Search results for: Lary C. Walker

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article

The Exceptional Vulnerability of Humans to Alzheimer’s Disease

Lary C. Walker, Mathias Jucker

Trends in Molecular Medicine > 2017 > 23 > 6 > 534-545

Like many humans, non-human primates deposit copious misfolded Aβ protein in the brain as they age. Nevertheless, the complete behavioral and pathologic phenotype of Alzheimer’s disease, including Aβ plaques, neurofibrillary (tau) tangles, and dementia, has not yet been identified in a non-human species. Recent research suggests that the crucial link between Aβ aggregation and tauopathy is somehow...

article

Comparative pathobiology of β-amyloid and the unique susceptibility of humans to Alzheimer's disease

Rebecca F. Rosen, Yasushi Tomidokoro, Aaron S. Farberg, Jeromy Dooyema, more

Neurobiology of Aging > 2016 > 44 > C > 185-196

The misfolding and accumulation of the protein fragment β-amyloid (Aβ) is an early and essential event in the pathogenesis of Alzheimer's disease (AD). Despite close biological similarities among primates, humans appear to be uniquely susceptible to the profound neurodegeneration and dementia that characterize AD, even though nonhuman primates deposit copious Aβ in senile plaques and cerebral amyloid-β...

article

What amyloid ligands can tell us about molecular polymorphism and disease

Harry LeVine, Lary C. Walker

Neurobiology of Aging > 2016 > 42 > C > 205-212

Brain-penetrant positron emission tomography imaging ligands selective for amyloid pathology in living subjects have sparked a revolution in presymptomatic biomarkers for Alzheimer's disease progression. As additional chemical structures were investigated, the heterogeneity of ligand-binding sites became apparent, as did discrepancies in binding of some ligands between human disease and animal models...

article

Progression of Seed‐Induced Aβ Deposition within the Limbic Connectome

Lan Ye, Tsuyoshi Hamaguchi, Sarah K. Fritschi, Yvonne S. Eisele, more

Brain Pathology > 25 > 6 > 743 - 752

An important early event in the pathogenesis of Alzheimer's disease (AD) is the aberrant polymerization and extracellular accumulation of amyloid‐β peptide (Aβ). In young transgenic mice expressing the human Aβ‐precursor protein (APP), deposits of Aβ can be induced by the inoculation of minute amounts of brain extract containing Aβ aggregates (“Aβ seeds”), indicative of a prion‐like seeding phenomenon...

article

Transport of cargo from periphery to brain by circulating monocytes

Amarallys F. Cintron, Nirjari V. Dalal, Jeromy Dooyema, Ranjita Betarbet, more

Brain Research > 2015 > 1622 > Complete > 328-338

The misfolding and aggregation of the Aβ peptide – a fundamental event in the pathogenesis of Alzheimer׳s disease – can be instigated in the brains of experimental animals by the intracranial infusion of brain extracts that are rich in aggregated Aβ. Recent experiments have found that the peripheral (intraperitoneal) injection of Aβ seeds induces Aβ deposition in the brains of APP-transgenic mice,...

article

A distinct subfraction of Aβ is responsible for the high‐affinity Pittsburgh compound B‐binding site in Alzheimer's disease brain

Sergey V. Matveev, Hans Peter Spielmann, Brittney M. Metts, Jing Chen, more

Journal of Neurochemistry > 131 > 3 > 356 - 368

The positron emission tomography (PET) ligand ¹¹C‐labeled Pittsburgh compound B (PIB) is used to image β‐amyloid (Aβ) deposits in the brains of living subjects with the intent of detecting early stages of Alzheimer's disease (AD). However, deposits of human‐sequence Aβ in amyloid precursor protein transgenic mice and non‐human primates bind very little PIB. The high stoichiometry of PIB:Aβ binding...

article

Aβ seeds resist inactivation by formaldehyde

Sarah K. Fritschi, Amarallys Cintron, Lan Ye, Jasmin Mahler, more

Acta Neuropathologica > 2014 > 128 > 4 > 477-484

Cerebral β-amyloidosis can be exogenously induced by the intracerebral injection of brain extracts containing aggregated β-amyloid (Aβ) into young, pre-depositing Aβ precursor protein- (APP) transgenic mice. Previous work has shown that the induction involves a prion-like seeding mechanism in which the seeding agent is aggregated Aβ itself. Here we report that the β-amyloid-inducing activity of Alzheimer’s...

article

Context dependence of protein misfolding and structural strains in neurodegenerative diseases

Anil K. Mehta, Rebecca F. Rosen, W. Seth Childers, John D. Gehman, more

Biopolymers > 100 > 6 > 722 - 730

Vast arrays of structural forms are accessible to simple amyloid peptides and environmental conditions can direct assembly into single phases. These insights are now being applied to the aggregation of the Aβ peptide of Alzheimer's disease and the identification of causative phases. We extend use of the imaging agent Pittsburgh compound B to discriminate among Aβ phases and begin to define conditions...

article

A new pathogenic pathway and causative treatment option for Alzheimer's disease: From aging to mitochondrial and ABC transporter dysfunction

Markus Krohn, Lary C. Walker, Jörg Gsponer, Jens Pahnke

Alzheimer's & Dementia > 2012 > 8 > 4(S) > P86

article

Exogenous seeding of cerebral β‐amyloid deposition in βAPP‐transgenic rats

Rebecca F. Rosen, Jason J. Fritz, Jeromy Dooyema, Amarallys F. Cintron, more

Journal of Neurochemistry > 120 > 5 > 660 - 666

J. Neurochem. (2012) 120, 660–666. AbstractDeposition of the amyloid‐β (Aβ) peptide in senile plaques and cerebral Aβ angiopathy (CAA) can be stimulated in Aβ‐precursor protein (APP)‐transgenic mice by the intracerebral injection of dilute brain extracts containing aggregated Aβ seeds. Growing evidence implicates a prion‐like mechanism of corruptive protein templating in this phenomenon, in which...

article

Mitochondrial DNA polymorphisms specifically modify cerebral β-amyloid proteostasis

Katja Scheffler, Markus Krohn, Tina Dunkelmann, Jan Stenzel, more

Acta Neuropathologica > 2012 > 124 > 2 > 199-208

Several lines of evidence link mutations and deletions in mitochondrial DNA (mtDNA) and its maternal inheritance to neurodegenerative diseases in the elderly. Age-related mutations of mtDNA modulate the tricarboxylic cycle enzyme activity, mitochondrial oxidative phosphorylation capacity and oxidative stress response. To investigate the functional relevance of specific mtDNA polymorphisms of inbred...

article

The presence of Aβ seeds, and not age per se, is critical to the initiation of Aβ deposition in the brain

Tsuyoshi Hamaguchi, Yvonne S. Eisele, Nicholas H. Varvel, Bruce T. Lamb, more

Acta Neuropathologica > 2012 > 123 > 1 > 31-37

The deposition of the β-amyloid (Aβ) peptide in senile plaques and cerebral Aβ-amyloid angiopathy can be seeded in β-amyloid precursor protein (APP)-transgenic mice by the intracerebral infusion of brain extracts containing aggregated Aβ. Previous studies of seeded β-amyloid induction have used relatively short incubation periods to dissociate seeded β-amyloid induction from endogenous β-amyloid deposition...

article

Pathogenic protein seeding in alzheimer disease and other neurodegenerative disorders

Mathias Jucker, Lary C. Walker

Annals of Neurology > 70 > 4 > 532 - 540

The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of neurodegenerative disorders. In Alzheimer disease (the most prevalent cerebral proteopathy), the two principal aggregating proteins are β‐amyloid (Aβ) and tau. The abnormal assemblies formed by conformational variants of these proteins range in size from small oligomers to the characteristic lesions...

article

PIB binding in aged primate brain: Enrichment of high-affinity sites in humans with Alzheimer's disease

Rebecca F. Rosen, Lary C. Walker, Harry LeVine

Neurobiology of Aging > 2011 > 32 > 2 > 223-234

Aged nonhuman primates accumulate large amounts of human-sequence amyloid β (Aβ) in the brain, yet they do not manifest the full phenotype of Alzheimer's disease (AD). To assess the biophysical properties of Aβ that might govern its pathogenic potential in humans and nonhuman primates, we incubated the benzothiazole imaging agent Pittsburgh Compound B (PIB) with cortical tissue homogenates from normal...

article

Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid‐β oligomers

Sam Gandy, Adam J. Simon, John W. Steele, Alex L. Lublin, more

Annals of Neurology > 68 > 2 > 220 - 230

ObjectiveRecent evidence suggests that high molecular weight soluble oligomeric Aβ (oAβ) assemblies (also known as Aβ‐derived diffusible ligands, or ADDLs) may represent a primary neurotoxic basis for cognitive failure in Alzheimer disease (AD). To date, most in vivo studies of oAβ/ADDLs have involved injection of assemblies purified from the cerebrospinal fluid of human subjects with AD or from the...

article

Transmission of Alzheimer amyloidosis to chimpanzees and monkeys: Revisited

Dmitry Goldgaber, Peter Davies, Pierluigi Gambetti, Lary C. Walker, more

Alzheimer's & Dementia > 2010 > 6 > 4(S) > S250

article

Evidence for dose-dependent neurotoxicity of amyloid-β oligomers/Aβ-derived diffusible ligands generated from physiological processing of transgenic human APP in situ in mouse brain

John W. Steele, Adam J. Simon, Alex L. Lublin, James J. Lah, more

Alzheimer's & Dementia > 2010 > 6 > 4(S) > S228

article

Mosaic aging

Lary C. Walker, James G. Herndon

Medical Hypotheses > 2010 > 74 > 6 > 1048-1051

Although all multicellular organisms undergo structural and functional deterioration with age, senescence is not a uniform process. Rather, each organism experiences a constellation of changes that reflect the heterogeneous effects of age on molecules, cells, organs and systems, an idiosyncratic pattern that we refer to as mosaic aging. Varying genetic, epigenetic and environmental factors (local...

article

Molecular polymorphism of Aβ in Alzheimer's disease

Harry LeVine, Lary C. Walker

Neurobiology of Aging > 2010 > 31 > 4 > 542-548

Alzheimer's disease is defined pathologically by the presence of senile plaques, which consist primarily of extracellular aggregates of fibrillar Aβ peptide, and neurofibrillary tangles, which are abnormal, intracellular bundles of fibrillar tau protein. The advent of amyloid binding agents as diagnostic imaging probes for Alzheimer's disease (AD) has made it imperative to understand at a molecular...

article

Deficient high-affinity binding of Pittsburgh compound B in a case of Alzheimer’s disease

Rebecca F. Rosen, Brian J. Ciliax, Thomas S. Wingo, Marla Gearing, more

Acta Neuropathologica > 2010 > 119 > 2 > 221-233

Radiolabeled Pittsburgh compound B (PIB) is a benzothiazole imaging agent that usually binds with high affinity, specificity, and stoichiometry to cerebral β-amyloid (Aβ) in patients with Alzheimer’s disease. Among a cohort of ten AD subjects examined postmortem, we describe a case of idiopathic, end-stage Alzheimer’s disease with heavy Aβ deposition yet substantially diminished high-affinity binding...

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INFONA - science communication portal

Search results for: Lary C. Walker

The Exceptional Vulnerability of Humans to Alzheimer’s Disease

Comparative pathobiology of β-amyloid and the unique susceptibility of humans to Alzheimer's disease

What amyloid ligands can tell us about molecular polymorphism and disease

Progression of Seed‐Induced Aβ Deposition within the Limbic Connectome

Transport of cargo from periphery to brain by circulating monocytes

A distinct subfraction of Aβ is responsible for the high‐affinity Pittsburgh compound B‐binding site in Alzheimer's disease brain

Aβ seeds resist inactivation by formaldehyde

Context dependence of protein misfolding and structural strains in neurodegenerative diseases

A new pathogenic pathway and causative treatment option for Alzheimer's disease: From aging to mitochondrial and ABC transporter dysfunction

Exogenous seeding of cerebral β‐amyloid deposition in βAPP‐transgenic rats

Mitochondrial DNA polymorphisms specifically modify cerebral β-amyloid proteostasis

The presence of Aβ seeds, and not age per se, is critical to the initiation of Aβ deposition in the brain

Pathogenic protein seeding in alzheimer disease and other neurodegenerative disorders

PIB binding in aged primate brain: Enrichment of high-affinity sites in humans with Alzheimer's disease

Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid‐β oligomers

Transmission of Alzheimer amyloidosis to chimpanzees and monkeys: Revisited

Evidence for dose-dependent neurotoxicity of amyloid-β oligomers/Aβ-derived diffusible ligands generated from physiological processing of transgenic human APP in situ in mouse brain

Mosaic aging

Molecular polymorphism of Aβ in Alzheimer's disease

Deficient high-affinity binding of Pittsburgh compound B in a case of Alzheimer’s disease

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