Amyloid-dependent and amyloid-independent stages of alzheimer disease

Archives of Neurology

Volumn 68, Issue 8, 2011, Pages 1062-1064

  Hyman, Bradley T ^a  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA SECRETASE; AMYLOID A PROTEIN; AMYLOID BETA PROTEIN; BETA SECRETASE; CASPASE; GAMMA SECRETASE INHIBITOR;

ALZHEIMER DISEASE; APOPTOSIS; CELL DEATH; COGNITION; HISTOPATHOLOGY; HUMAN; NEUROFIBRILLARY TANGLE; NOTE; POSITRON EMISSION TOMOGRAPHY; PRIMARY PREVENTION; PRIORITY JOURNAL; SENILE PLAQUE;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; ANIMALS; BRAIN CHEMISTRY; DISEASE PROGRESSION; DRUG DELIVERY SYSTEMS; DRUG DESIGN; HUMANS; NEURONS; PLAQUE, AMYLOID;

EID: 80051569682     PISSN: 00039942     EISSN: 15383687     Source Type: Journal    
DOI: 10.1001/archneurol.2011.70     Document Type: Note

References (28)

1. Bertram L, Lill CM, Tanzi RE. The genetics of Alzheimer disease: back to the future. Neuron. 2010;68(2):270-281.
2. Selkoe DJ. Biochemistry and molecular biology of amyloid beta-protein and the mechanism of Alzheimer's disease. Handb Clin Neurol. 2008;89:245-260.
3. Holmes C, Boche D, Wilkinson D, et al. Long-term effects of Abeta42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial. Lancet. 2008;372(9634):216-223. (Pubitemid 351978111)
4. Schenk DB, Seubert P, Grundman M, Black R. A beta immunotherapy: lessons learned for potential treatment of Alzheimer's disease. Neurodegener Dis. 2005;2(5):255-260. (Pubitemid 43805909)
5. Serrano-Pozo A, William CM, Ferrer I, et al. Beneficial effect of human anti-amyloid-beta active immunization on neurite morphology and tau pathology. Brain. 2010;133(pt 5):1312-1327.
6. Lilly halts development of semagacestat for Alzheimer's disease based on preliminary results of phase III clinical trials. http://newsroom.lilly.com/ releasedetail.cfm?releaseid=499794. Accessed February 15, 2011.
7. Citron M. Alzheimer's disease: strategies for disease modification. Nat Rev Drug Discov. 2010;9(5):387-398.
8. Arriagada PV, Growdon JH, Hedley-Whyte ET, Hyman BT. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease. Neurology. 1992;42(3, pt 1):631-639.
9. Hyman BT, Marzloff K, Arriagada PV. The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution. J Neuropathol Exp Neurol. 1993;52(6):594-600. (Pubitemid 23335735)
10. Ingelsson M, Fukumoto H, Newell KL, et al. Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain. Neurology. 2004;62(6):925-931. (Pubitemid 38435780)
11. Fagan AM, Mintun MA, Shah AR, et al. Cerebrospinal fluid tau and ptau(181) increase with cortical amyloid deposition in cognitively normal individuals: implications for future clinical trials of Alzheimer's disease. EMBO Mol Med. 2009;1(8-9):371-380.
12. Morris JC, Roe CM, Grant EA, et al. Pittsburgh compound B imaging and prediction of progression from cognitive normality to symptomatic Alzheimer disease. Arch Neurol. 2009;66(12):1469-1475.
13. Rentz DM, Locascio JJ, Becker JA, et al. Cognition, reserve, and amyloid deposition in normal aging. Ann Neurol. 2010;67(3):353-364.
14. Arriagada PV, Marzloff K, Hyman BT. Distribution of Alzheimer-type pathologic changes in non-demented elderly individuals matches the pattern in Alzheimer's disease. Neurology. 1992;42(9):1681-1688.
15. Gómez-Isla T, Hollister R, West H, et al. Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease. Ann Neurol. 1997;41(1):17-24. (Pubitemid 27057088)
16. Koffie RM, Meyer-Luehmann M, Hashimoto T, et al. Oligomeric amyloid beta associates with post-synaptic densities and correlates with excitatory synapse loss near senile plaques. Proc Natl Acad Sci U S A. 2009;106(10):4012-4017.
17. Li Z, Jo J, Jia JM, et al. Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization. Cell. 2010;141(5):859-871.
18. Kuchibhotla KV, Goldman ST, Lattarulo CR, Wu HY, Hyman BT, Bacskai BJ. Abeta plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks. Neuron. 2008;59(2):214-225. (Pubitemid 352033686)
19. Busche MA, Eichhoff G, Adelsberger H, et al. Clusters of hyperactive neurons near amyloid plaques in a mouse model of Alzheimer's disease. Science. 2008;321(5896):1686-1689.
20. Wu HY, Hudry E, Hashimoto T, et al. Amyloid beta induces the morphological neurodegenerative triad of spine loss, dendritic simplification, and neuritic dystrophies through calcineurin activation. J Neurosci. 2010;30(7):2636-2649.
21. Abdul HM, Sama MA, Furman JL, et al. Cognitive decline in Alzheimer's disease is associated with selective changes in calcineurin/NFAT signaling. J Neurosci. 2009;29(41):12957-12969.
22. D'Amelio M, Cavallucci V, Middei S, et al. Caspase-3 triggers early synaptic dysfunction in a mouse model of Alzheimer's disease. Nat Neurosci. 2011;14(1):69-76.
23. de Calignon A, Fox LM, Pitstick R, et al. Caspase activation precedes and leads to tangles. Nature. 2010;464(7292):1201-1204.
24. Quintanilla RA, Matthews-Roberson TA, Dolan PJ, Johnson GV. Caspase-cleaved tau expression induces mitochondrial dysfunction in immortalized cortical neurons: implications for the pathogenesis of Alzheimer disease. J Biol Chem. 2009;284(28):18754-18766.
25. Ittner LM, Ke YD, Delerue F, et al. Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. Cell. 2010;142(3):387-397.
26. Vossel KA, Zhang K, Brodbeck J, et al. Tau reduction prevents Abeta-induced defects in axonal transport. Science. 2010;330(6001):198.
27. Zempel H, Thies E, Mandelkow E, Mandelkow EM. Abeta oligomers cause localized Ca(2+) elevation, missorting of endogenous Tau into dendrites, Tau phosphorylation, and destruction of microtubules and spines. J Neurosci. 2010;30(36):11938-11950.
28. Becker J, Heden T, Carmasin J, et al. Amyloid-β associated cortical thinning in clinically normal elderly. Ann Neurol. doi:10.1002/ana.22333.