Morphological adaptive response of the synaptic junctional zones in the human dentate gyrus during aging and Alzheimer's disease

Bertoni–Freddari, Carlo; Fattoretti, Patrizia; Casoli, Tiziana; Meier‐Ruge, W.; Ulrich, J.

doi:10.1016/0006-8993(90)91009-6

Cited by 117 publications

(75 citation statements)

References 27 publications

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“…The synapse-to-neuron ratio was found to vary according to the brain regions from which the samples were taken and the individual's health [34]. No significant differences in the synapse-to-neuron ratio were found in samples taken from the cerebellum of adult and elderly persons without AD, and of elderly AD patients.…”

Section: Synaptic Damagementioning

confidence: 87%

Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

Reddy

Beal

2008

Trends in Molecular Medicine

819

642

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Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic AD mice suggest that oxidative damage, induced by amyloid beta, is associated with mitochondria early in AD progression. Amyloid beta and amyloid precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron transport chain, increase reactive oxygen species production, cause mitochondrial damage and prevent neurons from functioning normally. Further, accumulation of amyloid beta at synaptic terminals may contribute to synaptic damage and cognitive decline in patients with AD. This article describes the latest research in identifying factors that may affect AD progression, particularly synaptic damage and cognitive decline in AD patients.

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Section: Synaptic Damagementioning

confidence: 87%

Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

Reddy

Beal

2008

Trends in Molecular Medicine

819

642

View full text Add to dashboard Cite

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“…Synaptic loss is accompanied by synaptic hypertrophy in brains from Alzheimer's patients. 45,46 A striking feature of the synaptic morphology during disease progression was the change in the curvature of the PSDs. An increase in PSD curvature and thickness has been shown to occur after a delay in transcardial perfusion fixation of the mouse brain, a condition that induces ischemic stress.…”

Section: Discussionmentioning

confidence: 99%

Degenerating Synaptic Boutons in Prion Disease

Šišková

Page

O’Connor

et al. 2009

The American Journal of Pathology

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A growing body of evidence suggests that the loss of synapses is an early and major component of a number of neurodegenerative diseases. Murine prion disease offers a tractable preparation in which to study synaptic loss in a chronic neurodegenerative disease and to explore the underlying mechanisms. We have previously shown that synaptic loss in the hippocampus underpins the first behavioral changes and that there is a selective loss of presynaptic elements. The microglia have an activated morphology at this stage but they have an anti-inflammatory phenotype. We reasoned that the microglia might be involved in synaptic stripping, removing synapses undergoing a degenerative process, and that this gives rise to the anti-inflammatory phenotype. Analysis of synaptic density revealed a progressive loss from 12 weeks post disease initiation. The loss of synapses was not associated with microglia processes; instead, we found that the postsynaptic density of the dendritic spine was progressively wrapped around the degenerating presynaptic element with loss of subcellular components. Three-dimensional reconstructions of these structures from Dual Beam electron microscopy support the conclusion that the synaptic loss in prion disease is a neuron autonomous event facilitated without direct involvement of glial cells. Previous studies described synapse engulfment by developing and injured neurons, and we suggest that this mechanism may contribute to developmental and pathological changes in synapse numbers.

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“…Geinisman et al [15] extensively reviewed the data on neuronal numbers and densities in the hippocampus of aging subjects. Whereas some studies reported no age-associated loss in human hippocampal fields CA1-4 and the subiculum [10], other studies demonstrated a decrease of neuron numbers or densities in all or some of the hippocampal subfields or the dentate gyrus with advancing age [7,32,36,39]. Most, but not all, of these earlier studies made assumptions about size, shape, and distribution of the neurons, and for that reason these techniques are now designated as assumption-based counting techniques.…”

Section: Introductionmentioning

confidence: 99%

Preservation of hippocampal neuron numbers in aged rhesus monkeys

Keuker

Luiten

Fuchs

2003

Neurobiology of Aging

122

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Preservation of hippocampal neuron numbers in aged rhesus monkeys Keuker, J.I.H.; Luiten, P.G.M.; Fuchs, E. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. AbstractTo investigate whether or not aging of nonhuman primates is accompanied by a region-specific neuron loss in the hippocampal formation, we used the optical fractionator technique to obtain stereological estimates of unilateral neuron numbers of the hippocampi of eight young (0-4 years) and five aged (18-31 years) male rhesus monkeys (Macaca mulatta). Our results show a preservation of neurons (mean × 10 3 ± S.D. × 10 3 ) in the subiculum (young = 588 ± 124, aged = 612 ± 207), CA1 (young = 1051 ± 249, aged = 1318 ± 311), CA2 (young = 100 ± 18, aged = 113 ± 12), CA3 (young = 478 ± 125, aged = 509 ± 139), hilus (young = 337 ± 115, aged = 394 ± 90), and dentate gyrus (young = 5550 ± 1725, aged = 7799 ± 2087) of the hippocampal formation. These results confirm a previous stereological study in rhesus monkeys, but are in conflict with data for humans, showing age-dependent region-specific alterations in the hippocampal formation.

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Morphological adaptive response of the synaptic junctional zones in the human dentate gyrus during aging and Alzheimer's disease

Cited by 117 publications

References 27 publications

Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

Degenerating Synaptic Boutons in Prion Disease

Preservation of hippocampal neuron numbers in aged rhesus monkeys

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