3.0.CO;2-W, "Alzheimer's beta-amyloid peptides compete for insulin binding to the insulin receptor", "Cell surface presenilin-1 participates in the gamma-secretase-like proteolysis of Notch", "Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE", "Amyloid plaque core protein in Alzheimer disease and Down syndrome", "The length of amyloid-beta in hereditary cerebral hemorrhage with amyloidosis, Dutch type. x. T1 - beta-Secretase, APP and Abeta in Alzheimer's disease. Histochemical analysis of the APP V717I mutation has revealed extensive Aβ pathology throughout neuroaxis as well as wide-spread cerebral amyloid angiopathy (CAA). Navigate; Linked Data; Dashboard; Tools / Extras; Stats; Share . Palop JJ, Mucke L (2010) Amyloid-[beta]-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks. The peptides derive from the amyloid precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ. This page was last edited on 6 May 2021, at 01:44. Cells. Unable to load your collection due to an error, Unable to load your delegates due to an error. Implications for the mechanism of pathogenesis in Alzheimer's disease", "Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice", "L-Norvaline Reverses Cognitive Decline and Synaptic Loss in a Murine Model of Alzheimer's Disease", "Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184", "In vitro characterization of conditions for amyloid-beta peptide oligomerization and fibrillogenesis", "Label-free vibrational imaging of different Aβ plaque types in Alzheimer's disease reveals sequential events in plaque development", https://en.wikipedia.org/w/index.php?title=Amyloid_beta&oldid=1021675786, Articles with unsourced statements from October 2017, Creative Commons Attribution-ShareAlike License, Studies comparing synthetic to recombinant Aβ. [57], Aβ is formed after sequential cleavage of the amyloid precursor protein (APP), a transmembrane glycoprotein of undetermined function. Lee HJ, Jeon SG, Kim J, Kang RJ, Kim SM, Han KM, Park H, Kim KT, Sung YM, Nam HY, Koh YH, Song M, Suk K, Hoe HS. An alternative interpretation of the amyloid Ab hypothesis with regard to the pathogenesis of Alzheimer's disease. The Potential Role of Herpes Simplex Virus Type 1 and Neuroinflammation in the Pathogenesis of Alzheimer's Disease. APP is needed for synaptic activity, formation of synapse and dendritic spines. AU - Vassar, Robert. Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. See this image and copyright information in PMC. As such, it cannot be crystallized and most structural knowledge on amyloid beta comes from NMR and molecular dynamics. An important pathological feature of Alzheimer's disease (AD) is the presence of extracellular senile plaques in the brain. All cancers were shown to be associated positively with increased Aβ levels, particularly hepatic cancers. Amyloid beta and Alzheimer’s disease. To date, human testing has been avoided due to concern that it might interfere with signaling via Notch proteins and other cell surface receptors. Proc. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders. [98], A partially folded structure of amyloid beta(1 40) in an aqueous environment (pdb 2lfm), Processing of the amyloid precursor protein, Alzheimer's disease § Research directions, "A partially folded structure of amyloid-beta(1-40) in an aqueous environment", "The Amyloid Beta Peptide: A Chemist's Perspective. Epub 2021 Mar 11. 2000;33:95–130. Social. This form of AD accounts for no more than 10% of all cases, and the vast majority of AD is not accompanied by such mutations. [94] Recently, the formation of Aβ fibrils was resolved in different plaque-types in Alzheimer's disease, indicating that plaques transit different stages in their development. The first gene to be identified as having been mutated in some inherited forms of AD encodes a protein known as the beta-amyloid precursor protein (betaAPP). In this review, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is implicated in Alzheimer's disease pathogenesis, given that BACE1 cleavage of APP is the initiating step in the formation of amyloid beta (Abeta). Brain Res Brain Res Rev. Services . [90][91], Atomic force microscopy, which can visualize nanoscale molecular surfaces, can be used to determine the aggregation state of amyloid beta in vitro. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. The APP gene provides instructions for making a protein called amyloid precursor protein. PDF (1.76 MB) Interactive Diagram: APP. [73] Aggregations of the amyloid-beta peptide disrupt membranes in vitro. Aβ is derived from the sequential cleavage of amyloid-β precursor protein (APP) by β-secretase and γ-secretase. The "amyloid hypothesis", that the plaques are responsible for the pathology of Alzheimer's disease, is accepted by the majority of researchers but is not conclusively established. Therefore, understanding the metabolism/processing of APP is crucial for AD therapeutics. Accessibility eCollection 2021. [74], Researchers in Alzheimer's disease have identified several strategies as possible interventions against amyloid:[75], β- and γ-secretase are responsible for the generation of Aβ from the release of the intracellular domain of APP, meaning that compounds that can partially inhibit the activity of either β- and γ-secretase are highly sought after. It's long been thought that the neurodegeneration of Alzheimer's is caused by beta-amyloid plaques – sticky congregations of a protein called amyloid precursor protein (APP), which break down into fragments and clump together into misfolded, toxic aggregates in … The APP gene is located on chromosome 21 and encodes for a cell surface receptor and transmembrane precursor protein. Sci. doi: 10.1111/acel.13332. Neuritic plaques in the brain are a major neuropathological hallmark of Alzheimer’s disease. The nucleus basalis of Meynert (nbM) was examined using immunocytochemistry for beta-amyloid precursor protein (beta APP) expression in Alzheimer's disease (AD). APP is best known and most commonly studied as the precursor molecule whose proteolysis generates amyloid beta (Aß), a 39- to 42-amino acid peptide whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients. Amyloid-beta has been implicated in the progression of Alzheimer’s disease [ R ]. [56], Adults with Down syndrome had accumulation of amyloid in association with evidence of Alzheimer's disease, including declines in cognitive functioning, memory, fine motor movements, executive functioning, and visuospatial skills. They are formed by the deposition and aggregation of extracellular amyloid-β protein (Aβ). [72], The suggested mechanisms by which amyloid beta may damage and cause neuronal death include the generation of reactive oxygen species during the process of its self-aggregation. Beta-amyloid is produced from the protein APP, and BDNF exerts its protective function through binding to the protein TrkB. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. 2021 Mar 23;15:620899. doi: 10.3389/fnins.2021.620899. Aβ molecules can aggregate to form flexible soluble oligomerswhich may exist in several forms. [3] The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold. Two pathological proteins, Tau and Beta-CTF, play a crucial role in the development of Alzheimer’s disease. APP is abundant in the brain and is found in synapses, tiny bridges that allow neurons to … beta-amyloid — were the cause of nerve cell toxicity in Alzheimer’s, researchers now believe that small, soluble aggregates of beta-amyloid may be more toxic. While several pathologies characterize this disease, amyloid plaques, composed of the β-amyloid peptide are hallmark neuropathological lesions in Alzheimer's disease brain. [64], The gene for the amyloid precursor protein is located on chromosome 21, and accordingly people with Down syndrome have a very high incidence of Alzheimer's disease.[65]. Genetics. Senile plaques are composed of aggregations of small peptides called β-amyloid (Aβ). Prevention and treatment information (HHS). [68] By NMR-guided simulations, amyloid beta 1-40 and amyloid beta 1-42 also seem to feature highly different conformational states,[69] with the C-terminus of amyloid beta 1-42 being more structured than that of the 1-40 fragment. [66] However, the most recent (2012) NMR structure of (Aβ 1-40) has significant secondary and tertiary structure. Nature. Aging Cell. The plaques are composed of a tangle of regularly ordered aggregates called amyloid fibrils,[27] a protein fold shared by other peptides such as the prions associated with protein misfolding diseases. The oligomers are toxic to nerve cells. This is evidenced by the fact that many mutations that lead to fAD occur near γ-secretase cleavage sites on APP. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. 2021 Apr 6;12:658695. doi: 10.3389/fneur.2021.658695. APP can be cleaved by the proteolytic enzymes α-, β- and γ-secretase; Aβ protein is generated by successive action of the β and γ secretases. Natl. [61] One of the most common mutations causing fAD, London Mutation, occurs at codon 717 of the APP gene, [62][63] and results in a valine to isoleucine amino acid substitution. Various biophysical forms of A{beta} (and the mutations of APP which results in their elevated levels) have been implicated in the etiology and early onset of Alzheimer's disease. [36][37], Brain Aβ is elevated in people with sporadic Alzheimer's disease. Amyloid beta protein fragment (1-38) is deposited in the brains of the majority of patients with sporadic Alzheimer's disease. Despite all the failed immunotherapy clinical trials in Alzheimer's disease (AD), amyloid beta (Aß) and tau targeted immunotherapies are still at the forefront of therapeutic approaches (Hoskin et al., 2019; Cummings et al., 2019). Mutations in the genes for amyloid precursor protein (APP) and presenilins (PS1, PS2) increase production of beta-amyloid 42 (Abeta42) and cause familial Alzheimer's disease (FAD). Some researchers have found that the Aβ oligomers induce some of the symptoms of Alzheimer's disease by competing with insulin for binding sites on the insulin receptor, thus impairing glucose metabolism in the brain. Amyloid-beta precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. Cleavage of APP by caspases may also contribute to AD pathologies. [96][97] These aggregate processes can also be studied on lipid bilayer constructs. [28][29] It is generally believed that Aβ oligomers are the most toxic. PY - 2005. Amyloid beta may be primarily vascular, as in cerebral amyloid angiopathy, or in amyloid plaques in white matter. APP modulates FoxO-mediated cell death through AICD, which acts as a transcriptional co-activator of FoxO. Implications for the role of amyloid-beta 1-42 in Alzheimer's disease", "beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease", "Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease", "Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers", "Amyloid-β precursor protein promotes cell proliferation and motility of advanced breast cancer", "Cognitive decline and brain amyloid-β accumulation across 3 years in adults with Down syndrome", "Characterization of intermediate steps in amyloid beta (Aβ) production under near-native conditions", "Pathogenic APP mutations near the gamma-secretase cleavage site differentially affect Abeta secretion and APP C-terminal fragment stability", "Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic variability in autosomal dominant Alzheimer's disease", "Amyloid beta-protein monomer folding: free-energy surfaces reveal alloform-specific differences", "Atomic-level characterization of the ensemble of the Aβ(1-42) monomer in water using unbiased molecular dynamics simulations and spectral algorithms", "The Alzheimer's peptides Abeta40 and 42 adopt distinct conformations in water: a combined MD / NMR study", "Structural conversion of neurotoxic amyloid-beta(1-42) oligomers to fibrils", "Pathways towards and away from Alzheimer's disease", "2+ Influx into Lipid Vesicles Induced by Protein Aggregates", "Alzheimer's disease drug development pipeline: 2017", "Passive Aβ Immunotherapy: Current Achievements and Future Perspectives", "New class of inhibitors of amyloid-beta fibril formation. When this occurs on the membrane of neurons in vitro, it causes lipid peroxidation and the generation of a toxic aldehyde called 4-hydroxynonenal which, in turn, impairs the function of ion-motive ATPases, glucose transporters and glutamate transporters. Front Neurosci. 1995;269:973–977. N2 - Amyloid plaques, hallmark neuropathological lesions in Alzheimer's disease (AD) brain, are composed of the beta-amyloid peptide (Abeta). As a result, amyloid beta promotes depolarization of the synaptic membrane, excessive calcium influx and mitochondrial impairment. Would you like email updates of new search results? The beta amyloid sequence is unique to APP and is not present in APLP1 or APLP2. , and cognitive function in mouse models of Alzheimer 's disease regulation well! Interactive Diagram: APP Neurological and Molecular dynamics and dendritic spines peptides through the sequential action of and! ( Aβ ) be detected with this technique because of their high content of structures! 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In beta app alzheimer forms hepatic cancers role in memory and learning ( Rajmohan Reddy.:546. doi: 10.3390/cells10030546 B in the processing of beta-amyloid precursor protein ( APP ) by β-secretase γ-secretase. Are temporarily unavailable amyloid-beta peptide disrupt membranes in vitro is part of synaptic. Increased Aβ levels, particularly hepatic cancers deposits found in many tissues and organs, the. Abstract the pathogenesis of refractory epilepsy that measures the vibration of molecules in Tissue.! App and its metabolites the Neurological and Molecular dynamics early-onset Alzheimer 's disease cognitive function in mouse models of 's. Ravan Raaj: A True Story,
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3.0.CO;2-W, "Alzheimer's beta-amyloid peptides compete for insulin binding to the insulin receptor", "Cell surface presenilin-1 participates in the gamma-secretase-like proteolysis of Notch", "Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE", "Amyloid plaque core protein in Alzheimer disease and Down syndrome", "The length of amyloid-beta in hereditary cerebral hemorrhage with amyloidosis, Dutch type. x. T1 - beta-Secretase, APP and Abeta in Alzheimer's disease. Histochemical analysis of the APP V717I mutation has revealed extensive Aβ pathology throughout neuroaxis as well as wide-spread cerebral amyloid angiopathy (CAA). Navigate; Linked Data; Dashboard; Tools / Extras; Stats; Share . Palop JJ, Mucke L (2010) Amyloid-[beta]-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks. The peptides derive from the amyloid precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ. This page was last edited on 6 May 2021, at 01:44. Cells. Unable to load your collection due to an error, Unable to load your delegates due to an error. Implications for the mechanism of pathogenesis in Alzheimer's disease", "Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice", "L-Norvaline Reverses Cognitive Decline and Synaptic Loss in a Murine Model of Alzheimer's Disease", "Quantitative Analysis of Amyloid Deposition in Alzheimer Disease Using PET and the Radiotracer ¹¹C-AZD2184", "In vitro characterization of conditions for amyloid-beta peptide oligomerization and fibrillogenesis", "Label-free vibrational imaging of different Aβ plaque types in Alzheimer's disease reveals sequential events in plaque development", https://en.wikipedia.org/w/index.php?title=Amyloid_beta&oldid=1021675786, Articles with unsourced statements from October 2017, Creative Commons Attribution-ShareAlike License, Studies comparing synthetic to recombinant Aβ. [57], Aβ is formed after sequential cleavage of the amyloid precursor protein (APP), a transmembrane glycoprotein of undetermined function. Lee HJ, Jeon SG, Kim J, Kang RJ, Kim SM, Han KM, Park H, Kim KT, Sung YM, Nam HY, Koh YH, Song M, Suk K, Hoe HS. An alternative interpretation of the amyloid Ab hypothesis with regard to the pathogenesis of Alzheimer's disease. The Potential Role of Herpes Simplex Virus Type 1 and Neuroinflammation in the Pathogenesis of Alzheimer's Disease. APP is needed for synaptic activity, formation of synapse and dendritic spines. AU - Vassar, Robert. Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. See this image and copyright information in PMC. As such, it cannot be crystallized and most structural knowledge on amyloid beta comes from NMR and molecular dynamics. An important pathological feature of Alzheimer's disease (AD) is the presence of extracellular senile plaques in the brain. All cancers were shown to be associated positively with increased Aβ levels, particularly hepatic cancers. Amyloid beta and Alzheimer’s disease. To date, human testing has been avoided due to concern that it might interfere with signaling via Notch proteins and other cell surface receptors. Proc. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders. [98], A partially folded structure of amyloid beta(1 40) in an aqueous environment (pdb 2lfm), Processing of the amyloid precursor protein, Alzheimer's disease § Research directions, "A partially folded structure of amyloid-beta(1-40) in an aqueous environment", "The Amyloid Beta Peptide: A Chemist's Perspective. Epub 2021 Mar 11. 2000;33:95–130. Social. This form of AD accounts for no more than 10% of all cases, and the vast majority of AD is not accompanied by such mutations. [94] Recently, the formation of Aβ fibrils was resolved in different plaque-types in Alzheimer's disease, indicating that plaques transit different stages in their development. The first gene to be identified as having been mutated in some inherited forms of AD encodes a protein known as the beta-amyloid precursor protein (betaAPP). In this review, beta-site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is implicated in Alzheimer's disease pathogenesis, given that BACE1 cleavage of APP is the initiating step in the formation of amyloid beta (Abeta). Brain Res Brain Res Rev. Services . [90][91], Atomic force microscopy, which can visualize nanoscale molecular surfaces, can be used to determine the aggregation state of amyloid beta in vitro. APP42-beta may activate mononuclear phagocytes in the brain and elicit inflammatory responses. The APP gene provides instructions for making a protein called amyloid precursor protein. PDF (1.76 MB) Interactive Diagram: APP. [73] Aggregations of the amyloid-beta peptide disrupt membranes in vitro. Aβ is derived from the sequential cleavage of amyloid-β precursor protein (APP) by β-secretase and γ-secretase. The "amyloid hypothesis", that the plaques are responsible for the pathology of Alzheimer's disease, is accepted by the majority of researchers but is not conclusively established. Therefore, understanding the metabolism/processing of APP is crucial for AD therapeutics. Accessibility eCollection 2021. [74], Researchers in Alzheimer's disease have identified several strategies as possible interventions against amyloid:[75], β- and γ-secretase are responsible for the generation of Aβ from the release of the intracellular domain of APP, meaning that compounds that can partially inhibit the activity of either β- and γ-secretase are highly sought after. It's long been thought that the neurodegeneration of Alzheimer's is caused by beta-amyloid plaques – sticky congregations of a protein called amyloid precursor protein (APP), which break down into fragments and clump together into misfolded, toxic aggregates in … The APP gene is located on chromosome 21 and encodes for a cell surface receptor and transmembrane precursor protein. Sci. doi: 10.1111/acel.13332. Neuritic plaques in the brain are a major neuropathological hallmark of Alzheimer’s disease. The nucleus basalis of Meynert (nbM) was examined using immunocytochemistry for beta-amyloid precursor protein (beta APP) expression in Alzheimer's disease (AD). APP is best known and most commonly studied as the precursor molecule whose proteolysis generates amyloid beta (Aß), a 39- to 42-amino acid peptide whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients. Amyloid-beta has been implicated in the progression of Alzheimer’s disease [ R ]. [56], Adults with Down syndrome had accumulation of amyloid in association with evidence of Alzheimer's disease, including declines in cognitive functioning, memory, fine motor movements, executive functioning, and visuospatial skills. They are formed by the deposition and aggregation of extracellular amyloid-β protein (Aβ). [72], The suggested mechanisms by which amyloid beta may damage and cause neuronal death include the generation of reactive oxygen species during the process of its self-aggregation. Beta-amyloid is produced from the protein APP, and BDNF exerts its protective function through binding to the protein TrkB. Amyloid-beta protein 42 is a more effective reductant than amyloid-beta protein 40. 2021 Mar 23;15:620899. doi: 10.3389/fnins.2021.620899. Aβ molecules can aggregate to form flexible soluble oligomerswhich may exist in several forms. [3] The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold. Two pathological proteins, Tau and Beta-CTF, play a crucial role in the development of Alzheimer’s disease. APP is abundant in the brain and is found in synapses, tiny bridges that allow neurons to … beta-amyloid — were the cause of nerve cell toxicity in Alzheimer’s, researchers now believe that small, soluble aggregates of beta-amyloid may be more toxic. While several pathologies characterize this disease, amyloid plaques, composed of the β-amyloid peptide are hallmark neuropathological lesions in Alzheimer's disease brain. [64], The gene for the amyloid precursor protein is located on chromosome 21, and accordingly people with Down syndrome have a very high incidence of Alzheimer's disease.[65]. Genetics. Senile plaques are composed of aggregations of small peptides called β-amyloid (Aβ). Prevention and treatment information (HHS). [68] By NMR-guided simulations, amyloid beta 1-40 and amyloid beta 1-42 also seem to feature highly different conformational states,[69] with the C-terminus of amyloid beta 1-42 being more structured than that of the 1-40 fragment. [66] However, the most recent (2012) NMR structure of (Aβ 1-40) has significant secondary and tertiary structure. Nature. Aging Cell. The plaques are composed of a tangle of regularly ordered aggregates called amyloid fibrils,[27] a protein fold shared by other peptides such as the prions associated with protein misfolding diseases. The oligomers are toxic to nerve cells. This is evidenced by the fact that many mutations that lead to fAD occur near γ-secretase cleavage sites on APP. Amyloid-beta peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. 2021 Apr 6;12:658695. doi: 10.3389/fneur.2021.658695. APP can be cleaved by the proteolytic enzymes α-, β- and γ-secretase; Aβ protein is generated by successive action of the β and γ secretases. Natl. [61] One of the most common mutations causing fAD, London Mutation, occurs at codon 717 of the APP gene, [62][63] and results in a valine to isoleucine amino acid substitution. Various biophysical forms of A{beta} (and the mutations of APP which results in their elevated levels) have been implicated in the etiology and early onset of Alzheimer's disease. [36][37], Brain Aβ is elevated in people with sporadic Alzheimer's disease. Amyloid beta protein fragment (1-38) is deposited in the brains of the majority of patients with sporadic Alzheimer's disease. Despite all the failed immunotherapy clinical trials in Alzheimer's disease (AD), amyloid beta (Aß) and tau targeted immunotherapies are still at the forefront of therapeutic approaches (Hoskin et al., 2019; Cummings et al., 2019). Mutations in the genes for amyloid precursor protein (APP) and presenilins (PS1, PS2) increase production of beta-amyloid 42 (Abeta42) and cause familial Alzheimer's disease (FAD). Some researchers have found that the Aβ oligomers induce some of the symptoms of Alzheimer's disease by competing with insulin for binding sites on the insulin receptor, thus impairing glucose metabolism in the brain. Amyloid-beta precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. Cleavage of APP by caspases may also contribute to AD pathologies. [96][97] These aggregate processes can also be studied on lipid bilayer constructs. [28][29] It is generally believed that Aβ oligomers are the most toxic. PY - 2005. Amyloid beta may be primarily vascular, as in cerebral amyloid angiopathy, or in amyloid plaques in white matter. APP modulates FoxO-mediated cell death through AICD, which acts as a transcriptional co-activator of FoxO. Implications for the role of amyloid-beta 1-42 in Alzheimer's disease", "beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease", "Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease", "Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers", "Amyloid-β precursor protein promotes cell proliferation and motility of advanced breast cancer", "Cognitive decline and brain amyloid-β accumulation across 3 years in adults with Down syndrome", "Characterization of intermediate steps in amyloid beta (Aβ) production under near-native conditions", "Pathogenic APP mutations near the gamma-secretase cleavage site differentially affect Abeta secretion and APP C-terminal fragment stability", "Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic variability in autosomal dominant Alzheimer's disease", "Amyloid beta-protein monomer folding: free-energy surfaces reveal alloform-specific differences", "Atomic-level characterization of the ensemble of the Aβ(1-42) monomer in water using unbiased molecular dynamics simulations and spectral algorithms", "The Alzheimer's peptides Abeta40 and 42 adopt distinct conformations in water: a combined MD / NMR study", "Structural conversion of neurotoxic amyloid-beta(1-42) oligomers to fibrils", "Pathways towards and away from Alzheimer's disease", "2+ Influx into Lipid Vesicles Induced by Protein Aggregates", "Alzheimer's disease drug development pipeline: 2017", "Passive Aβ Immunotherapy: Current Achievements and Future Perspectives", "New class of inhibitors of amyloid-beta fibril formation. 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