Synaptic slaughter in Alzheimer's disease

Coleman, Paul D.; Yao, Pamela J.

doi:10.1016/j.neurobiolaging.2003.09.001

Cited by 332 publications

(238 citation statements)

References 18 publications

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“…Thus, increasing CREB in the CA1 region does not improve spatial memory through a mechanism of Ab clearance. This coincides with other studies that suggest the extent of synapse loss is a more robust correlate of cognitive impairment in AD patients than that of either b-amyloid or neurofibrillary tangle pathology (Coleman and Yao, 2003). Perhaps strategies that enhance the CREB signaling cascades can restore learning and memory through compensatory mechanisms that circumvent b-amyloid pathology (Figure 1).…”

supporting

confidence: 89%

Is CREB the Angry Bird that Releases Memory in Alzheimer's?

Wang

Bibb

2011

Neuropsychopharmacol

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supporting

confidence: 89%

Is CREB the Angry Bird that Releases Memory in Alzheimer's?

Wang

Bibb

2011

Neuropsychopharmacol

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“…The issue of axonal sorting is important because missorting of Tau into the somatodendritic compartment is recognized as one of the earliest signs of neurodegeneration in AD and in mouse models (Braak et al 1994;Coleman and Yao 2003). Entry of Tau into dendrites (e.g., triggered by Ab, glutamate, oxidative stress, etc.)…”

Section: Tau Protein In Neurofibrillary Degenerationmentioning

confidence: 99%

Biochemistry and Cell Biology of Tau Protein in Neurofibrillary Degeneration

Mandelkow

2012

Cold Spring Harbor Perspectives in Medicine

663

636

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Tau represents the subunit protein of one of the major hallmarks of Alzheimer disease (AD), the neurofibrillary tangles, and is therefore of major interest as an indicator of disease mechanisms. Many of the unusual properties of Tau can be explained by its nature as a natively unfolded protein. Examples are the large number of structural conformations and biochemical modifications ( phosphorylation, proteolysis, glycosylation, and others), the multitude of interaction partners (mainly microtubules, but also other cytoskeletal proteins, kinases, and phosphatases, motor proteins, chaperones, and membrane proteins). The pathological aggregation of Tau is counterintuitive, given its high solubility, but can be rationalized by short hydrophobic motifs forming b structures. The aggregation of Tau is toxic in cell and animal models, but can be reversed by suppressing expression or by aggregation inhibitors. This review summarizes some of the structural, biochemical, and cell biological properties of Tau and Tau fibers. Further aspects of Tau as a diagnostic marker and therapeutic target, its involvement in other Tau-based diseases, and its histopathology are covered by other chapters in this volume.

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“…Generation of Ab, a characteristics hallmark of AD, is also associated with ER [102,103]. Ab is reported to induce Ca 2?…”

Section: Er Stress and Alzheimer's Diseasementioning

confidence: 99%

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

2015

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Endoplasmic reticulum (ER) is the site of protein synthesis, protein folding, maintainance of calcium homeostasis, synthesis of lipids and sterols. Genetic or environmental insults can alter its function generating ER stress. ER senses stress mainly by three stress sensor pathways, namely protein kinase R-like endoplasmic reticulum kinase-eukaryotic translation-initiation factor 2a, inositol-requiring enzyme 1a-X-box-binding protein 1 and activating transcription factor 6-CREBH, which induce unfolded protein responses (UPR) after the recognition of stress. Recent studies have demonstrated that ER stress and UPR signaling are involved in cancer, metabolic disorders, inflammatory diseases, osteoporosis and neurodegenerative diseases. However, the precise knowledge regarding involvement of ER stress in different disease processes is still debatable. Here we discuss the possible role of ER stress in various disorders on the basis of existing literature. An attempt has also been made to highlight the present knowledge of this field which may help to elucidate and conjure basic mechanisms and novel insights into disease processes which could assist in devising better future diagnostic and therapeutic strategies.

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Synaptic slaughter in Alzheimer's disease

Cited by 332 publications

References 18 publications

Is CREB the Angry Bird that Releases Memory in Alzheimer's?

Is CREB the Angry Bird that Releases Memory in Alzheimer's?

Biochemistry and Cell Biology of Tau Protein in Neurofibrillary Degeneration

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

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