Pathways towards and away from Alzheimer's disease

By Mark P. Mattson. Nature, 2004

3,041 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/de6ad547088e72099581097f8819f6d6e8dd6336

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In Cellular and Molecular Neuroscience

In Pharmacology

In Physiology

Citations in the corpus

The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease (2007, neutral): “dtd" [ ]> The accumulation of Aβ peptide, a neurotoxic proteolytic derivative of APP, is a central event in the pathogenesis of Alzheimer diseas”
Integrative single-cell analysis of transcriptional and epigenetic states in the human adult brain (2017, positive): “It provides a coherent framework to consolidate previous GWAS findings, such as the relative contributions of glia, microglia and neurons to sporadic AD 58 , and could potentially extend to single-neuron genomic mosaicism that also becomes altered in this disease 14 .”
Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases (2015, background): “which are abundant numbers of “plaques” and “tangles” by postmortem examination [85].”
Inflammatory processes in Alzheimer's disease. (2007, positive): “This brain volume reduction is due to a profound degeneration of neurons and synapses (Mattson, 2004).”
Critical role of soluble amyloid-β for early hippocampal hyperactivity in a mouse model of Alzheimer’s disease (2012, background): “A disease (AD) is associated with multiple neuronal dysfunctions, including impairments underlying the storage and processing of information in the brain (1).”
Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers (2009, background): “Significant attention focuses on strategies that could neutralize the mechanism(s) initiating memory loss, the major manifestation of early AD (1, 2).”
The Brain's Default Network (2008, methodology): “A more recent approach that identiﬁes brain systems via intrinsic activity correlations (e.g., Biswal et al. 1995) has also revealed a similar estimate of the anatomy of the default network (Greicius et al. 2003, 2004).”
NMDA receptor trafficking in synaptic plasticity and neuropsychiatric disorders (2007, background): “Accumulation of amyloid-β, a small secreted peptide with a high propensity to form aggregates, is a central causative factor in Alzheimer's diseas”
Cortical Hubs Revealed by Intrinsic Functional Connectivity: Mapping, Assessment of Stability, and Relation to Alzheimer’s Disease (2009, background): “AD is associated with the pathological accumulation of misfolded proteins, including amyloid- (A ) (Mattson, 2004; Walsh and Selkoe, 2004).”
Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Such oxidative damage to membranes is believed to play major roles in a range of disorders, including myocardial infarction (172), stroke and traumatic brain injury (254), and Alzheimer’s disease (AD) (286).”