Experts and Doctors on alzheimer disease in Switzerland


Locale: Switzerland
Topic: alzheimer disease

Top Publications

  1. Noetzli M, Eap C. Pharmacodynamic, pharmacokinetic and pharmacogenetic aspects of drugs used in the treatment of Alzheimer's disease. Clin Pharmacokinet. 2013;52:225-41 pubmed publisher
    ..The aim of this review is to summarize the pharmacodynamics and pharmacokinetics of the four commonly used anti-dementia drugs and to give an overview on the current knowledge of pharmacogenetics in this field. ..
  2. Paganetti P, Calanca V, Galli C, Stefani M, Molinari M. beta-site specific intrabodies to decrease and prevent generation of Alzheimer's Abeta peptide. J Cell Biol. 2005;168:863-8 pubmed
  3. Schneider N, Yvon C. A review of multidomain interventions to support healthy cognitive ageing. J Nutr Health Aging. 2013;17:252-7 pubmed publisher
    ..Larger high-quality randomized controlled trials are required to systematically investigate the cognitive effect of programs comprising physical and mental activity as well as nutritional aspects. ..
  4. Gast H, Gordic S, Petrzilka S, Lopez M, Muller A, Gietl A, et al. Transforming growth factor-beta inhibits the expression of clock genes. Ann N Y Acad Sci. 2012;1261:79-87 pubmed publisher
    ..TGF-β2-induced dysregulation of clock genes may alter neuronal pathways, which may be causally related to abnormal sleep-wake rhythms in AD patients. ..
  5. Woltering T, Wostl W, Hilpert H, Rogers Evans M, Pinard E, Mayweg A, et al. BACE1 inhibitors: a head group scan on a series of amides. Bioorg Med Chem Lett. 2013;23:4239-43 pubmed publisher
  6. Finder V. Alzheimer's disease: a general introduction and pathomechanism. J Alzheimers Dis. 2010;22 Suppl 3:5-19 pubmed publisher
  7. Pfeil A, Kressig R, Szucs T. Alzheimer's dementia: budget impact and cost-utility analysis of a combination treatment of a cholinesterase inhibitor and memantine in Switzerland. Swiss Med Wkly. 2012;142:w13676 pubmed publisher
    ..From a health care perspective, the combination treatment would decrease costs over five years by CHF 50 million. Based on long term considerations, the combination treatment was the dominant strategy over the mono treatment. ..
  8. Vishwanathan R, Schalch W, Johnson E. Macular pigment carotenoids in the retina and occipital cortex are related in humans. Nutr Neurosci. 2016;19:95-101 pubmed publisher
    ..Total macular pigment density measured via non-invasive, psychophysical techniques can be used as a biomarker to ascertain brain lutein and zeaxanthin status in clinical studies. ..
  9. Gay B, Taylor K, Hohl U, Tolnay M, Staehelin H. The validity of clinical diagnoses of dementia in a group of consecutively autopsied memory clinic patients. J Nutr Health Aging. 2008;12:132-7 pubmed
    ..This study reaffirms the need for internationally accepted criteria for clinical and neuropathological diagnoses, as well as further clinical-neuropathological investigations to further refine the clinical diagnostic process. ..

More Information


  1. Ovchinnikova O, Finder V, Vodopivec I, Nitsch R, Glockshuber R. The Osaka FAD mutation E22? leads to the formation of a previously unknown type of amyloid ? fibrils and modulates A? neurotoxicity. J Mol Biol. 2011;408:780-91 pubmed publisher
    ..Because A?1-40 is the major A? form in vivo, the gain of toxic function caused by the E22 deletion may explain the development of familial AD in mutation carriers. ..
  2. Savaskan E, Schnitzler C, Schröder C, Cajochen C, Muller Spahn F, Wirz Justice A. Treatment of behavioural, cognitive and circadian rest-activity cycle disturbances in Alzheimer's disease: haloperidol vs. quetiapine. Int J Neuropsychopharmacol. 2006;9:507-16 pubmed
    ..The study provides evidence that quetiapine at a moderate dose may be efficacious in treating behavioural disturbances in AD, with better tolerability than haloperidol. ..
  3. Grimminger Marquardt V, Lashuel H. Structure and function of the molecular chaperone Hsp104 from yeast. Biopolymers. 2010;93:252-76 pubmed publisher
  4. Riederer B, Leuba G, Vernay A, Riederer I. The role of the ubiquitin proteasome system in Alzheimer's disease. Exp Biol Med (Maywood). 2011;236:268-76 pubmed publisher
    ..It is essential to discuss therapeutic ways to investigate the UPS dysfunction in the human brain and to identify specific targets to hold or stop cell decay. ..
  5. Aguzzi A, Barres B, Bennett M. Microglia: scapegoat, saboteur, or something else?. Science. 2013;339:156-61 pubmed publisher
    ..It also seems increasingly likely that microglial dysfunction can underlie certain neurological diseases without an obvious immune component. ..
  6. Hilpert H, Guba W, Woltering T, Wostl W, Pinard E, Mauser H, et al. ?-Secretase (BACE1) inhibitors with high in vivo efficacy suitable for clinical evaluation in Alzheimer's disease. J Med Chem. 2013;56:3980-95 pubmed publisher
    ..The effect was long lasting, showing a significant reduction of A?40 and 42 even after 24 h. In contrast to 89, compound 1b lacking the CF3 group was virtually inactive in vivo. ..
  7. Gobbi L, Knust H, Körner M, Honer M, Czech C, Belli S, et al. Identification of Three Novel Radiotracers for Imaging Aggregated Tau in Alzheimer's Disease with Positron Emission Tomography. J Med Chem. 2017;60:7350-7370 pubmed publisher
  8. Wiessner C, Wiederhold K, Tissot A, Frey P, Danner S, Jacobson L, et al. The second-generation active A? immunotherapy CAD106 reduces amyloid accumulation in APP transgenic mice while minimizing potential side effects. J Neurosci. 2011;31:9323-31 pubmed publisher
    ..They reacted with A? monomers and oligomers and blocked A? toxicity in cell culture. We conclude that CAD106 immunization is suited to interfere with A? aggregation and its downstream detrimental effects. ..
  9. Hogg R, Bertrand D. Nicotinic acetylcholine receptors as drug targets. Curr Drug Targets CNS Neurol Disord. 2004;3:123-30 pubmed
    ..Beneficial and possible undesirable actions of agonists, antagonists and allosteric modulators are discussed and placed in perspective of our most recent knowledge. ..
  10. AbdAlla S, Langer A, Fu X, Quitterer U. ACE inhibition with captopril retards the development of signs of neurodegeneration in an animal model of Alzheimer's disease. Int J Mol Sci. 2013;14:16917-42 pubmed publisher
    ..Taken together, our data present strong evidence that ACE inhibition with a widely used cardiovascular drug could interfere with Abeta-dependent neurodegeneration. ..
  11. Sevigny J, Chiao P, Bussiere T, Weinreb P, Williams L, Maier M, et al. The antibody aducanumab reduces A? plaques in Alzheimer's disease. Nature. 2016;537:50-6 pubmed publisher
    ..These results justify further development of aducanumab for the treatment of AD. Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis. ..
  12. Stoppe G, Knoblauch A, Haak S, Maeck L. [Physicians' competence regarding the early diagnosis of dementia: differences between family physicians and primary care neuropsychiatrists in Germany]. Psychiatr Prax. 2007;34:134-8 pubmed
    ..Vascular concepts prevail. However, both groups differ with regard to the diagnostic work-up. An increase of competence seems to be necessary in both groups. ..
  13. Alberi L, Hoey S, Brai E, Scotti A, Marathe S. Notch signaling in the brain: in good and bad times. Ageing Res Rev. 2013;12:801-14 pubmed publisher
  14. Princz Kranz F, Mueggler T, Knobloch M, Nitsch R, Rudin M. Vascular response to acetazolamide decreases as a function of age in the arcA beta mouse model of cerebral amyloidosis. Neurobiol Dis. 2010;40:284-92 pubmed publisher
    ..High diagnostic accuracy of the combined readouts in detecting vascular dysfunction in arcA beta mice was found. ..
  15. Aguzzi A, O CONNOR T. Protein aggregation diseases: pathogenicity and therapeutic perspectives. Nat Rev Drug Discov. 2010;9:237-48 pubmed publisher
  16. Savaskan E. The role of the brain renin-angiotensin system in neurodegenerative disorders. Curr Alzheimer Res. 2005;2:29-35 pubmed
    ..The aim of this brief review is to summarize the current state of research in this field with emphasis on RAS-related alterations during the course of neurodegenerative disorders. ..
  17. Téllez J, Krishnakumar J, Bungener M, Le Galès C. Capability deprivation of people with Alzheimer's disease: An empirical analysis using a national survey. Soc Sci Med. 2016;151:56-68 pubmed publisher
    ..Hence they need a special attention in policy-making. ..
  18. Pache M, Smeets C, Gasio P, Savaskan E, Flammer J, Wirz Justice A, et al. Colour vision deficiencies in Alzheimer's disease. Age Ageing. 2003;32:422-6 pubmed
    ..0008) than the controls. No relation between test performance and severity of Alzheimer's disease was found. Alzheimer's disease patients have an unspecific colour vision deficiency independent of the severity of the disease. ..
  19. Probst A, Herzig M, Mistl C, Ipsen S, Tolnay M. Perisomatic granules (non-plaque dystrophic dendrites) of hippocampal CA1 neurons in Alzheimer's disease and Pick's disease: a lesion distinct from granulovacuolar degeneration. Acta Neuropathol. 2001;102:636-44 pubmed
    ..In addition PSG should be acknowledged among main histological changes associated with hippocampal neurons in AD and Pick's disease. ..
  20. Wollmer M, Kapaki E, Hersberger M, Muntwyler J, Brunner F, Tsolaki M, et al. Ethnicity-dependent genetic association of ABCA2 with sporadic Alzheimer's disease. Am J Med Genet B Neuropsychiatr Genet. 2006;141B:534-6 pubmed
    ..These data suggest that ABCA2 may exert population-dependent effects on the genetic risk for sporadic AD and support a role of ABC lipid transporters in the pathogenesis of this disease...
  21. Hua H, Münter L, Harmeier A, Georgiev O, Multhaup G, Schaffner W. Toxicity of Alzheimer's disease-associated A? peptide is ameliorated in a Drosophila model by tight control of zinc and copper availability. Biol Chem. 2011;392:919-26 pubmed publisher
    ..These results show that a tight control of zinc and copper availability can minimize cellular damage associated with A?42 expression. ..
  22. Rudinskiy N, Grishchuk Y, Vaslin A, Puyal J, Delacourte A, Hirling H, et al. Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration. J Biol Chem. 2009;284:12447-58 pubmed publisher
  23. Udayar V, Buggia Prévot V, Guerreiro R, Siegel G, Rambabu N, Soohoo A, et al. A paired RNAi and RabGAP overexpression screen identifies Rab11 as a regulator of β-amyloid production. Cell Rep. 2013;5:1536-51 pubmed publisher
    ..Our results reveal trafficking pathways that regulate Aβ levels and show how systems biology approaches can unravel the molecular complexity underlying AD. ..
  24. Beckmann N, Gerard C, Abramowski D, Cannet C, Staufenbiel M. Noninvasive magnetic resonance imaging detection of cerebral amyloid angiopathy-related microvascular alterations using superparamagnetic iron oxide particles in APP transgenic mouse models of Alzheimer's disease: application to passive Abeta immunot. J Neurosci. 2011;31:1023-31 pubmed publisher
    ..Our data demonstrate that MRI has the sensitivity to noninvasively monitor the development of vascular pathology and its possible enhancement by amyloid ? immunotherapy in transgenic mice modeling AD. ..
  25. Briand C, Kozlov S, Sonderegger P, Grutter M. Crystal structure of neuroserpin: a neuronal serpin involved in a conformational disease. FEBS Lett. 2001;505:18-22 pubmed
    ..We propose that these mutations could delay the insertion of the reactive center loop into the central beta-sheet A, an essential step in the inhibition and possibly in the polymerization of neuroserpin. ..
  26. Papassotiropoulos A, Streffer J, Tsolaki M, Schmid S, Thal D, Nicosia F, et al. Increased brain beta-amyloid load, phosphorylated tau, and risk of Alzheimer disease associated with an intronic CYP46 polymorphism. Arch Neurol. 2003;60:29-35 pubmed
    ..4 for apolipoprotein E epsilon4 alone (95% CI, 2.8-6.8; P<.001). CYP46 influences brain beta-amyloid load, cerebrospinal fluid levels of beta-amyloid peptides and phosphorylated tau, and the genetic risk of late-onset sporadic AD. ..
  27. Kunze A, Meissner R, Brando S, Renaud P. Co-pathological connected primary neurons in a microfluidic device for Alzheimer studies. Biotechnol Bioeng. 2011;108:2241-5 pubmed publisher
    ..g., in Alzheimer), as well as simultaneous drug effects on connected healthy and diseased cell populations. ..
  28. Boncristiano S, Calhoun M, Kelly P, Pfeifer M, Bondolfi L, Stalder M, et al. Cholinergic changes in the APP23 transgenic mouse model of cerebral amyloidosis. J Neurosci. 2002;22:3234-43 pubmed
    ..Moreover, our results suggest that disruption of the basal cholinergic forebrain system does not promote cerebral amyloidosis in APP23 transgenic mice. ..
  29. Jan A, Adolfsson O, Allaman I, Buccarello A, Magistretti P, Pfeifer A, et al. Abeta42 neurotoxicity is mediated by ongoing nucleated polymerization process rather than by discrete Abeta42 species. J Biol Chem. 2011;286:8585-96 pubmed publisher
  30. Miklossy J. Emerging roles of pathogens in Alzheimer disease. Expert Rev Mol Med. 2011;13:e30 pubmed publisher
    ..Global attention and action is needed to support this emerging field of research because dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy. ..
  31. von Kienlin M, Künnecke B, Metzger F, Steiner G, Richards J, Ozmen L, et al. Altered metabolic profile in the frontal cortex of PS2APP transgenic mice, monitored throughout their life span. Neurobiol Dis. 2005;18:32-9 pubmed
    ..These noninvasive biomarkers can be exploited in preclinical pharmaceutical research to cope with the high variability in transgenic animal models and to enhance the power of drug efficacy studies. ..
  32. Janssens J, Pautex S, Hilleret H, Michel J. Sleep disordered breathing in the elderly. Aging (Milano). 2000;12:417-29 pubmed
    ..The possibility of SDB should be considered in the elderly in the differential diagnosis of "reversible dementias", increased daytime sleepiness, or unexplained right-sided heart failure...
  33. Abramowski D, Rabe S, Upadhaya A, Reichwald J, Danner S, Staab D, et al. Transgenic expression of intraneuronal A?42 but not A?40 leads to cellular A? lesions, degeneration, and functional impairment without typical Alzheimer's disease pathology. J Neurosci. 2012;32:1273-83 pubmed publisher
    ..While intracellular membrane expression of A?1-42 in APP48 mice does not lead to the AD-typical lesions, A? aggregates develop within cells accompanied by considerable neurodegeneration. ..
  34. Dubovik S, Bouzerda Wahlen A, Nahum L, Gold G, Schnider A, Guggisberg A. Adaptive reorganization of cortical networks in Alzheimer's disease. Clin Neurophysiol. 2013;124:35-43 pubmed publisher
    ..Not only dysfunctional but also adaptive network reorganization occurs in early AD. The network mechanisms for preserved cognitive functioning may inform novel treatment strategies for AD in the future. ..
  35. Yalak G, Vogel V. Extracellular phosphorylation and phosphorylated proteins: not just curiosities but physiologically important. Sci Signal. 2012;5:re7 pubmed publisher
  36. Jan A, Gokce O, Luthi Carter R, Lashuel H. The ratio of monomeric to aggregated forms of Abeta40 and Abeta42 is an important determinant of amyloid-beta aggregation, fibrillogenesis, and toxicity. J Biol Chem. 2008;283:28176-89 pubmed publisher
  37. Freidel S, Martin Sölch C, Schreiter Gasser U. [Alzheimer's dementia or cerebral toxoplasmosis? Case study of dementia following toxoplasmosis infection]. Nervenarzt. 2002;73:874-8 pubmed
    ..Since the results of the PET examination indicated changes in the glucose metabolism typical of Alzheimer's disease, we infer a comorbidity of cerebral toxoplasmosis and dementia of Alzheimer type. ..
  38. Jeong J, Ansaloni A, Mezzenga R, Lashuel H, Dietler G. Novel mechanistic insight into the molecular basis of amyloid polymorphism and secondary nucleation during amyloid formation. J Mol Biol. 2013;425:1765-81 pubmed publisher
    ..g., diffuse versus amyloid plaques), and of the structural basis of A? toxicity. ..
  39. Fischer F, Molinari M, Bodendorf U, Paganetti P. The disulphide bonds in the catalytic domain of BACE are critical but not essential for amyloid precursor protein processing activity. J Neurochem. 2002;80:1079-88 pubmed
  40. Miklossy J. Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria. J Neuroinflammation. 2011;8:90 pubmed publisher
    ..Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia. ..
  41. Krstic D, Pfister S, Notter T, Knuesel I. Decisive role of Reelin signaling during early stages of Alzheimer's disease. Neuroscience. 2013;246:108-16 pubmed publisher
  42. Dimitrov M, Alattia J, Lemmin T, Lehal R, Fligier A, Houacine J, et al. Alzheimer's disease mutations in APP but not ?-secretase modulators affect epsilon-cleavage-dependent AICD production. Nat Commun. 2013;4:2246 pubmed publisher
    ..Molecular simulations suggest that familial Alzheimer's disease mutations modulate the flexibility of the APP transmembrane domain and the presentation of its ?-site, modifying at the same time, the solvation of the ?-site. ..
  43. Karagöz G, Duarte A, Akoury E, Ippel H, Biernat J, Morán Luengo T, et al. Hsp90-Tau complex reveals molecular basis for specificity in chaperone action. Cell. 2014;156:963-74 pubmed publisher
    ..Our model resolves the paradox of how Hsp90 specifically selects for late folding intermediates but also for some intrinsically disordered proteins-through the eyes of Hsp90 they look the same. ..
  44. Giannakopoulos P, Gold G, Duc M, Michel J, Hof P, Bouras C. Neuroanatomic correlates of visual agnosia in Alzheimer's disease: a clinicopathologic study. Neurology. 1999;52:71-7 pubmed
    ..To examine the neuroanatomic correlates of visual agnosia in AD...
  45. Giannakopoulos P, Kovari E, French L, Viard I, Hof P, Bouras C. Possible neuroprotective role of clusterin in Alzheimer's disease: a quantitative immunocytochemical study. Acta Neuropathol. 1998;95:387-94 pubmed
  46. Ostrowitzki S, Deptula D, Thurfjell L, Barkhof F, Bohrmann B, Brooks D, et al. Mechanism of amyloid removal in patients with Alzheimer disease treated with gantenerumab. Arch Neurol. 2012;69:198-207 pubmed publisher
    ..Gantenerumab induced phagocytosis of human amyloid in a dose-dependent manner ex vivo. Gantenerumab treatment resulted in a dose-dependent reduction in brain amyloid level, possibly through an effector cell-mediated mechanism of action. ..
  47. Zurbriggen R, Amacker M, Kammer A, Westerfeld N, Borghgraef P, Van Leuven F, et al. Virosome-based active immunization targets soluble amyloid species rather than plaques in a transgenic mouse model of Alzheimer's disease. J Mol Neurosci. 2005;27:157-66 pubmed
    ..The high specific antibody responses, obtained without eliciting T-cell reactivity, demonstrate that immunostimulating reconstituted influenza virosomes are a promising antigen carrier system against the neuropathology of AD. ..
  48. von Rotz R, Kins S, Hipfel R, von der Kammer H, Nitsch R. The novel cytosolic RING finger protein dactylidin is up-regulated in brains of patients with Alzheimer's disease. Eur J Neurosci. 2005;21:1289-98 pubmed
    ..However, the up-regulation of dactylidin in highly vulnerable brain tissues of AD patients was confirmed by a quantitative PCR approach, suggesting that dactylidin may function early in the progression of neurodegenerative diseases. ..
  49. Reichwald J, Danner S, Wiederhold K, Staufenbiel M. Expression of complement system components during aging and amyloid deposition in APP transgenic mice. J Neuroinflammation. 2009;6:35 pubmed publisher
    ..The low expression of C3 and C5 and failure to upregulate C5 and downstream components differs from human AD brain and likely contributes to the lack of full complement activation in APP transgenic mice. ..
  50. Hock C, Heese K, Muller Spahn F, Hulette C, Rosenberg C, Otten U. Decreased trkA neurotrophin receptor expression in the parietal cortex of patients with Alzheimer's disease. Neurosci Lett. 1998;241:151-4 pubmed
    ..These results reveal a central specific role of the high affinity NGF receptor during neurodegeneration in AD. ..
  51. Zekry D, Herrmann F, Irminger Finger I, Graf C, Genet C, Vitale A, et al. Telomere length and ApoE polymorphism in mild cognitive impairment, degenerative and vascular dementia. J Neurol Sci. 2010;299:108-11 pubmed publisher
    ..9; p=0.016). This longitudinal study in very old patients provided no evidence suggesting that telomere length alone could be used to distinguish between the different types of dementia or MCI, nor combined with the ApoE polymorphism. ..
  52. Bot N, Schweizer C, Ben Halima S, Fraering P. Processing of the synaptic cell adhesion molecule neurexin-3beta by Alzheimer disease alpha- and gamma-secretases. J Biol Chem. 2011;286:2762-73 pubmed publisher
    ..We further report that this processing is altered by several PS1 mutations in the catalytic subunit of the ?-secretase that cause early-onset familial Alzheimer disease. ..
  53. Wollmer M, Streffer J, Tsolaki M, Grimaldi L, Lutjohann D, Thal D, et al. Genetic association of acyl-coenzyme A: cholesterol acyltransferase with cerebrospinal fluid cholesterol levels, brain amyloid load, and risk for Alzheimer's disease. Mol Psychiatry. 2003;8:635-8 pubmed
    ..005). This polymorphism of SOAT1 is also associated with reduced risk for Alzheimer's disease in ethnically distinct populations (P=0.0001, odds ratio: 0.6, 95% confidence interval 0.4-0.8). ..
  54. Wollmer M, Papassotiropoulos A, Streffer J, Grimaldi L, Kapaki E, Salani G, et al. Genetic polymorphisms and cerebrospinal fluid levels of tissue inhibitor of metalloproteinases 1 in sporadic Alzheimer's disease. Psychiatr Genet. 2002;12:155-60 pubmed
    ..In addition, no significant differences were observed after stratification for TIMP 1 genotypes. Our data show that neither genetic variability nor protein levels of TIMP-1 are associated with AD. ..
  55. Boncristiano S, Calhoun M, Howard V, Bondolfi L, Kaeser S, Wiederhold K, et al. Neocortical synaptic bouton number is maintained despite robust amyloid deposition in APP23 transgenic mice. Neurobiol Aging. 2005;26:607-13 pubmed
    ..Our results suggest that cerebral amyloidosis is not sufficient to account for the global synapse loss in AD. Alternatively, a putative trophic effect of APP may prevent, compensate, or delay a loss of synapses in this mouse model. ..
  56. Papassotiropoulos A, Bagli M, Becker K, Jessen F, Maier W, Rao M, et al. No association between an intronic biallelic polymorphism of the FE65 gene and Alzheimer's disease. Int J Mol Med. 2000;6:587-9 pubmed
    ..We conclude that, whereas FE65 is implicated in AD pathology, the gene encoding FE65 does not appear to confer a substantial risk for AD. ..
  57. Mbefo M, Paleologou K, Boucharaba A, Oueslati A, Schell H, Fournier M, et al. Phosphorylation of synucleins by members of the Polo-like kinase family. J Biol Chem. 2010;285:2807-22 pubmed publisher
  58. Burgermeister P, Calhoun M, Winkler D, Jucker M. Mechanisms of cerebrovascular amyloid deposition. Lessons from mouse models. Ann N Y Acad Sci. 2000;903:307-16 pubmed
    ..The possibility to cross genetically defined mouse models of CAA with other mutant mice now has the potential to identify molecular mechanisms of CAA. ..
  59. Beeler N, Riederer B, Waeber G, Abderrahmani A. Role of the JNK-interacting protein 1/islet brain 1 in cell degeneration in Alzheimer disease and diabetes. Brain Res Bull. 2009;80:274-81 pubmed publisher
    ..This review discusses the role of the IB1/JIP-1 and the JNK pathway in the molecular pathogenesis of AD and T2D. ..
  60. Riederer I, Schiffrin M, Kovari E, Bouras C, Riederer B. Ubiquitination and cysteine nitrosylation during aging and Alzheimer's disease. Brain Res Bull. 2009;80:233-41 pubmed publisher
    ..Since reactive astrocytes localized prominently around senile plaques one can speculate that elements of plaques such as beta-amyloid proteins may activate surrounding glial elements and proteins. ..
  61. Pietropaolo S, Sun Y, Li R, Brana C, Feldon J, Yee B. The impact of voluntary exercise on mental health in rodents: a neuroplasticity perspective. Behav Brain Res. 2008;192:42-60 pubmed publisher
  62. Gschwind M, Huber G. Introduction of hereditary disease-associated mutations into the beta-amyloid precursor protein gene of mouse embryonic stem cells: a comparison of homologous recombination methods. Mol Cell Biol. 1998;18:4651-8 pubmed
    ..For further improvements, optimization of the homologous recombination efficiency could be envisaged. ..