions for Alzheimers disease; namely, Progressive Muscle Relaxation (PMR) and Cognitive Stimulation Therapy (CST).. The researchers ...
Fagan, A. M., Mintun, M. A., Shah, A. R., Aldea, P., Roe, C. M., Mach, R. H., Marcus, D., Morris, J. C. and Holtzman, D. M. (2009), Cerebrospinal fluid tau and ptau181 increase with cortical amyloid deposition in cognitively normal individuals: Implications for future clinical trials of Alzheimers disease. EMBO Mol Med, 1: 371-380. doi: 10.1002/emmm.200900048 ...
BACKGROUND: Knowledge of the evolution of cognitive deficits in Alzheimer disease is important for our understanding of disease progression. Previous reports, however, have either lacked detail or have not covered the presymptomatic stages. OBJECTIVE: To delineate the onset and progression of clinical and neuropsychological abnormalities in familial Alzheimer disease. METHODS: Nineteen subjects with familial Alzheimer disease underwent serial clinical and neuropsychological assessments. Eight of these had undergone presymptomatic assessments. The follow-up period was 1 to 10 years (mean, 5 years). The relative timing of the occurrence of 3 markers of disease onset and progression (onset of symptoms, Mini-Mental State Examination score , or = 24, and impaired scores on a range of neuropsychological tests) were compared using the binomial exact test. RESULTS: Neurological abnormalities were not prominent, although myoclonus appeared early in some. Mini-Mental State Examination score was not ...
Title: Serum Amyloid Beta Peptides in Patients with Dementia and Age-Matched Non-Demented Controls as Detected by Surface-Enhanced Laser Desorption Ionisation-Time of Flight Mass Spectrometry (SELDI-TOF MS). VOLUME: 3 ISSUE: 3. Author(s):Suzanne V. Frankfort, Jos P.C.M. van Campen, Linda R. Tulner and Jos H. Beijnen. Affiliation:Department of Pharmacy&Pharmacology, Slotervaart Hospital, Louwesweg 6, 1066 EC Amsterdam, The Netherlands.. Keywords:Serum Amyloid Beta Peptides, dementia, SELDI-TOF MS, Alzheimers Disease, CSF profile, diagnosis, DNA Isolation, Genotype Analysis. Abstract: Background: By using surface enhanced laser desorption/ionisation- time of flight mass spectrometry (SELDITOF MS) an amyloid ß (Aß) profile was shown in cerebrospinal fluid (CSF) of patients with dementia. Objective: To investigate the Aβ-profile in serum with SELDI-TOF MS, to evaluate if this profile resembles CSF profiles and to investigate the correlation between intensity of Aβ-peptide-peaks in serum and ...
- Treatment with Nypta(R) (Tideglusib) (NP-12) was tolerated and produced positive effects on Alzheimers patients in four of the five efficacy variables examined in the trial.
The uridine nucleotide-activated P2Y2, P2Y4 and P2Y6 receptors are widely expressed in the brain and are involved in many CNS processes, including those which malfunction in Alzheimers disease (AD). However, the status of these receptors in the AD neocortex, as well as their putative roles in the pathogenesis of neuritic plaques and neurofibrillary tangles, remain unclear. In this study, we used immunoblotting to measure P2Y2, P2Y4 and P2Y6 receptors in two regions of the postmortem neocortex of neuropathologically assessed AD patients and aged controls. P2Y2 immunoreactivity was found to be selectively reduced in the AD parietal cortex, while P2Y4 and P2Y6 levels were unchanged. In contrast, all three receptors were preserved in the occipital cortex, which is known to be minimally affected by AD neuropathology. Furthermore, reductions in parietal P2Y2 immunoreactivity correlated both with neuropathologic scores and markers of synapse loss. These results provide a basis for considering P2Y2 receptor
Most people with Alzheimers disease have the late-onset form of the disease, in which symptoms become apparent in their mid-60s.The apolipoprotein E (APOE) gene is involved in late-onset Alzheimers. This gene has several forms. One of them, APOE ε4, increases a persons risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop Alzheimers disease, and people with no APOE ε4 may also develop the disease.. Also, scientists have identified a number of regions of interest in the genome (an organisms complete set of DNA) that may increase a persons risk for late-onset Alzheimers to varying degrees.. Early-onset Alzheimers disease occurs in people age 30 to 60 and represents less than 5 percent of all people with Alzheimers. Most cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimers disease, ...
The Pentacam HR Scheimpflug imaging was performed on 10 eyes from 10 Alzheimers disease patients and 10 eyes of 10 age and sex matched control patients (Figure). The average age of Alzheimers disease patients was 72.3±9.9 years and that of control patients was 68.3±6.78 years. The average and maximum densities of the supranuclear lens region were consistently higher in Alzheimers disease patients (12.28±1.25 and 24.72±6.01, respectively), when compared to age and sex matched controls (11.82±1.67 and 22.40±4.3). However, there was no statistically significant difference in these variables between the two groups (p=0.33 and p=0.50).. ...
Dr. Richard Mayeux is the Gertrude H. Sergievsky Professor of Neurology, Psychiatry and Epidemiology, chair of the Department of Neurology at Columbia University College of Physicians and Surgeons, and Neurologist-in-Chief at NewYork-Presbyterian/Columbia University Medical Center. Dr. Mayeux is also director of the Gertrude H. Sergievsky Center, a center devoted to the epidemiologic investigation of neurological diseases, and co-director of the Taub Institute for Research on Alzheimers Disease and the Aging Brain at Columbia University Medical Center.. Dr. Mayeux graduated with distinction from the University of Oklahoma School of Health Sciences and trained in Internal Medicine at the Boston City Hospital and in Neurology at the Columbia Presbyterian Medical Center in New York. He completed a fellowship in the study of disorders of behavior, language, and cognition with the late D.Frank Benson in Boston. Dr. Mayeux completed graduate work in epidemiology at the Columbia University Mailman ...
The progression and symptoms of early-onset Alzheimers Disease, typically identified in patients in their 40s or 50s, can vary dramatically depending on the individual. According to the Alzheimers Association,
The study involved 20 subjects with Alzheimers disease or mild cognitive impairment who, on separate days, were given either emulsified MCTs or a placebo. The researchers observed a significant increase in blood plasma levels of the ketone body beta-hydroxylutyrate (beta-OHB) after only 90 minutes of treatment, and depending on the apolipoprotein E genotype of the subject tested, beta-OHB levels either continued to rise or held constant between the 90 and 120 minute blood draws in the treatment condition. Remarkably, cognitive testing revealed that this brief MCT treatment facilitated improved performance on the Alzheimers Disease Assessment Scale-Cognitive Subscale (ADAS-cog) in 4 subjects within the study group. Moreover, "higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02)."[i ...
On October 4, the Alzheimer Society of B.C., Brain Canada, Genome British Columbia, the Michael Smith Foundation for Health Research and the Pacific Alzheimer Research Foundation will have an in-depth discussion of how research is moving towards a cure for Alzheimers disease and other dementias. An expert panel will break down the current state of dementia research, including the crucial role played by individuals and families living with the disease. Afterwards, a Q&A session will open the floor for public discussion.. If you or someone in your life is living with the disease, or if youre interested in how B.C. researchers are confronting it, dont miss out. Registration is free, but spaces are limited.. Event details: ...
The CLU gene is located on p21-p12 of human chromosome 8, with CLU as its encoded product, which has various physiological functions, including participating in lipid metabolism (28), oxidative stress reaction (29), and cell cycle regulation (30). CLU is highly expressed in cerebrospinal fluid and amyloid plaques in brain tissues, and is involved in the pathogenesis of AD (4,5,31). Yerbury et al (32) demonstrated that the deposition of CLU in senile plaques and neurofibrillary tangles of AD. Howlett et al (33) further reported a correlation between CLU and senile plaque Aβ40 in the brain cortex of patients with AD. Martin-Rehrmann et al (34) demonstrated the presence of dysfunctional neurons with phosphorylated tau protein surrounding the senile plaques in 71% of CLU-positive patients with AD. Furthermore, they also showed that the tau and phosphorylated tau protein were significantly increased in the rat hippocampus, following the injection of a CLU-rich solution (34). It was suggested that ...
The new potential treatment offers a different approach from the traditional tactic of targeting the amyloid plaques and tangles that develop in the brains of Alzheimers patients. Until recently, most researchers believed these plaques and tangles caused the cognitive decline. But the failure of this hypothesis to lead to an effective treatment for Alzheimers disease has caused some scientists to theorize that, though the plaques and tangles are always associated with the disease, they may not be the main cause of the dementia, nor the best target for treating it ...
Objective: To investigate the particular pathology of the Arctic APP (APParc) early-onset familial Alzheimer disease (eoFAD) mutation for the first time in vivo with PET in comparison with other eoFAD mutations and sporadic Alzheimer disease (sAD).. Methods: We examined 2 APParc mutation carriers together with 5 noncarrier siblings cross-sectionally with C-11-labeled Pittsburgh compound B (PiB) and F-18-fluorodeoxyglucose (FDG) PET, as well as MRI, CSF biomarkers, and neuropsychological tests. Likewise, we examined 7 patients with sAD, 1 carrier of a presenilin 1 (PSEN1) mutation, 1 carrier of the Swedish APP (APPswe) mutation, and 7 healthy controls (HCs).. Results: Cortical PiB retention was very low in the APParc mutation carriers while cerebral glucose metabolism and CSF levels of A beta(1-42), total and phosphorylated tau were clearly pathologic. This was in contrast to the PSEN1 and APPswe mutation carriers revealing high PiB retention in the cortex and the striatum in combination with ...
Alzheimers disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ) production and clearance leading to Aβ accumulation in the central nervous system (CNS). Aβ production and clearance are key targets in the development of disease-modifying therapeutic agents for Alzheimers disease. However, there has not been direct evidence of altered Aβ production or clearance in Alzheimers disease. Using metabolic labeling, we measured Aβ42 and Aβ40 production and clearance rates in the CNS of participants with Alzheimers disease and cognitively normal controls. Clearance rates for both Aβ42 and Aβ40 were impaired in Alzheimers disease compared to controls. On average, there were no differences in Aβ40 or Aβ42 production rates. Thus, the common late-onset form of Alzheimers disease is characterized by an overall impairment in Aβ clearance.. ...
17/Jun/2013 Although a family history of Alzheimers disease is a primary risk factor for the devastating neurological disorder, mutations in only three genes - the amyloid precursor protein and presenilins 1 and 2 - have been established as causative for inherited, early-onset Alzheimers, accounting for about half of such cases. Now Massachusetts General Hospital (MGH) researchers have discovered a type of mutation known as copy-number variants (CNVs) - deletions, duplications, or rearrangements of human genomic DNA - in affected members of 10 families with early-onset Alzheimers. Notably, different genomic changes were identified in the Alzheimers patients in each family.. The study was conducted as part of the Alzheimers Genome Project - directed by Rudolph Tanzi, PhD, director of the Genetics and Aging Research Unit at Massachusetts General Hospital (MGH) and a co-discoverer of the first three early-onset genes - and was supported by the Cure Alzheimers Fund and the National Institute ...
Altered proteome profiles have been reported in both postmortem brain tissues and body fluids of subjects with Alzheimer disease (AD), but their broad relationships with AD pathology, amyloid pathology, and tau-related neurodegeneration have not yet been fully explored. Using a robust automated MS-based proteomic biomarker discovery workflow, we measured cerebrospinal fluid (CSF) proteomes to explore their association with well-established markers of core AD pathology. Cross-sectional analysis was performed on CSF collected from 120 older community-dwelling adults with normal (n = 48) or impaired cognition (n = 72). LC-MS quantified hundreds of proteins in the CSF. CSF concentrations of β-amyloid 1-42 (Aβ1-42), tau, and tau phosphorylated at threonine 181 (P-tau181) were determined with immunoassays. First, we explored proteins relevant to biomarker-defined AD. Then, correlation analysis of CSF proteins with CSF markers of amyloid pathology, neuronal injury, and tau hyperphosphorylation (i.e., Aβ1-42
Pfizer Inc. (NYSE PFE) , together with its collaborator on the Alzheimer s Immunotherapy Program, Janssen Alzheimer Immunotherapy, presented new research this w
Dr. Lawrence Honigs principal medical and scientific interests are in aging and neurodegenerative diseases of the brain. These latter include Alzheimers disease, Lewy Body dementia, vascular cognitive impairment, and Creutzfeldt-Jakob disease, and also include the frontotemporal degeneration disease family including corticobasal degeneration, ALS-dementia, and progressive aphasia. His laboratory efforts are concentrated on molecular processes that occur in aging and degenerative brain diseases, including changes in chromosomal telomeres, and changes involved in protein processing and in the losses of nerve cells and their connections, the synapses. His research involves analysis of changes in human blood, fluid, and tissues, as well as the use of model systems including mice and cell culture. In addition to his laboratory investigations, he carries out clinical research on diagnosis, imaging, and drug treatment trials of patients with Alzheimers disease and other degenerative brain ...
TY - JOUR. T1 - Association between Later Life Lifestyle Factors and Alzheimers Disease Biomarkers in Non-Demented Individuals. T2 - A Longitudinal Descriptive Cohort Study. AU - Reijs, Babette L.R.. AU - Vos, Stephanie J.B.. AU - Soininen, Hilkka. AU - Lötjonen, Jyrki. AU - Koikkalainen, Juha. AU - Pikkarainen, Maria. AU - Hall, Anette. AU - Vanninen, Ritva. AU - Liu, Yawu. AU - Herukka, Sanna-Kaisa. AU - Freund-Levi, Yvonne. AU - Frisoni, Giovanni B.. AU - Frölich, Lutz. AU - Nobili, Flavio. AU - Rikkert, Marcel Olde. AU - Spiru, Luiza. AU - Tsolaki, Magda. AU - Wallin, Åsa K.. AU - Scheltens, Philip. AU - Verhey, Frans. AU - Visser, Pieter Jelle. PY - 2017. Y1 - 2017. N2 - Background: Lifestyle factors have been associated with the risk of dementia, but the association with Alzheimers disease (AD) remains unclear. Objective: To examine the association between later life lifestyle factors and AD biomarkers (i.e., amyloid-ß 1-42 (Aß 42) and tau in cerebrospinal fluid (CSF), and ...
This award-winning blog is a must-read for individuals experiencing early-onset Alzheimers. Less common than standard age-related dementias, early onset Alzheimers is virtually always a surprise to diagnosed individuals. Linda Fisher, blogger and author, knows the difficulty of this condition firsthand.. In her Early Onset Alzheimers blog, she teaches readers not just how to manage such a frightening condition, but also how to live life to the fullest. Her passion for helping others - showing everyone that life with Alzheimers is worth living - is a tremendous gift. Thank you, Linda! ...