Beta Amyloid Peptide: August 2011

Beta Amyloid Protein Alzheimer's ~ Research Papers on Beta Amyloid Protein Alzheimer's


Beta Amyloid Protein Alzheimer's ~ Research Papers on Beta Amyloid Protein Alzheimer's

Wang HY, Lee DH, D'Andrea MR, Peterson PA, Shank RP, Reitz AB. beta-Amyloid(1-42) binds to alpha7 nicotinic acetylcholine receptor with high affinity. Implications for Alzheimer's disease pathology. J Biol Chem. 2000 Feb 25;275(8):5626-32.

Corrigan FM, Wienburg CL, Shore RF, Daniel SE, Mann D. Organochlorine insecticides in substantia nigra in Parkinson's disease. J Toxicol Environ Health A. 2000 Feb 25;59(4):229-34.


Gong CX, Lidsky T, Wegiel J, Zuck L, Grundke-Iqbal I, Iqbal K. Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease. J Biol Chem. 2000 Feb 25;275(8):5535-44.

  
Mulnard RA, Cotman CW, Kawas C, van Dyck CH, Sano M, Doody R, Koss E, Pfeiffer E, Jin S, Gamst A, Grundman M, Thomas R, Thal LJ. Estrogen replacement therapy for treatment of mild to moderate Alzheimer disease: a randomized controlled trial. Alzheimer's Disease Cooperative Study. JAMA. 2000 Feb 23;283(8):1007-15.
    

Manly JJ, Merchant CA, Jacobs DM, Small SA, Bell K, Ferin M, Mayeux R. Endogenous estrogen levels and Alzheimer's disease among postmenopausal women. Neurology. 2000 Feb 22;54(4):833-7.

Ala TA, Beh GO, Frey WH. Pure hippocampal sclerosis: a rare cause of dementia mimicking Alzheimer's disease. Neurology. 2000 Feb 22;54(4):843-8.

Tapiola T, Pirttilä T, Mikkonen M, Mehta PD, Alafuzoff I, Koivisto K, Soininen H. Three-year follow-up of cerebrospinal fluid tau, beta-amyloid 42 and 40 concentrations in Alzheimer's disease. Neurosci Lett. 2000 Feb 18;280(2):119-22. ,

MacManus A, Ramsden M, Murray M, Henderson Z, Pearson HA, Campbell VA. Enhancement of (45)Ca(2+) influx and voltage-dependent Ca(2+) channel activity by beta-amyloid-(1-40) in rat cortical synaptosomes and cultured cortical neurons. Modulation by the proinflammatory cytokine interleukin-1beta. J Biol Chem. 2000 Feb 18;275(7):4713-8.

Kosasa T, Kuriya Y, Matsui K, Yamanishi Y. Inhibitory effect of orally administered donepezil hydrochloride (E2020), a novel treatment for Alzheimer's disease, on cholinesterase activity in rats. Eur J Pharmacol. 2000 Feb 18;389(2-3):173-9.


Troy CM, Rabacchi SA, Friedman WJ, Frappier TF, Brown K, Shelanski ML. Caspase-2 mediates neuronal cell death induced by beta-amyloid. J Neurosci. 2000 Feb 15;20(4):1386-92.


Mattson MP, Zhu H, Yu J, Kindy MS. Presenilin-1 mutation increases neuronal vulnerability to focal ischemia in vivo and to hypoxia and glucose deprivation in cell culture: involvement of perturbed calcium homeostasis. J Neurosci. 2000 Feb 15;20(4):1358-64.

Rockwell P, Yuan H, Magnusson R, Figueiredo-Pereira ME. Proteasome inhibition in neuronal cells induces a proinflammatory response manifested by upregulation of cyclooxygenase-2, its accumulation as ubiquitin conjugates, and production of the prostaglandin PGE(2). Arch Biochem Biophys. 2000 Feb 15;374(2):325-33.

  
Lin X, Koelsch G, Wu S, Downs D, Dashti A, Tang J. Human aspartic protease memapsin 2 cleaves the beta-secretase site of beta-amyloid precursor protein. Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1456-60.


Giasson BI, Jakes R, Goedert M, Duda JE, Leight S, Trojanowski JQ, Lee VM. A panel of epitope-specific antibodies detects protein domains distributed throughout human alpha-synuclein in Lewy bodies of Parkinson's disease. J Neurosci Res. 2000 Feb 15;59(4):528-33.

Panegyres PK, Zafiris-Toufexis K, Kakulas BA. Amyloid precursor protein gene isoforms in Alzheimer's disease and other neurodegenerative disorders. J Neurol Sci. 2000 Feb 15;173(2):81-92.

Blain H, Jouzeau JY, Blain A, Terlain B, Tréchot P, Touchon J, Netter P, Jeandel C. [Non-steroidal anti-inflammatory drugs with selectivity for cyclooxygenase-2 in Alzheimer's disease. Rationale and perspectives] Presse Med. 2000 Feb 12;29(5):267-73.

Theuns J, Del-Favero J, Dermaut B, van Duijn CM, Backhovens H, Van den Broeck MV, Serneels S, Corsmit E, Van Broeckhoven CV, Cruts M. Genetic variability in the regulatory region of presenilin 1 associated with risk for Alzheimer's disease and variable expression. Hum Mol Genet. 2000 Feb 12;9(3):325-31. ,

Hamanaka H, Katoh-Fukui Y, Suzuki K, Kobayashi M, Suzuki R, Motegi Y, Nakahara Y, Takeshita A, Kawai M, Ishiguro K, Yokoyama M, Fujita SC. Altered cholesterol metabolism in human apolipoprotein E4 knock-in mice. Hum Mol Genet. 2000 Feb 12;9(3):353-61.
 

Wetterberg L. [Mental disease a heritage. New genetic knowledge can reveal "public diseases" such as autism, dyslexia, alcoholism, anorexia, schizophrenia] Lakartidningen. 2000 Feb 9;97(6):558-62, 565-7.


Aisen PS, Davis KL, Berg JD, Schafer K, Campbell K, Thomas RG, Weiner MF, Farlow MR, Sano M, Grundman M, Thal LJ. A randomized controlled trial of prednisone in Alzheimer's disease. Alzheimer's Disease Cooperative Study. Neurology. 2000 Feb 8;54(3):588-93.

Xu W, Liu L, Emson P, Harrington CR, McKeith IG, Perry RH, Morris CM, Charles IG. The CCTTT polymorphism in the NOS2A gene is associated with dementia with Lewy bodies. Neuroreport. 2000 Feb 7;11(2):297-9. ,

Matsumoto A. The 68K protease has beta-secretase-like activity for lymphocyte precursor protein but not for brain substrate. Neuroreport. 2000 Feb 7;11(2):373-7.

Jarskog LF, Gilmore JH. Developmental expression of Bcl-2 protein in human cortex. Brain Res Dev Brain Res. 2000 Feb 7;119(2):225-30.

Evin G, Le Brocque D, Culvenor JG, Galatis D, Weidemann A, Beyreuther K, Masters CL, Cappai R. Presenilin I expression in yeast lowers secretion of the amyloid precursor protein. Neuroreport. 2000 Feb 7;11(2):405-8.

Lovell MA, Xie C, Markesbery WR. Decreased base excision repair and increased helicase activity in Alzheimer's disease brain. Brain Res. 2000 Feb 7;855(1):116-23.

Ho LH, Ratnaike RN, Zalewski PD. Involvement of intracellular labile zinc in suppression of DEVD-caspase activity in human neuroblastoma cells. Biochem Biophys Res Commun. 2000 Feb 5;268(1):148-54.

Shirotani K, Takahashi K, Araki W, Maruyama K, Tabira T. Mutational analysis of intrinsic regions of presenilin 2 that determine its endoproteolytic cleavage and pathological function. J Biol Chem. 2000 Feb 4;275(5):3681-6.

Sester M, Feuerbach D, Frank R, Preckel T, Gutermann A, Burgert HG. The amyloid precursor-like protein 2 associates with the major histocompatibility complex class I molecule K(d). J Biol Chem. 2000 Feb 4;275(5):3645-54.


Kimberly WT, Xia W, Rahmati T, Wolfe MS, Selkoe DJ. The transmembrane aspartates in presenilin 1 and 2 are obligatory for gamma-secretase activity and amyloid beta-protein generation. J Biol Chem. 2000 Feb 4;275(5):3173-8.

Romas SN, Mayeux R, Rabinowitz D, Tang MX, Zadroga HR, Lantigua R, Medrano M, Tycko B, Knowles JA. The deletion polymorphism and Val1000Ile in alpha-2-macroglobulin and Alzheimer disease in Caribbean Hispanics. Neurosci Lett. 2000 Feb 4;279(3):133-6. ,

Ikegami S, Harada A, Hirokawa N. Muscle weakness, hyperactivity, and impairment in fear conditioning in tau-deficient mice. Neurosci Lett. 2000 Feb 4;279(3):129-32.

Roberts JS. Anticipating response to predictive genetic testing for Alzheimer's disease: a survey of first-degree relatives. Gerontologist. 2000 Feb 1;40(1):43-52.

Taylor R. National Adult Reading Test performance in established dementia. Arch Gerontol Geriatr. 2000 Feb;29(3):291-296.

Ishii H, Meguro K, Ishizaki J, Shimada M, Yamaguchi S, Sano I, Ambo H, Ohtake H, Shimada Y, Someya K, Sato M, Shibuya Y, Kato M, Sekita Y, Yamadori A. Prevalence of senile dementia in a rural community in Japan: the Tajiri project. Arch Gerontol Geriatr. 2000 Feb;29(3):249-265.

Zaman SH, Parent A, Laskey A, Lee MK, Borchelt DR, Sisodia SS, Malinow R. Enhanced synaptic potentiation in transgenic mice expressing presenilin 1 familial Alzheimer's disease mutation is normalized with a benzodiazepine. Neurobiol Dis. 2000 Feb;7(1):54-63.

Bregman DB, Pestell RG, Kidd VJ. Cell cycle regulation and RNA polymerase II. Front Biosci. 2000 Feb 1;5:D244-57.


Chui HC, Mack W, Jackson JE, Mungas D, Reed BR, Tinklenberg J, Chang FL, Skinner K, Tasaki C, Jagust WJ. Clinical criteria for the diagnosis of vascular dementia: a multicenter study of comparability and interrater reliability. Arch Neurol. 2000 Feb;57(2):191-6.

Farrer LA, Sherbatich T, Keryanov SA, Korovaitseva GI, Rogaeva EA, Petruk S, Premkumar S, Moliaka Y, Song YQ, Pei Y, Sato C, Selezneva ND, Voskresenskaya S, Golimbet V, Sorbi S, Duara R, Gavrilova S, St George-Hyslop PH, Rogaev EI. Association between angiotensin-converting enzyme and Alzheimer disease. Arch Neurol. 2000 Feb;57(2):210-4. , ,

Maruyama H, Toji H, Harrington CR, Sasaki K, Izumi Y, Ohnuma T, Arai H, Yasuda M, Tanaka C, Emson PC, Nakamura S, Kawakami H. Lack of an association of estrogen receptor alpha gene polymorphisms and transcriptional activity with Alzheimer disease. Arch Neurol. 2000 Feb 1;57(2):236-40. ,


Gouras GK, Xu H, Gross RS, Greenfield JP, Hai B, Wang R, Greengard P. Testosterone reduces neuronal secretion of Alzheimer's beta-amyloid peptides. Proc Natl Acad Sci U S A. 2000 Feb 1;97(3):1202-5.


Grundman M. Vitamin E and Alzheimer disease: the basis for additional clinical trials. Am J Clin Nutr. 2000 Feb;71(2):630S-636S.


St George-Hyslop PH. Molecular genetics of Alzheimer's disease. Biol Psychiatry. 2000 Feb 1;47(3):183-99.

Schippling S, Kontush A, Arlt S, Buhmann C, Stürenburg HJ, Mann U, Müller-Thomsen T, Beisiegel U. Increased lipoprotein oxidation in Alzheimer's disease. Free Radic Biol Med. 2000 Feb 1;28(3):351-60.

Licastro F, Pedrini S, Caputo L, Annoni G, Davis LJ, Ferri C, Casadei V, Grimaldi LM. Increased plasma levels of interleukin-1, interleukin-6 and alpha-1-antichymotrypsin in patients with Alzheimer's disease: peripheral inflammation or signals from the brain? J Neuroimmunol. 2000 Feb 1;103(1):97-102. ,

Yamaguchi S, Tsuchiya H, Yamagata S, Toyoda G, Kobayashi S. Event-related brain potentials in response to novel sounds in dementia. Clin Neurophysiol. 2000 Feb;111(2):195-203.

Grant WB. Fish consumption, cancer, and Alzheimer disease. Am J Clin Nutr. 2000 Feb;71(2):599-600.

Altamirano CV, Bartels CF, Lockridge O. The butyrylcholinesterase K-variant shows similar cellular protein turnover and quaternary interaction to the wild-type enzyme. J Neurochem. 2000 Feb;74(2):869-77.

Hellström-Lindahl E, Moore H, Nordberg A. Increased levels of tau protein in SH-SY5Y cells after treatment with cholinesterase inhibitors and nicotinic agonists. J Neurochem. 2000 Feb;74(2):777-84.

Mattson MP, Culmsee C, Yu Z, Camandola S. Roles of nuclear factor kappaB in neuronal survival and plasticity. J Neurochem. 2000 Feb;74(2):443-56.

Yasuda M, Maeda S, Kawamata T, Tamaoka A, Yamamoto Y, Kuroda S, Maeda K, Tanaka C. Novel presenilin-1 mutation with widespread cortical amyloid deposition but limited cerebral amyloid angiopathy. J Neurol Neurosurg Psychiatry. 2000 Feb;68(2):220-3.

Pastor P, Ezquerra M, Muñoz E, Martí MJ, Blesa R, Tolosa E, Oliva R. Significant association between the tau gene A0/A0 genotype and Parkinson's disease. Ann Neurol. 2000 Feb;47(2):242-5.

Cotman SL, Halfter W, Cole GJ. Agrin binds to beta-amyloid (Abeta), accelerates abeta fibril formation, and is localized to Abeta deposits in Alzheimer's disease brain. Mol Cell Neurosci. 2000 Feb;15(2):183-98.

Yoshiyama Y, Asahina M, Hattori T. Selective distribution of matrix metalloproteinase-3 (MMP-3) in Alzheimer's disease brain. Acta Neuropathol (Berl). 2000 Feb;99(2):91-5.

Stoltzner SE, Grenfell TJ, Mori C, Wisniewski KE, Wisniewski TM, Selkoe DJ, Lemere CA. Temporal accrual of complement proteins in amyloid plaques in Down's syndrome with Alzheimer's disease. Am J Pathol. 2000 Feb;156(2):489-99.

Mizuno K, Wakai M, Takeda A, Sobue G. Medial temporal atrophy and memory impairment in early stage of Alzheimer's disease: an MRI volumetric and memory assessment study. J Neurol Sci. 2000 Feb 1;173(1):18-24.

Arlt S, Finckh B, Beisiegel U, Kontush A. Time-course of oxidation of lipids in human cerebrospinal fluid in vitro. Free Radic Res. 2000 Feb;32(2):103-14.

Shimohama S. [Changes in apoptosis-regulating proteins in Alzheimer's disease: comparison with development and aging] Tanpakushitsu Kakusan Koso. 2000 Feb;45(3 Suppl):532-6.

Ruotsalainen S, Miettinen R, MacDonald E, Koivisto E, Sirviö J. Blockade of muscarinic, rather than nicotinic, receptors impairs attention, but does not interact with serotonin depletion. Psychopharmacology (Berl). 2000 Feb;148(2):111-23.

Metzger MM. Glucose enhancement of a facial recognition task in young adults. Physiol Behav. 2000 Feb;68(4):549-53.

Hösli E, Rühl W, Hösli L. Histochemical and electrophysiological evidence for estrogen receptors on cultured astrocytes: colocalization with cholinergic receptors. Int J Dev Neurosci. 2000 Feb;18(1):101-11.

Celsis P. Age-related cognitive decline, mild cognitive impairment or preclinical Alzheimer's disease? Ann Med. 2000 Feb;32(1):6-14.

Bartolomeo AC, Morris H, Buccafusco JJ, Kille N, Rosenzweig-Lipson S, Husbands MG, Sabb AL, Abou-Gharbia M, Moyer JA, Boast CA. The preclinical pharmacological profile of WAY-132983, a potent M1 preferring agonist. J Pharmacol Exp Ther. 2000 Feb;292(2):584-96.

Vickers JC, Dickson TC, Adlard PA, Saunders HL, King CE, McCormack G. The cause of neuronal degeneration in Alzheimer's disease. Prog Neurobiol. 2000 Feb 1;60(2):139-65.

Rivas-Vazquez RA, Carrazana EJ, Rey GJ, Blais MA, Racher DA. Alzheimer's disease: pharmacological treatment and management. Clin Neuropsychol. 2000 Feb;14(1):93-109.

Hugon J, Esclaire F, Terro F, Yardin C. [Apoptosis and Alzheimer disease. Contribution of cellular and transgenic models] Rev Neurol (Paris). 2000 Feb;156(2):123-5.

Fankhauser F, Ricka J, Rol P, Kwasniewska S, Niederer P. [Protein-condensation diseases--molecular basis of cataract formation] Klin Monatsbl Augenheilkd. 2000 Feb;216(2):75-8.

Schölzel-Dorenbos CJ. [Measurement of quality of life in patients with dementia of Alzheimer type and their caregivers: Schedule for the Evaluation of Individual Quality of Life (SEIQoL)] Tijdschr Gerontol Geriatr. 2000 Feb;31(1):23-6.

De Groot CJ, Montagne L, Janssen I, Ravid R, Van Der Valk P, Veerhuis R. Isolation and characterization of adult microglial cells and oligodendrocytes derived from postmortem human brain tissue. Brain Res Brain Res Protoc. 2000 Feb;5(1):85-94.

Skovronsky DM, Pijak DS, Doms RW, Lee VM. A distinct ER/IC gamma-secretase competes with the proteasome for cleavage of APP. Biochemistry. 2000 Feb 1;39(4):810-7.

Williams RS, Harwood AJ. Lithium therapy and signal transduction. Trends Pharmacol Sci. 2000 Feb;21(2):61-4.

Wang Z, Natte , Berliner , van Duinen , Vinters . Toxicity of Dutch (E22Q) and Flemish (A21G) mutant amyloid beta proteins to human cerebral microvessel and aortic smooth muscle cells. Stroke. 2000 Feb;31(2):534-8. Abstract

Kwok JB, Li QX, Hallupp M, Whyte S, Ames D, Beyreuther K, Masters CL, Schofield PR. Novel Leu723Pro amyloid precursor protein mutation increases amyloid beta42(43) peptide levels and induces apoptosis. Ann Neurol. 2000 Feb;47(2):249-53.

  
Lütjohann D, Papassotiropoulos A, Björkhem I, Locatelli S, Bagli M, Oehring RD, Schlegel U, Jessen F, Rao ML, von Bergmann K, Heun R. Plasma 24S-hydroxycholesterol (cerebrosterol) is increased in Alzheimer and vascular demented patients. J Lipid Res. 2000 Feb;41(2):195-8. ,

Gieffers J, Reusche E, Solbach W, Maass M. Failure to detect Chlamydia pneumoniae in brain sections of Alzheimer's disease patients. J Clin Microbiol. 2000 Feb;38(2):881-2.
    

Metodiewa D, Koska C. Reactive oxygen species and reactive nitrogen species: relevance to cyto(neuro)toxic events and neurologic disorders. An overview. Neurotox Res. 2000 Feb;1(3):197-233.


Shoji M, Kawarabayashi T, Matsubara E, Ikeda M, Ishiguro K, Harigaya Y, Okamoto K. Distribution of amyloid beta protein precursor in the Alzheimer's disease brain. Psychiatry Clin Neurosci. 2000 Feb;54(1):45-54.

Ishii H, Meguro K, Ishizaki J, Shimada M, Yamaguchi S, Sano I, Ambo H, Ohtake H, Shimada Y, Someya K, Sato M, Shibuya Y, Kato M, Sekita Y, Yamadori A. Prevalence of senile dementia in a rural community in Japan: the Tajiri project. Arch Gerontol Geriatr. 2000 Feb;29(3):249-65.

Londos E, Passant U, Gustafson L. Blood pressure and drug treatment in clinically diagnosed Lewy body dementia and Alzheimer's disease. Arch Gerontol Geriatr. 2000 Feb;30(1):35-46.

Clare L, Wilson BA, Carter G, Breen K, Gosses A, Hodges JR. Intervening with everyday memory problems in dementia of Alzheimer type: an errorless learning approach. J Clin Exp Neuropsychol. 2000 Feb;22(1):132-46.

Camps P, Cusack B, Mallender WD, El Achab RE, Morral J, Muñoz-Torrero D, Rosenberry TL. Huprine X is a novel high-affinity inhibitor of acetylcholinesterase that is of interest for treatment of Alzheimer's disease. Mol Pharmacol. 2000 Feb;57(2):409-17.

Ramassamy C, Averill D, Beffert U, Theroux L, Lussier-Cacan S, Cohn JS, Christen Y, Schoofs A, Davignon J, Poirier J. Oxidative insults are associated with apolipoprotein E genotype in Alzheimer's disease brain. Neurobiol Dis. 2000 Feb;7(1):23-37.

van Dyck CH, Newhouse P, Falk WE, Mattes JA. Extended-release physostigmine in Alzheimer disease: a multicenter, double-blind, 12-week study with dose enrichment. Physostigmine Study Group. Arch Gen Psychiatry. 2000 Feb;57(2):157-64.

Shimohama S. Apoptosis in Alzheimer's disease--an update. Apoptosis. 2000 Feb;5(1):9-16.

Lackey BR, Gray SL, Henricks DM. Actions and interactions of the IGF system in Alzheimer's disease: review and hypotheses. Growth Horm IGF Res. 2000 Feb;10(1):1-13.

Ribaut-Barassin C, Moussaoui S, Brugg B, Haeberlé AM, Huber G, Imperato A, Delhaye-Bouchaud N, Mariani J, Bailly YJ. Hemisynaptic distribution patterns of presenilins and beta-APP isoforms in the rodent cerebellum and hippocampus. Synapse. 2000 Feb;35(2):96-110.

Frederikse PH, Zigler SJ, Farnsworth PN, Carper DA. Prion protein expression in mammalian lenses. Curr Eye Res. 2000 Feb;20(2):137-43.

Walker LC, LeVine H. The cerebral proteopathies: neurodegenerative disorders of protein conformation and assembly. Mol Neurobiol. 2000 Feb-Apr;21(1-2):83-95.

Tunstall N, Owen MJ, Williams J, Rice F, Carty S, Lillystone S, Fraser L, Kehoe P, Neill D, Rudrasingham V, Sham P, Lovestone S. Familial influence on variation in age of onset and behavioural phenotype in Alzheimer's disease. Br J Psychiatry. 2000 Feb;176:156-9.

Salib E. Risk factors for Alzheimer's disease. Elder Care. 2000 Feb;11(10):12-5.

McLendon BM, Chen GG, Doraiswamy PM. Current and future treatments for cognitive deficits in dementia. Curr Psychiatry Rep. 2000 Feb;2(1):20-3.


Iwata N, Tsubuki S, Takaki Y, Watanabe K, Sekiguchi M, Hosoki E, Kawashima-Morishima M, Lee HJ, Hama E, Sekine-Aizawa Y, Saido TC. Identification of the major Abeta1-42-degrading catabolic pathway in brain parenchyma: suppression leads to biochemical and pathological deposition. Nat Med. 2000 Feb;6(2):143-50.

Glabe C. Does Alzheimer disease tilt the scales of amyloid degradation versus accumulation? Nat Med. 2000 Feb;6(2):133-4.

Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res. 2000 Feb;32(2):115-24.

APP Beta Amyloid ~ Definition: Overview & Research Papers of APP Beta Amyloid



APP Beta Amyloid ~ Definition: Overview
& Research Papers of APP Beta Amyloid

Amyloid Definition: A type of extracellularly deposited substance composed of an amyloid protein and additional components including HEPARAN SULFATE PROTEOGLYCAN; LAMININ; COLLAGEN TYPE IV; SERUM AMYLOID P-COMPONENT; and APOLIPOPROTEINS E which together form characteristic amyloid fibrils. The core of amyloid fibrils is formed by the stacking of overlapping beta-pleated sheet domains of the amyloid protein. There are many different amyloid proteins that have been found forming the core of the fibrils in vivo. However, amyloid can be formed from any protein that exposes beta-pleated strand conformations during unfolding or refolding. A common characteristic of amyloid is the ability to bind such dyes as CONGO RED and thioflavine.

Amyloid A Protein Definition: The non-circulating form of serum amyloid A protein. It is found deposited in a variety of tissues during AMYLOIDOSIS.
Serum Amyloid A Protein Definition: An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.

Amyloidosis Definition: A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.

amyloidosis Definition: any disease manifested by the pathogenic accumulation of amyloid in organs and tissues.
amyloidosis Definition: A group of diseases in which protein is deposited in specific organs (localized amyloidosis) or throughout the body (systemic amyloidosis). Amyloidosis may be either primary (plasma cell neoplasm) or secondary (caused by a long standing infection or another disease or some types of cancer). Generally, primary amyloidosis affects the nerves, skin, tongue, joints, heart, and liver; secondary amyloidosis often affects the spleen, kidneys, liver, and adrenal glands.

Amyloid beta-Protein Definition: A 4-kDa protein, 39-43 amino acids long, expressed by a gene located on chromosome 21. It is the major protein subunit of the vascular and plaque amyloid filaments in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The protein is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.

Amyloid beta-Protein Precursor Definition: A precursor to the AMYLOID BETA-PROTEIN (beta/A4). Alterations in the expression of the amyloid beta-protein precursor (ABPP) gene, located on chromosome 21, plays a role in the development of the neuropathology common to both ALZHEIMER DISEASE and DOWN SYNDROME. ABPP is associated with the extensive extracellular matrix secreted by neuronal cells. Upon cleavage, this precursor produces three proteins of varying amino acid lengths: 695, 751, and 770. The beta/A4 (695 amino acids) or beta-amyloid protein is the principal component of the extracellular amyloid in senile plaques found in ALZHEIMER DISEASE; DOWN SYNDROME and, to a limited extent, in normal aging.
Cerebral Amyloid Angiopathy Definition: A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)
Amyloid Neuropathies Definition: Disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. Familial, primary (nonfamilial), and secondary forms have been described. Some familial subtypes demonstrate an autosomal dominant pattern of inheritance. Clinical manifestations include sensory loss, mild weakness, autonomic dysfunction, and CARPAL TUNNEL SYNDROME. (Adams et al., Principles of Neurology, 6th ed, p1349)
Senile Plaques Definition: Spherical masses consisting of amyloid fibrils and neuronal processes.
neuritic plaque Definition: plaques consist of amyloid deposits surrounded by a web of astrocytic processes, swollen neurites, and neuron terminals; seen in the cerebral cortex in Alzheimer's disease.

Amyloid Beta A4 Protein Precursor Definition: Encoded by human APP Gene (APP Family), Amyloid Beta A4 Protein Precursor is an N-/O-glycosylated sulfated metal ion-binding type I cell surface protein containing a BPTI protease inhibitor domain. Widely expressed APP is processed by secretases into soluble peptides, membrane-anchored fragments, plaque amyloid components, and cytotoxic fragments. Phosphorylation by Casein Kinases, CDC5, CDC2, and MAPK10 can affect processing, interaction with Fe65, and SHC binding. A kinesin I membrane receptor for cell mobility, adhesion, and axonogenesis/synaptogenesis, APP variants inhibit Notch signaling, regulate copper homeostasis, bind lipoproteins, activate transcription, and enhance apoptosis via G(O) and JIP pathways. NPXY is required for binding protein PID domains, endocytosis, and BaSS sorting. APP defects cause Alzheimer's disease and cerebroarterial amyloidosis.

amyloid protein Definition: OBSOLETE (was not defined before being made obsolete). [GOC:mah]

amyloid protein Definition: extracellular glycoprotein that accumulates in certain pathological conditions, e.g., the paired helical filaments of neuritic plaques in Alzheimer's disease and Down's syndrome; use this term for both the precursor and beta form.
Amyloid Proteins Definition: Proteins that form the core of amyloid fibrils. For example, the core of amyloid A is formed from amyloid A protein, also known as serum amyloid A protein or SAA protein.

Amyloid Beta-Peptide Pathway Definition: Alzheimer's disease is associated with dense aggregations of proteins in the brain called amyloid plaques that contain beta-amyloid fragments as a primary component. If the development of amyloid plaques is responsible for neurodegeneration in Alzheimer's disease, reduction of beta-amyloid formation may prevent the development and progression of disease symptoms. Beta-amyloid fragments are derived from proteolytic processing of amyloid precursor protein (APP) in neurons, and the subsequent release of fragments into the extracellular space. APP in the ER is cleaved at residue 17 by alpha-secretase protease activity encoded by ADAM-10 and TACE. Beta-secretase activity, recently identified as BACE, cleaves in the N-terminus of the beta-amyloid fragment. Gamma-secretase cuts APP within the transmembrane domain at amino acids 40 and 42, releasing the beta-amyloid fragment containing residues 1-40/42 as well as shorter products such as p3 (residues 17-40/42) that requires alpha-secretase cleavage. The gamma-secretase activity requires the transmembrane protein Presenilin-1 that is itself cleaved into an N-terminal and C-terminal fragment that both are required for gamma-secretase activity. Mutations in presenilin-1 have been genetically associated with familial forms of Alzheimer's disease, further supporting the role of APP processing the development of the disease. Inhibition of the beta- or gamma-secretases may provide a mechanism to treat this disease. Other mechanisms may include altering degradation of beta-amyloid, and the use of vaccines against beta-amyloid to remove aggregates. (BioCarta) http://de.dict.md/definition/amyloid
The Hallmarks of AD

Alzheimer’s disease disrupts critical metabolic processes that keep neurons healthy. These disruptions cause nerve cells in the brain to stop working, lose connections with other nerve cells, and finally die. The destruction and death of nerve cells causes the memory failure, personality changes, problems in carrying out daily activities, and other features of the disease.

The brains of people with AD have an abundance of two abnormal structures—amyloid plaques and neurofibrillary tangles—that are made of misfolded proteins (see "Protein Misfolding" for more information). This is especially true in certain regions of the brain that are important in memory.

The third main feature of AD is the loss of connections between cells. This leads to diminished cell function and cell death.

AMYLOID PLAQUES

Amyloid plaques are found in the spaces between the brain’s nerve cells. They were first described by Dr. Alois Alzheimer in 1906. Plaques consist of largely insoluble deposits of an apparently toxic protein peptide, or fragment, called beta-amyloid.

We now know that some people develop some plaques in their brain tissue as they age. However, the AD brain has many more plaques in particular brain regions. We still do not know whether amyloid plaques themselves cause AD or whether they are a by-product of the AD process. We do know that genetic mutations can increase production of beta-amyloid and can cause rare, inherited forms of AD (see "Genes and Early-Onset Alzheimer’s Disease" for more on inherited AD).

To view a video showing what happens to the brain in AD, go to www.nia.nih.gov/Alzheimers/ADvideo .

Amyloid precursor protein (APP) is an integral membrane protein expressed in many tissues and concentrated in the synapses of neurons. Its primary function is not known, though it has been implicated as a regulator of synapse formation[2], neural plasticity[3] and iron export.[4] APP is best known and most commonly studied as the precursor molecule whose proteolysis generates beta amyloid (Aβ), a 39- to 42-amino acid peptide whose amyloid fibrillar form is the primary component of amyloid plaques found in the brains of Alzheimer's disease patients.

Genetics

In humans, the gene for APP is located on chromosome 21 and contains at least 18 exons in 240 kilobases.[5][6] Several alternative splicing isoforms of APP have been observed in humans, ranging in length from 365 to 770 amino acids, with certain isoforms preferentially expressed in neurons; changes in the neuronal ratio of these isoforms have been associated with Alzheimer's disease.[7] Homologous proteins have been identified in other organisms such as Drosophila (fruit flies), C. elegans (roundworms), and all mammals.[8] The amyloid beta region of the protein, located in the membrane-spanning domain, is not well conserved across species and has no obvious connection with APP's native-state biological functions.[8]
Mutations in critical regions of Amyloid Precursor Protein, including the region that generates amyloid beta, are known to cause familial susceptibility to Alzheimer's disease.[9][10][11] For example, several mutations outside the Aβ region associated with familial Alzheimer's have been found to dramatically increase production of Aβ
Structure

A number of distinct, largely independently-folding structural domains have been identified in the APP sequence. The extracellular region, much larger than the intracellular region, is divided into the E1 and E2 domains, linked by an acidic domain (AcD); E1 contains two subdomains including a growth factor-like domain (GFLD) and a copper-binding domain (CuBD) interacting tightly together.[13] A serine protease inhibitor domain, absent from the isoform differentially expressed in the brain, is found between acidic region and E2 domain.[14] The complete crystal structure of APP has not yet been solved; however, individual domains have been successfully crystallized, the growth factor-like domain[15], the copper-binding domain[16], the complete E1 domain[13] and the E2 domain.

Post-translational processing

APP undergoes extensive post-translational modification including glycosylation, phosphorylation, and tyrosine sulfation, as well as many types of proteolytic processing to generate peptide fragments.[17] It is commonly cleaved by proteases in the secretase family; alpha secretase and beta secretase both remove nearly the entire extracellular domain to release membrane-anchored carboxy-terminal fragments that may be associated with apoptosis.[8] Cleavage by gamma secretase within the membrane-spanning domain generates the amyloid-beta fragment; gamma secretase is a large multi-subunit complex whose components have not yet been fully characterized, but include presenilin, whose gene has been identified as a major genetic risk factor for Alzheimer's.

The amyloidogenic processing of APP has been linked to its presence in lipid rafts. When APP molecules occupy a lipid raft region of membrane, they are more accessible to and differentially cleaved by beta secretase, whereas APP molecules outside a raft are differentially cleaved by the non-amyloidogenic alpha secretase.[19] Gamma secretase activity has also been associated with lipid rafts.[20] The role of cholesterol in lipid raft maintenance has been cited as a likely explanation for observations that high cholesterol and apolipoprotein E genotype are major risk factors for Alzheimer's disease.

Biological function

Although the native biological role of APP is of obvious interest to Alzheimer's research, thorough understanding has remained elusive.
Synaptic formation and repair

The most-substantiated role for APP is in synaptic formation and repair;[2] its expression is upregulated during neuronal differentiation and after neural injury. Roles in cell signaling, long-term potentiation, and cell adhesion have been proposed and supported by as-yet limited research.[8] In particular, similarities in post-translational processing have invited comparisons to the signaling role of the surface receptor protein Notch.[22] APP knockout mice are viable and have relatively minor phenotypic effects including impaired long-term potentiation and memory loss without general neuron loss.[23] On the other hand, transgenic mice with upregulated APP expression have also been reported to show impaired long-term potentiation.[24] The logical inference is that because Aβ accumulates excessively in Alzheimer's disease its precursor, APP, would be elevated as well. However, neuronal cell bodies contain less APP as a function of their proximity to amyloid plaques.[25] The data indicate that this deficit in APP results from a decline in production rather than an increase in catalysis. Loss of a neuron's APP may affect physiological deficits that contribute to dementia.
Iron export

A different perspective on Alzheimer's is revealed by a mouse study that has found that APP possesses ferroxidase activity similar to ceruloplasmin, facilitating iron export through interaction with ferroportin; it seems that this activity is blocked by zinc trapped by accumulated Aβ in Alzheimer's.

Hormonal regulation of AβPP expression and processing during embryogenesis and Alzheimer’s disease

The amyloid-β precursor protein (AβPP) and all associated secretases are expressed early in development and plays a key role in the endocrinology of reproduction – with the differential processing of AβPP by secretases regulating human embryonic stem cell (hESC) proliferation as well as their differentiation into neural precursor cells (NPC). The pregnancy hormone human chorionic gonadotropin (hCG) increases AβPP expression [26] and hESC proliferation while progesterone directs AβPP processing towards the non-amyloidogenic pathway which promotes hESC differentiation into NPC

APP and its cleavage products do not promote the proliferation and differentiation of post-mitotic neurons; rather the overexpression of either wild-type or mutant AβPP in post-mitotic neurons induces apoptotic death following their re-entry into the cell cycle (McPhie et al., 2003, J. Neurosci.). It is postulated that the loss of sex steroids (including progesterone) but the elevation in luteinizing hormone, the adult equivalent of hCG, post-menopause and during andropause drives amyloid-β production (Bowen et al., 2004) and re-entry of post-mitotic neurons into the cell cycle.
Arthritis
Recently amyloid precursor protein (APP) origin was demonstrated with arthritogenic animals. The source noted is breakdown of immune complexes, where the amyloid aggregates are left degraded and binds together to form coil like structure that is not resorbed. Finally it induces secondary inflammation which may cause local damage.[30]
Interactions

Amyloid precursor protein has been shown to interact with APBA3,[31][32] CLSTN1,[33][34] APPBP1,[35] Gelsolin,[36] BCAP31,[37] Caveolin 1,[38] FBLN1,[39] Collagen, type XXV, alpha 1,[40] APBB1,[41][42][43][44][45] APBA2,[31][34][46] APBA1,[31][41] APPBP2,[47] HSD17B10,[48] BLMH[49] and SHC1.

One group of scientists reports that APP interacts with reelin, a protein implicated in a number of brain disorders, including Alzheimer's disease. http://en.wikipedia.org/wiki/Amyloid_precursor_protein

Amyloid precursor protein (APP), the starting point for amyloid plaques, is one of many proteins associated with the cell membrane, the barrier that encloses the cell. As it is being made inside the cell, APP becomes embedded in the membrane, like a toothpick stuck through the skin of an orange

In a number of cell compartments, including the outermost cell membrane, specific enzymes snip, or cleave, APP into discrete fragments. In 1999 and 2000, scientists identified the enzymes responsible for cleaving APP. These enzymes are called alpha-secretase, beta-secretase, and gamma-secretase. In a major breakthrough, scientists then discovered that, depending on which enzyme is involved and the segment of APP where the cleaving occurs, APP processing can follow one of two pathways that have very different consequences for the cell.

In the benign pathway, alpha-secretase cleaves the APP molecule within the portion that has the potential to become beta-amyloid. This eliminates the production of the beta-amyloid peptide and the potential for plaque buildup. The cleavage releases from the neuron a fragment called sAPPα, which has beneficial properties, such as promoting neuronal growth and survival. The remaining APP fragment, still tethered in the neuron’s membrane, is then cleaved by gamma-secretase at the end of the beta-amyloid segment. The smaller of the resulting fragments also is released into the space outside the neuron, while the larger fragment remains within the neuron and interacts with factors in the nucleus (Figure 2).

In the harmful pathway, beta-secretase first cleaves the APP molecule at one end of the beta-amyloid peptide, releasing sAPPβ from the cell (Figure 3). Gamma-secretase then cuts the resulting APP fragment, still tethered in the neuron’s membrane, at the other end of the beta-amyloid peptide. Following the cleavages at each end, the beta-amyloid peptide is released into the space outside the neuron and begins to stick to other beta-amyloid peptides (Figure 4). These small, soluble aggregates of two, three, four, or even up to a dozen beta-amyloid peptides are called oligomers. Specific sizes of oligomers may be responsible for reacting with receptors on neighboring cells and synapses, affecting their ability to function.

It is likely that some oligomers are cleared from the brain. Those that cannot be cleared clump together with more beta-amyloid peptides. As the process continues, oligomers grow larger, becoming entities called protofibrils and fibrils. Eventually, other proteins and cellular material are added, and these increasingly insoluble entities combine to become the well-known plaques that are characteristic of AD.

For many years, scientists thought that plaques might cause all of the damage to neurons that is seen in AD. However, that concept has evolved greatly in the past few years. Many scientists now think that oligomers may be a major culprit. Many scientists also think that plaques actually may be a late-stage attempt by the brain to get this harmful beta-amyloid away from neurons. http://www.nia.nih.gov/Alzheimers/Publications/Unraveling/Part2/hallmarks.htm

From APP to Beta Amyloid

APP is one of many proteins associated with the cell membrane, the barrier that encloses the cell. As it is being made inside the cell, APP becomes embedded in the membrane, like a toothpick stuck through the skin of an orange.

There are three enzymes involved in the cleavage of APP: α-secretase, β-secretase and γ-secretase. Depending on which enzyme is involved and the segment of APP where the cleaving occurs, APP processing can follow one of two pathways that have very different consequences for the cell.

In the benign pathway, α-secretase cleaves the APP molecule within the portion that has the potential to become beta-amyloid (Figure). This eliminates the production of the Aβ peptide and the potential for plaque buildup. The cleavage releases from the neuron a fragment called sAPPα, which has beneficial properties, such as promoting neuronal growth and survival. http://www.web-books.com/eLibrary/Medicine/Neurological/Alzheimer_Amyloid.htm

A4, β—amyloid Neurology A 4 kD polypeptide encoded on chromosome 21 arising from altered processing of amyloid precursor protein, an integral membrane glycoprotein secreted as a truncated carboxyl-terminal molecule; BA forms plaques in the brains of Pts with Alzheimer's disease–AD, Down syndrome, infectious encephalopathy, cerebral amyloid angiopathy; BA is found in skin, intestine, adrenal gland. See Alzheimer's disease, Amyloid, Presenilin. Cf Alpha2-macroglobulin. http://medical-dictionary.thefreedictionary.com/beta-amyloid

Amyloid: Any of a number of complex proteins that are deposited in tissues and that share selected laboratory features such as a change in the fluorescence intensity of certain aromatic dyes like Congo Red.

The deposition of amyloid occurs in a number of diseases. In many of these, there is disagreement as to whether amyloid causes the disease or is simply a sign of the disease downstream from the cause. (In Alzheimer's disease, those who believe that the deposition of beta-amyloid protein kills neurons are called baptists.)

Amyloid may be deposited widely in the body, as in systemic amyloidosis. Or the deposition of amyloid may be organ-specific and limited, for instance, to the pancreas, as in type 2 diabetes, or the central nervous system, as in Alzheimer's disease, Parkinson's disease, Huntington disease, Creutzfeldt-Jakob disease and bovine spongiform encephalopathy (mad cow disease).

The term amyloid comes from amylo- (starch) + -oid (like) = like starch. This reflects the mistaken identification of the substance as starch based on crude staining techniques.

Camandola S, Poli G, Mattson MP. The lipid peroxidation product 4-hydroxy-2,3-nonenal inhibits constitutive and inducible activity of nuclear factor kappa B in neurons. Brain Res Mol Brain Res. 2000 Dec 28;85(1-2):53-60. http://www.medterms.com/script/main/art.asp?articlekey=38323

What is the official name of the APP gene?

The official name of this gene is “amyloid beta (A4) precursor protein.”
APP is the gene's official symbol. The APP gene is also known by other names, listed below.

What is the normal function of the APP gene?

The APP gene provides instructions for making a protein called amyloid precursor protein. This protein is found in many tissues and organs, including the brain and spinal cord (central nervous system). Little is known about the function of amyloid precursor protein. Researchers speculate that it may bind to other proteins on the surface of cells or help cells attach to one another.
Amyloid precursor protein is cut by enzymes to create smaller fragments (peptides), some of which are released outside the cell. Two of these fragments are called soluble amyloid precursor protein (sAPP) and amyloid beta peptide. Recent evidence suggests that sAPP has growth-promoting properties and may play a role in the formation of nerve cells (neurons) in the brain both before and after birth. Other functions of sAPP and amyloid beta peptide are under investigation.

How are changes in the APP gene related to health conditions?

Alzheimer disease - caused by mutations in the APP gene More than 25 different mutations in the APP gene can cause early-onset Alzheimer disease. These mutations are responsible for 10 percent to 15 percent of all early-onset cases of the disorder.
The most common APP mutation changes one of the protein building blocks (amino acids) in the amyloid precursor protein. This mutation replaces the amino acid valine with the amino acid isoleucine at protein position 717 (written as Val717Ile or V717I). Mutations in the APP gene can lead to an increased amount of the amyloid beta peptide or to the production of a slightly longer and stickier form of the peptide. When these protein fragments are released from the cell, they can accumulate in the brain and form clumps called amyloid plaques. These plaques are characteristic of Alzheimer disease. A buildup of toxic amyloid beta peptide and amyloid plaques may lead to the death of neurons and the progressive signs and symptoms of this disorder.
other disorders - caused by mutations in the APP gene Certain mutations in the APP gene can also result in brain abnormalities other than Alzheimer disease. For example, a particular APP mutation causes a disorder called hereditary cerebral hemorrhage with amyloidosis-Dutch type. This disorder is characterized by recurring episodes of bleeding in the brain (hemorrhagic strokes) that lead to the deterioration of memory, concentration, and judgment. Most people with this disorder develop signs and symptoms in mid-adulthood. The mutation that causes this disorder replaces the amino acid glutamic acid with the amino acid glutamine at position 22 of amyloid precursor protein (written as Glu22Gln or E22Q). The E22Q mutation likely affects processing of this protein, leading to the formation of amyloid plaques in brain tissue and the walls of blood vessels that serve the brain.

Where is the APP gene located?

Cytogenetic Location: 21q21
image:app.jpg
Molecular Location on chromosome 21: base pairs 26,174,731 to 26,465,002

The APP gene is located on the long (q) arm of chromosome 21 at position 21.
More precisely, the APP gene is located from base pair 26,174,731 to base pair 26,465,002 on chromosome 21.
See How do geneticists indicate the location of a gene? in the Handbook.

Where can I find additional information about APP?

You and your healthcare professional may find the following resources about APP helpful.
·         Educational resources - Information pages
·         Basic Neurochemistry: Molecular, Cellular, and Medical Aspects (sixth edition, 2006): Alzheimer's Disease Is the Most Common Neurodegenerative Disorder
·         Gene Reviews - Clinical summary
·         Gene Tests - DNA tests ordered by healthcare professionals
You may also be interested in these resources, which are designed for genetics professionals and researchers.
·         PubMed - Recent literature
·         OMIM - Genetic disorder catalog (2 links)
·         Research Resources - Tools for researchers (6 links)

What other names do people use for the APP gene or gene products?

·         A4
·         A4_HUMAN
·         AAA
·         ABETA
·         ABPP
·         AD1
·         Amyloid A4 Protein Precursor
·         amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)
·         amyloid beta-peptide
·         Amyloid Of Aging and Alzheimer Disease; AAA
·         amyloid precursor protein
·         APPI
·         Cerebral Vascular Amyloid Peptide
·         CVAP
·         PN-II
·         PreA4
·         protease nexin 2
·         Protease nexin-II
See How are genetic conditions and genes named? in the Handbook.

Where can I find general information about genes?

The Handbook provides basic information about genetics in clear language.
·         What is DNA?
·         What is a gene?
·         How do genes direct the production of proteins?
·         How can gene mutations affect health and development?
These links provide additional genetics resources that may be useful.
·         Genetics education
·         Human Genome Project
·         Resources for Genetic Researchers
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·         Caille I, Allinquant B, Dupont E, Bouillot C, Langer A, Muller U, Prochiantz A. Soluble form of amyloid precursor protein regulates proliferation of progenitors in the adult subventricular zone. Development. 2004 May;131(9):2173-81. Epub 2004 Apr 08. PubMed citation
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·         Harman D. Alzheimer's disease pathogenesis: role of aging. Ann N Y Acad Sci. 2006 May;1067:454-60. Review. PubMed citation
·         Kerr ML, Small DH. Cytoplasmic domain of the beta-amyloid protein precursor of Alzheimer's disease: Function, regulation of proteolysis, and implications for drug development. J Neurosci Res. 2005 Jan 25; [Epub ahead of print]. PubMed citation
·         Levy E, Prelli F, Frangione B. Studies on the first described Alzheimer's disease amyloid beta mutant, the Dutch variant. J Alzheimers Dis. 2006;9(3 Suppl):329-39. Review. PubMed citation
·         Maat-Schieman M, Roos R, van Duinen S. Hereditary cerebral hemorrhage with amyloidosis-Dutch type. Neuropathology. 2005 Dec;25(4):288-97. Review. PubMed citation
·         Majersik JJ, Skalabrin EJ. Single-gene stroke disorders. Semin Neurol. 2006 Feb;26(1):33-48. Review. PubMed citation
·         Papassotiropoulos A, Fountoulakis M, Dunckley T, Stephan DA, Reiman EM. Genetics, transcriptomics, and proteomics of Alzheimer's disease. J Clin Psychiatry. 2006 Apr;67(4):652-70. Review. PubMed citation
·         Rocchi A, Pellegrini S, Siciliano G, Murri L. Causative and susceptibility genes for Alzheimer's disease: a review. Brain Res Bull. 2003 Jun 30; 61(1): 1-24. Review. PubMed citation
·         Wolfe MS, Guénette SY. APP at a glance. J Cell Sci. 2007 Sep 15;120(Pt 18):3157-61. Review. No abstract available. PubMed citation

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Mattson MP. Neuroprotective signaling and the aging brain: take away my food and let me run. Brain Res. 2000 Dec 15;886(1-2):47-53.

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Gulesserian T, Engidawork E, Cairns N, Lubec G. Increased protein levels of serotonin transporter in frontal cortex of patients with Down syndrome. Neurosci Lett. 2000 Dec 15;296(1):53-7.

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The secret of Eta Black by Ananya Sharma

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