Decreased presence of perforated synapses in a triple-transgenic mouse model of Alzheimer's disease

Rejuvenation Research

Volumn 11, Issue 2, 2008, Pages 309-313

  Bertoni Freddari, Carlo ^a   Sensi, Stefano L ^b   Giorgetti, Belinda ^a   Balietti, Marta ^a   Di Stefano, Giuseppina ^a   Canzoniero, Lorella M T ^c   Casoli, Tiziana ^a   Fattoretti, Patrizia ^a  

^a INRCA   (Italy)

^b UNIVERSITY OF CHIETI   (Italy)

^c UNIVERSITY OF SANNIO   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN;

ALZHEIMER DISEASE; ANIMAL MODEL; ARTICLE; BRAIN FUNCTION; CONTROLLED STUDY; GENOTYPE; HIPPOCAMPUS; MORPHOMETRICS; MOUSE; NERVE CELL PLASTICITY; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; SYNAPSE;

AGING; ALZHEIMER DISEASE; ANIMALS; DISEASE MODELS, ANIMAL; MICE; MICE, TRANSGENIC; SYNAPSES;

MUS; MUS MUSCULUS;

EID: 42649141628     PISSN: 15491684     EISSN: None     Source Type: Journal    
DOI: 10.1089/rej.2008.0660     Document Type: Article

References (24)

1. La Ferla FM, Oddo S. Alzheimer's disease: Aβ, tau and synaptic dysfunction. Trends Mol Med 2005;11:170-176.
2. Selkoe DJ. Alzheimer's disease is a synaptic failure. Science 2002;298:789-791.
3. Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 2002;298:962-964.
4. Klein WL. Abeta toxicity in Alzheimer's disease: globular oligomers (ADDLs) as new vaccine and drug targets. Neurochem Int 2002;41:345-352.
5. Tanzi RE. The synaptic Aβ hypothesis of Alzheimer disease. Nature Neurosci 2005;8:977-979.
6. La Ferla FM, Green KN, Oddo S. Intracellular amyloid-β in Alzheimer's disease. Nat Rev 2007;8:499-509.
7. Lambert MP Barlow AK, et al. Diffusible nonfibrillar ligands derived from Abeta 1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 1998;95:6448-6453.
8. Tsai J, Grutzendler J, Duff K, et al. Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches. Nat Neurosci 2004;7:1181-1183.
9. Snyder EM, Nong Y, Almeida CG, et al. Regulation of NMDA receptor trafficking by amyloid-beta. Nat Neurosci 2005;8:1051-1058.
10. Shrestha BR, Vitolo OV, Joshi P, et al. Amyloid beta peptide adversely affects spine number and motility in hippocampal neurons. Mol Cell Neurosci 2006;33:274-282.
11. Oddo S, Caccamo A, Shepherd JD, et al. Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Aβ and synaptic dysfunction. Neuron 2003;39:409-421.
12. Billings LM, Oddo S, Green KN, et al. Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice. Neuron 2005;45:639-642.
13. Bertoni-Freddari C, Fattoretti P, Giorgetti B, et al. Synaptic pathology in the brain cortex of old monkeys as an early alteration in senile plaque formation. Rejuvenation Res 2006;9:85-88.
14. Coggesshall RE, Lekan HA. Methods for determining number of cells and synapses: a case for more uniform standard review. J Comp Neurol 1996;364:6-15.
15. Genisman Y, de-Toledo-Morrell L, Morrell F. Induction of long-term potentiation is associated with an increase in the number of axospinous synapses with segmented postsynaptic densities. Brain Res 1991;566:77-88.
16. Guldner FH, Phillips SC. Structural plasticity of synaptic contacts in the central nervous system. In: Jones DG (ed): Current Topics in Research on Synapses. New York: Liss, 1986, pp. 147-169.
17. Hillman DE, Chen S. Reciprocal relationship between size of postsynaptic densities and their number. Constancy in contact area. Brain Res 1984;295:325-343.
18. Bertoni-Freddari C, Fattoretti P, Casoli T, et al. Neurobiology of the aging brain. In: Conn PM (ed.): Handbook of Models for the Study of Human Aging. St. Louis: Elsevier, 2006, pp. 485-506.
19. Chen YR, Glabe C. Distinct early folding and aggregation properties of Alzheimer amyloid-β peptides Aβ40 and Aβ42: stable trimer or tetramer formation by Aβ42. J Biol Cem 2006;281:24414-24422.
20. Fedulov V, Rex CS, Simmons DA, et al. Evidence that long-term potentiation occurs within individual hippocampal synapses during learning. J Neurosci 2007;27:8031-8039.
21. Jones DG, Harris RJ. An analysis of contemporary morphological concepts of synaptic remodelling in the CNS: perforated synapses revisited. Rev Neurosci 1995;6:177-219.
22. Calverley RKS, Jones DG. Contribution of dendritic spines and perforated synapses to synaptic plasticity. Brain Res Rev 1990;15:215-249.
23. Geinisman Y, deToledo-Morrel L, Morrel F. Aged rats need a preserved complement of perforated axospinous synapses per hippocampal neuron to maintain good spatial memory. Brain Res 1986;398:266-275.
24. Genisman Y, de-Toledo-Morrel L, Morrell F. Loss of perforated synapses in the dentate gyrus: morphological substrate of memory deficit in aged rats. Proc Natl Acad Sci USA 1986;83:3027-3031.