For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
19
views
57
references
 Top references
cited by
91
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      351
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Looking backward to move forward: early detection of neurodegenerative disorders.

      Author(s):
      Publication date:
      Journal: Science (New York, N.Y.)
      Keywords: Aging, Alzheimer Disease, diagnosis, genetics, metabolism, pathology, Biological Markers, analysis, Brain, Cognition Disorders, Diagnostic Imaging, Dopamine, Genetic Markers, Genetic Predisposition to Disease, Humans, Huntington Disease, Memory, Mutation, Neurodegenerative Diseases, Parkinson Disease, Time Factors

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Early detection of neurodegenerative disorders would provide clues to the underlying pathobiology of these diseases and would enable more effective diagnosis and treatment of patients. Recent advances in molecular neuroscience have begun to provide the tools to detect diseases like Alzheimer's disease, Parkinson's disease, and others early in their course and potentially even before the development of clinical manifestations of disease. These genetic, imaging, clinical, and biochemical tools are being validated in a number of studies. Early detection of these slowly progressive diseases offers the promise of presymptomatic diagnosis and, ultimately, of disease-modifying medications for use early in disease and during the presymptomatic period.

          Related collections

          Most cited references57

          • Record: found
          • Abstract: found
          • Article: not found

          Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

          Dale Schenk, Robin Barbour, Whitney Dunn … (1999)
          Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.
          Article 0 comments Cited 502 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain.

            D. Price, Robert G. Struble, Anthony Coyle … (1982)
            Recent evidence indicates that the nucleus basalis of Meynert, a distinct population of basal forebrain neurons, is a major source of cholinergic innervation of the cerebral cortex. Postmortem studies have previously demonstrated profound reduction in the presynaptic markers for cholinergic neurons in the cortex of patients with Alzheimer's disease and senile dementia of the Alzheimer's type. The results of this study show that neurons of the nucleus basalis of Meynert undergo a profound (greater than 75 percent) and selective degeneration in these patients and provide a pathological substrate of the cholinergic deficiency in their brains. Demonstration of selective degeneration of such neurons represents the first documentation of a loss of a transmitter-specific neuronal population in a major disorder of higher cortical function and, as such, points to a critical subcortical lesion in Alzheimer's patients.
            Article 0 comments Cited 222 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease.

              D Morgan, D Diamond, P Gottschall … (2001)
              Vaccinations with amyloid-beta peptide (A beta) can dramatically reduce amyloid deposition in a transgenic mouse model of Alzheimer's disease. To determine if the vaccinations had deleterious or beneficial functional consequences, we tested eight months of A beta vaccination in a different transgenic model for Alzheimer's disease in which mice develop learning deficits as amyloid accumulates. Here we show that vaccination with A beta protects transgenic mice from the learning and age-related memory deficits that normally occur in this mouse model for Alzheimer's disease. During testing for potential deleterious effects of the vaccine, all mice performed superbly on the radial-arm water-maze test of working memory. Later, at an age when untreated transgenic mice show memory deficits, the A beta-vaccinated transgenic mice showed cognitive performance superior to that of the control transgenic mice and, ultimately, performed as well as nontransgenic mice. The A beta-vaccinated mice also had a partial reduction in amyloid burden at the end of the study. This therapeutic approach may thus prevent and, possibly, treat Alzheimer's dementia.
              Article 0 comments Cited 221 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                PubMed ID:: 14593169
                DOI:: 10.1126/science.1090349

                ScienceOpen disciplines: Chemistry
                Keywords: Aging,Alzheimer Disease,diagnosis,genetics,metabolism,pathology,Biological Markers,analysis,Brain,Cognition Disorders,Diagnostic Imaging,Dopamine,Genetic Markers,Genetic Predisposition to Disease,Humans,Huntington Disease,Memory,Mutation,Neurodegenerative Diseases,Parkinson Disease,Time Factors
                Data availability:
                ScienceOpen disciplines: Chemistry
                Keywords: Aging, Alzheimer Disease, diagnosis, genetics, metabolism, pathology, Biological Markers, analysis, Brain, Cognition Disorders, Diagnostic Imaging, Dopamine, Genetic Markers, Genetic Predisposition to Disease, Humans, Huntington Disease, Memory, Mutation, Neurodegenerative Diseases, Parkinson Disease, Time Factors

                Comments

                Comment on this article

                scite_

                Similar content351

                See all similar

                Cited by90

                See all cited by

                Most referenced authors1,564

                See all reference authors