European Journal of Neuroscience

Cover image for Vol. 37 Issue 12

Special Issue: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE

June 2013

Volume 37, Issue 12

Pages 1885–2018

  1. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE

    1. Top of page
    2. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
    3. Special Issue: The Neurobiology of Aging and Alzheimer's Disease
    4. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
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      The neurobiology of aging and Alzheimer's disease: walking down the same road? (pages 1885–1886)

      Jannic Boehm, Karl Fernandes, Nicole Leclerc and Richard Robitaille

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12261

    2. The adaptive aging brain: evidence from the preservation of communication abilities with age (pages 1887–1895)

      Jennyfer Ansado, Yannick Marsolais, Ikram Methqal, Flamine Alary and Yves Joanette

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12252

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      Neurofunctional reorganization with age is suspected to occur for many cognitive components including communication abilities. Several functional neuroimaging studies of elderly individuals have reported the occurrence of an interhemispheric neurofunctional reorganization characterized by more bilateral activation patterns.

    3. Alterations in hippocampal network oscillations and theta–gamma coupling arise before Aβ overproduction in a mouse model of Alzheimer's disease (pages 1896–1902)

      Romain Goutagny, Ning Gu, Chelsea Cavanagh, Jesse Jackson, Jean-Guy Chabot, Rémi Quirion, Slavica Krantic and Sylvain Williams

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12233

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      Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by memory impairments. Brain oscillatory activity is critical for cognitive function and is altered in AD patients.

    4. Impact of aging brain circuits on cognition (pages 1903–1915)

      Rachel D. Samson and Carol A. Barnes

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12183

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      Brain networks that engage the hippocampus and prefrontal cortex are central for enabling effective interactions with our environment. Some of the cognitive processes that these structures mediate, such as encoding and retrieving episodic experience, wayfinding, working memory and attention are known to be altered across the lifespan.

    5. Functional alteration patterns of default mode networks: comparisons of normal aging, amnestic mild cognitive impairment and Alzheimer's disease (pages 1916–1924)

      Jungho Cha, Hang Joon Jo, Hee Jin Kim, Sang Won Seo, Han-Soo Kim, Uicheul Yoon, Hyunjin Park, Duk L. Na and Jong-Min Lee

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12177

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      Functional connectivity in default mode network was significantly different in amnestic mild cognitive impairment and Alzheimer's disease. And the functional connectivity is associated with the Mini-Mental State Examination scores in aMCI and AD. An increment in connectivity in the middle frontal gyrus may compensate for the loss of function in the posterior cingulate cortex, middle temporal gyrus, and parahippocampal gyrus via compensatory mechanisms that occur in cortico-cortical connections.

  2. Special Issue: The Neurobiology of Aging and Alzheimer's Disease

    1. Top of page
    2. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
    3. Special Issue: The Neurobiology of Aging and Alzheimer's Disease
    4. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
    1. A ‘danse macabre’: tau and Fyn in STEP with amyloid beta to facilitate induction of synaptic depression and excitotoxicity (pages 1925–1930)

      Jannic Boehm

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12251

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      Alzheimer disease, with its two most prominent pathological factors amyloid beta and tau protein, can be described as a disease of the synapse. In this review I will summarise recent evidence showing that the NMDA-receptor links the effects of extracellular amyloid-beta with intracellular tau protein. Furthermore the antagonistic roles of Fyn and STEP in NMDA-receptor regulation, synaptic dysfunction and induction of synaptic depression will be discussed.

    2. Serine racemase as a prime target for age-related memory deficits (pages 1931–1938)

      J.-M. Billard

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12226

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      The learning and memory deficits associated with non pathological aging mainly result from alterations to the plasticity of neuronal network dynamics within the hippocampus. Besides the broad spectrum of changes that affect the morphology and function of hippocampal excitatory circuits in the aging brain, the impaired activation of the N-methyl-d-aspartate subtype of glutamate receptors (NMDA-R) by D-serine is a typical feature, altering the induction and maintenance of long-term potentiation (LTP), a major form of synaptic plasticity.

    3. Spreading of tau pathology in Alzheimer's disease by cell-to-cell transmission (pages 1939–1948)

      Nguyen-Vi Mohamed, Thibaut Herrou, Vanessa Plouffe, Nicolas Piperno and Nicole Leclerc

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12229

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      The present review focuses on the new concept that the spreading of tau pathology in Alzheimer brain would result from a cell-to-cell transmission of tau aggregates. Consistent with this concept, recent studies have reported that tau can be released by an active process of secretion and can be taken up by endocytosis by both non-neuronal and neuronal cells.

    4. Autophagy failure in Alzheimer's disease and the role of defective lysosomal acidification (pages 1949–1961)

      Devin M. Wolfe, Ju-hyun Lee, Asok Kumar, Sooyeon Lee, Samantha J. Orenstein and Ralph A. Nixon

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12169

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      Autophagy is a process to recycle cellular waste that relies on correct functioning of the lysosome. The complex regulation of lysosomal pH makes this process vulnerable to disruption by many factors and reliable lysosomal pH measurements are increasingly important in investigations of disease mechanisms. Here we evaluate the most commonly used pH probes and review evidence that lysosomal acidification is defective in Alzheimer's disease (AD), extending our original findings of elevated lysosomal pH in presenilin 1 knockout cells.

    5. Amyloid-β protein (Aβ) Glu11 is the major β-secretase site of β-site amyloid-β precursor protein-cleaving enzyme 1(BACE1), and shifting the cleavage site to Aβ Asp1 contributes to Alzheimer pathogenesis (pages 1962–1969)

      Yu Deng, Zhe Wang, Ruitao Wang, Xiaozhu Zhang, Shuting Zhang, Yili Wu, Matthias Staufenbiel, Fang Cai and Weihong Song

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12235

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      Cleavage of wild type and Swedish mutant APP proteins by BACE1. The schematic diagram showed that the major β-secretase cleavage site of wild type APP by BACE1 locates at Glu11 to generate C89, whereas the major β-secretase cleavage site of Swedish mutant APP by BACE1 locates at Asp1 to generate C99.

  3. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE

    1. Top of page
    2. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
    3. Special Issue: The Neurobiology of Aging and Alzheimer's Disease
    4. SPECIAL ISSUE: THE NEUROBIOLOGY OF AGING AND ALZHEIMER'S DISEASE
    1. BACE2 degradation mediated by the macroautophagy–lysosome pathway (pages 1970–1977)

      Xi Liu, Zhe Wang, Yili Wu, Jianping Wang and Weihong Song

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12204

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      Lysosomal inhibition facilitates non-amyloidogenic processing pathway by promoting BACE2-mediated APP cleavage. BACE1 cleaves APP at the Asp1 β-secretase site to generate Aβ. APP cleavage by BACE2 at the θ site precludes Aβ production. Lysosomal inhibition induces BACE2 accumulation, promoting APP processing through non-amyloidogenic pathway.

    2. Aging and neurogenesis in the adult forebrain: what we have learned and where we should go from here (pages 1978–1986)

      Laura K. Hamilton, Sandra E. Joppé, Loїc M. Cochard and Karl J. L. Fernandes

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12207

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      To understand when, how and why adult neurogenesis decreases in the aging brain, we critically reviewed the scientific literature on aging of the rodent subventricular zone, the neurogenic niche of the forebrain. Our analysis revealed that deficits in the neurogenic pathway occur by middle-age, but that there remains striking ambiguity in the underlying mechanisms, especially at the level of stem and progenitor cells. We discuss several issues that have led to these gaps in our knowledge.

      Corrected by:

      Corrigendum: Aging and neurogenesis in the adult forebrain: what we have learned and where we should go from here

      Vol. 38, Issue 2, 2339, Version of Record online: 14 JUL 2013

    3. Calorie restriction alleviates the age-related decrease in neural progenitor cell division in the aging brain (pages 1987–1993)

      June-Hee Park, Zachary Glass, Kasim Sayed, Tatyana V. Michurina, Alexander Lazutkin, Olga Mineyeva, Dmitry Velmeshev, Walter F. Ward, Arlan Richardson and Grigori Enikolopov

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12249

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      We examined the response of adult stem and progenitor cells in the hippocampus to an extended period of calorie restriction and rapamycin supplementation by using a reporter mouse line in which expression of GFP marks adult stem and progenitor cells. Upper left image shows the hippocampus of a young (3 weeks) animal for comparison. We found that calorie restriction increases proliferation of neural stem and progenitor cells in aging females.

    4. Cerebrovascular contributions to Alzheimer's disease pathophysiology and potential therapeutic interventions in mouse models (pages 1994–2004)

      Lynsie A. M. Thomason, Bojana Stefanovic and JoAnne McLaurin

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12181

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      The interrelationship between vascular dysfunction and Alzheimer's disease pathology is not clearly understood, however, it is clear that the accumulation of Aβ and loss of vascular function contribute to the cognitive decline detected in patients. At present, imaging modalities can monitor the downstream effects of vascular dysfunction such as cerebral blood flow alterations, white and grey matter lacunes, and ischemic lesions, however it cannot distinguish parenchymal plaques from cerebrovascular amyloid.

    5. Caspase-6 as a novel early target in the treatment of Alzheimer's disease (pages 2005–2018)

      Andrea C. LeBlanc

      Version of Record online: 16 JUN 2013 | DOI: 10.1111/ejn.12250

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      Caspase-6 activity is intimately associated with Alzheimer Disease pathological hallmarks and cognitive impairment. The action of Caspase-6 results in the proteolysis of several neuronal proteins that could affect in parallel many cellular functions. This paper summarizes the evidence for Caspase-6 in Alzheimer Disease and examines the possibility that inhibiting Caspase-6 may provide an efficient treatment against early cognitive impairment and progression to dementia in Alzheimer Disease.

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