The isotropic fractionator provides evidence for differential loss of hippocampal neurons in two mouse models of Alzheimer's disease

Molecular Neurodegeneration

Volumn 7, Issue 1, 2012, Pages

  Brautigam, Hannah ^a   Steele, John W ^a,b,c   Westaway, David ^d   Fraser, Paul E ^e   George Hyslop, Peter H St ^e,f   Gandy, Sam ^a,b   Hof, Patrick R ^a   Dickstein, Dara L ^a,g  

^a MOUNT SINAI SCHOOL OF MEDICINE   (United States)

^b VETERANS AFFAIRS MEDICAL CENTER   (United States)

^c ROCKEFELLER UNIVERSITY   (United States)

^d UNIVERSITY OF ALBERTA   (Canada)

^e UNIVERSITY OF TORONTO   (Canada)

^f UNIVERSITY OF CAMBRIDGE   (United Kingdom)

^g HESS CORPORATION   (United States)

Author keywords

Alzheimer's disease; Amyloid beta (A ); Isotropic fractionator; Mouse models; Neuronal loss

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN;

ACCURACY; ALZHEIMER DISEASE; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL COUNT; CELL DENSITY; CELL LOSS; CELL POPULATION; CONTROLLED STUDY; HIPPOCAMPUS; ISOTROPIC FRACTIONATOR METHOD; MOUSE; NONHUMAN; PROCEDURES CONCERNING CELLS;

ALZHEIMER DISEASE; ANIMALS; CELL COUNT; CELL FRACTIONATION; DISEASE MODELS, ANIMAL; HIPPOCAMPUS; MICE; MICE, TRANSGENIC; NEURONS;

MUS; MUS MUSCULUS;

EID: 84869861999     PISSN: None     EISSN: 17501326     Source Type: Journal    
DOI: 10.1186/1750-1326-7-58     Document Type: Article

References (17)

1. Alzheimer's disease results from the cerebral accumulation and cytotoxicity of amyloid beta-protein. Selkoe DJ, J Alzheimers Dis 2001 3 75 80 12214075
2. A mouse model of amyloid beta oligomers: their contribution to synaptic alteration, abnormal tau phosphorylation, glial activation, and neuronal loss in vivo. Tomiyama T, Matsuyama S, Iso H, Umeda T, Takuma H, Ohnishi K, Ishibashi K, Teraoka R, Sakama N, Yamashita T, Nishitsuji K, Ito K, Shimada H, Lambert MP, Klein WL, Mori H, J Neurosci 2010 30 4845 56 10.1523/JNEUROSCI.5825-09.2010 20371804
3. Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomers. Gandy S, Simon AJ, Steele JW, Lublin AL, Lah JJ, Walker LC, Levey AI, Krafft GA, Levy E, Checler F, Glabe C, Bilker WB, Abel T, Schmeidler J, Ehrlich ME, Ann Neurol 2010 68 220 30 20641005
4. Amyloid deposition and advanced age fails to induce Alzheimer's type progression in a double knock-in mouse model. Malthankar-Phatak GH, Lin YG, Giovannone N, Siman R, Aging Dis 2012 3 141 55 22724075
5. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695. Chishti MA, Yang DS, Janus C, Phinney AL, Horne P, Pearson J, Strome R, Zuker N, Loukides J, French J, Turner S, Lozza G, Grilli M, Kunicki S, Morissette C, Paquette J, Gervais F, Bergeron C, Fraser PE, Carlson GA, George-Hyslop PS, Westaway D, J Biol Chem 2001 276 21562 70 10.1074/jbc.M100710200 11279122 (Pubitemid 37413154)
6. Isotropic fractionator: a simple, rapid method for the quantification of total cell and neuron numbers in the brain. Herculano-Houzel S, Lent R, J Neurosci 2005 25 2518 21 10.1523/JNEUROSCI.4526-04.2005 15758160 (Pubitemid 40365162)
7. Cellular scaling rules for rodent brains. Herculano-Houzel S, Mota B, Lent R, Proc Natl Acad Sci U S A 2006 103 12138 43 10.1073/pnas.0604911103 16880386 (Pubitemid 44215824)
8. Developmental increase of total cell numbers in the murine cerebellum. Surchev L, Nazwar TA, Weisheit G, Schilling K, Cerebellum 2007 1 6
9. Neuron loss in APP transgenic mice. Calhoun ME, Wiederhold KH, Abramowski D, Phinney AL, Probst A, Sturchler-Pierrat C, Staufenbiel M, Sommer B, Jucker M, Nature 1998 395 755 6 10.1038/27351 9796810 (Pubitemid 28485431)
10. Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease. Schmitz C, Rutten BP, Pielen A, Schafer S, Wirths O, Tremp G, Czech C, Blanchard V, Multhaup G, Rezaie P, Korr H, Steinbusch HW, Pradier L, Bayer TA, Am J Pathol 2004 164 1495 502 10.1016/S0002-9440(10)63235-X 15039236 (Pubitemid 38387814)
11. Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model. Casas C, Sergeant N, Itier JM, Blanchard V, Wirths O, van der Kolk N, Vingtdeux V, van de Steeg E, Ret G, Canton T, Drobecq H, Clark A, Bonici B, Delacourte A, Benavides J, Schmitz C, Tremp G, Bayer TA, Benoit P, Pradier L, Am J Pathol 2004 165 1289 300 10.1016/S0002-9440(10)63388-3 15466394 (Pubitemid 39297734)
12. APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy. Breyhan H, Wirths O, Duan K, Marcello A, Rettig J, Bayer TA, Acta Neuropathol 2009 117 677 85 10.1007/s00401-009-0539-7 19387667
13. Amyloid-beta oligomers: possible roles as key neurotoxins in Alzheimer's Disease. Lublin AL, Gandy S, Mt Sinai J Med 2010 77 43 9 10.1002/msj.20160 20101723
14. Soluble fibrillar oligomer levels are elevated in Alzheimer's disease brain and correlate with cognitive dysfunction. Tomic JL, Pensalfini A, Head E, Glabe CG, Neurobiol Dis 2009 35 352 8 10.1016/j.nbd.2009.05.024 19523517
15. Memory deficits in APP23/Abca1+/- mice correlate with the level of Abeta oligomers. Lefterov I, Fitz NF, Cronican A, Lefterov P, Staufenbiel M, Koldamova R, ASN Neuro 2009 1
16. Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease. Gouras GK, Tampellini D, Takahashi RH, Capetillo-Zarate E, Acta Neuropathol 2010 119 523 41 10.1007/s00401-010-0679-9 20354705
17. Changes in dendritic complexity and spine morphology in transgenic mice expressing human wild-type tau. Dickstein DL, Brautigam H, Stockton SD Jr, Schmeidler J, Hof PR, Brain Struct Funct 2010 214 161 79 10.1007/s00429-010- 0245-1 20213269