Age-related amyloid β deposition in transgenic mice overexpressing both alzheimer mutant presenilin 1 and amyloid β precursor protein swedish mutant is not associated with global neuronal loss

American Journal of Pathology

Volumn 157, Issue 1, 2000, Pages 331-339

  Takeuchi, Ayano ^a   Irizarry, Michael C ^b   Duff, Karen ^c   Saido, Takaomi C ^d   Ashe, Karen Hsiao ^e   Hasegawa, Masato ^a   Mann, David M A ^f   Hyman, Bradley T ^b   Iwatsubo, Takeshi ^a  

^a UNIVERSITY OF TOKYO   (Japan)

^b MASSACHUSETTS GENERAL HOSPITAL   (United States)

^c NEW YORK UNIVERSITY   (United States)

^d RIKEN BRAIN SCIENCE INSTITUTE   (Japan)

^e UNIVERSITY OF MINNESOTA   (United States)

^f UNIVERSITY OF MANCHESTER   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN; PRESENILIN 1; SYNAPTOPHYSIN;

ALZHEIMER DISEASE; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DENTATE GYRUS; FRONTAL LOBE; GENE OVEREXPRESSION; HIPPOCAMPUS; IMMUNOREACTIVITY; MOUSE; NEOCORTEX; NONHUMAN; PATHOGENESIS; PRIORITY JOURNAL; SENILE PLAQUE; TRANSGENIC MOUSE;

EID: 0033872024     PISSN: 00029440     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0002-9440(10)64544-0     Document Type: Article

References (50)

1. Consensus recommendations for the postmortem diagnosis of Alzheimer disease from the National Institute on Aging and the Reagan Institute Working Group on diagnostic criteria for the neuropathological assessment of Alzheimer disease
2. An increased percentage of long amyloid β-protein is secreted by familial amyloid β-protein precursor (βAPP717) mutants
3. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1
4. Familial Alzheimer's disease-linked presenilin 1 variants elevate Aβ1-42/1-40 ratio in vitro and in vivo
5. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
6. The presenilin 2 mutation (N141l) linked to familial Alzheimer disease (Volga German families) increases the secretion of amyloid β protein ending at the 42nd (or 43rd) residue
7. Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ-monoclonals: Evidence that an initially deposited species is Aβ42(43)
8. Predominant deposition of amyloid β42(43) in plaques in cases of Alzheimer's disease and hereditary cerebral hemorrhage associated with mutations in the APP gene
9. The E280A presenilin 1 Alzheimer mutation produces increased Aβ42 deposition and severe cerebellar pathology
10. Amyloid β protein (Aβ) deposition in chromosome 14-linked Alzheimer's disease: Predominance of Aβ42(43)
11. Seeding 'one-dimensional crystallization' of amyloid: A pathogenic mechanism in Alzheimer's disease and scrapie?
12. The impact of different presenilin 1 and presenilin 2 mutations on amyloid deposition, neurofibrillary changes and neuronal loss in the familial Alzheimer's disease brain: Evidence for other phenotype-modifying factors
13. Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease
14. Differences in the pattern of hippocampal neuronal loss in normal ageing and Alzheimer's disease
15. Plaques, tangles and dementia. A quantitative study
16. Physical basis of cognitive alterations in Alzheimer's disease: Synapse loss is the major correlate of cognitive impairment
17. The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution
18. Profound loss of layer entorhinal cortex neurons occurs in very mild Alzheimer's disease
19. Aβ deposition is associated with neuropil changes, but not with overt neuronal loss in the human amyloid precursor protein V717F (PDAPP) transgenic mouse
20. APPSw transgenic mice develop age-related Aβ deposits and neuropil abnormalities, but no neuronal loss in CA1
21. Neuron loss in APP transgenic mice
22. Transgenic mice with Alzheimer presenilin 1 mutations show accelerated neurodegeneration without amyloid plaque formation
23. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins
24. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes
25. Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice
26. Abnormal pathology development in transgenic mice over-expressing both mutant amyloid precursor protein and mutant presenilin 1 transgenes
27. Spatial resolution of the primary β-amyloidogenic process induced in postischemic hippocampus
28. Full-length amyloid-β(1-42(43)) as well as amino-terminally modified and truncated amyloid-β42(43) deposit in diffuse plaques
29. Amyloid precursor protein processing and Aβ42 deposition in a transgenic mouse model of Alzheimer's disease
30. Unbiased stereological estimation of the number of neurons in the human hippocampus
31. New stereologic methods for counting neurons
32. The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution
33. Proline-directed and non-proline-directed phosphorylation of PHF-tau
34. Structural correlates of cognition in dementia: Quantification and assessment of synapse change
35. Synaptotrophic effects of human amyloid β protein precursors in the cortex of transgenic mice
36. Pathogenic mechanisms of Alzheimer's disease analyzed in the APP23 transgenic mouse model
37. Reorganization of cholinergic terminals in the cerebral cortex and hippocampus in transgenic mice carrying mutated presenilin-1 and amyloid precursor protein transgenes
38. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models
39. β-amyloid neurotoxicity requires fibril formation and is inhibited by congo red
40. Neurodegeneration induced by β-amyloid peptides in vitro: The role of peptide assembly state
41. Clinical, pathological, and neurochemical changes in dementia: A subgroup with preserved mental status and numerous neocortical plaques
42. Amyloid β protein (Aβ) deposition in normal aging has the same characteristics as that in Alzheimer's disease: Predominance of Aβ42(43) and association of Aβ40 with cored plaques
43. Alzheimer's presenilin mutation sensitizes neural cells to apoptosis induced by trophic factor withdrawal and amyloid β-peptide: Involvement of calcium and oxyradicals
44. Mutant presenilin-1 induces apoptosis and downregulates Akt/PKB
45. Participation of presenilin 2 in apoptosis: Enhanced basal activity conferred by an Alzheimer mutation
46. Alzheimer-associated presenilin-2 confers increased sensitivity to apoptosis in PC12 cells
47. The tauopathies: Toward an experimental animal model
48. Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17
49. Apoptosis. Dead end for neurodegeneration?
50. Brain trauma induces massive hippocampal neuron death linked to a surge in β-amyloid levels in mice overexpressing mutant amyloid precursor protein