My research has been focused on studying how intracellular trafficking is important for cellular function, in particular for neuronal function. It remains fairly unknown how the regulation of intracellular trafficking is important for synaptic function and dysfunction.
Currently, my major goal is to identify which mechanisms of intracellular trafficking in neurons become impaired with aging thus contributing to Alzheimer’s disease development.
We are currently working to answer the following questions:
1. How does neuronal intracellular trafficking contribute to the degradation of beta-amyloid in neurons?
2. How regulators of intracellular trafficking contribute to beta-amyloid accumulation in neurons?
3. How does cellular aging, the main risk factor for Alzheimer’s disease, contribute to beta-amyloid accumulation in neurons?
To answer these questions we use primary neuronal cultures as cellular model. We image the dynamics of intracellular transport in live cells using photoactivatable live reporters, cellular synchronization techniques and high-resolution spinning disk confocal microscopy, in addition to cell biology and biochemistry techniques.
Discover more about the Neuronal Trafficking in Aging Lab
- Investigador FCT
- Marie Curie Integration Grant “Traffic in AD” 2013-2017
- Santander Totta/NOVA University of Lisbon Award
- Guimas Almeida C, Sadat Mirfakhar F, Perdigão C, Burrinha T. (2018) Impact of late-onset Alzheimer's genetic risk factors on beta-amyloid endocytic production. Cell Mol Life Sci. 2018 Apr 27. doi: 10.1007/s00018-018-2825-9. [Epub ahead of print]
- Ubelmann F, Burrinha T, Salavessa L, Gomes R, Ferreira C, Moreno N, Guimas Almeida C. (2016) Bin1 and CD2AP polarise the endocytic generation of beta-amyloid. EMBO Rep. 2016 Nov 28. pii: e201642738. [Epub ahead of print]
- Almeida CG, Yamada A, Tenza D, Louvard D, Raposo G, Coudrier E. Myosin 1b promotes the formation of post-Golgi carriers by regulating actin assembly and membrane remodelling at the trans-Golgi network. Nat Cell Bio. 2011, Jun 12;13(7):779-89. (10 citations; IF = 19.407)
- Tampellini D, Magrane J, Takahashi RH, Li F, Lin MT, Almeida CG, Gouras GK. Internalized Antibodies to the Abeta Domain of APP Reduce Neuronal Abeta and Protect against Synaptic Alterations. J Biol Chem. 2007 Jun 29;282(26):18895-906. (61 citations; IF = 3.603)
- Sahlin C, Lord A, Magnusson K, Englund H, Almeida CG, Greengard P, Nyberg F, Gouras GK, Lannfelt L, Nilsson LN. The Arctic Alzheimer mutation favors intracellular amyloid-beta production by making amyloid precursor protein less available to alpha-secretase. J Neurochem. 2007 May;101(3):854-62. (22 citations; IF = 4.337)
- Almeida CG, Takahashi RH, Gouras GK. Aβ42 accumulation impairs multivesicular body sorting by inhibiting the ubiquitin-proteasome system. J Neuroscience. Apr 19;26(16):4277-88. (90 citations; IF = 7.271)
- Almeida CG, Tampellini D, Takahashi RH, Greengard P, Lin MT, Snyder EM, Gouras GK. Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses. Neurobiol Dis. 2005 Nov;20(2):187-98 (145 citations; IF = 5.121)
- Snyder EM, Nong Y, Almeida CG, Paul S, Moran T, Choi EY, Nairn AC, Salter MW, Lombroso PJ, Gouras GK, Greengard P. Regulation of NMDA receptor trafficking by amyloid-beta. Nat Neurosci. 2005 Aug;8(8):1051-8. (551 citations; IF = 14.191)
- Gouras GK, Almeida CG, Takahashi RH. Intraneuronal Abeta accumulation and origin of plaques in Alzheimer's disease. Neurobiol Aging. 2005 Oct;26(9):1235-44. (125 citations; IF = 6.634)
- Stenh C, Englund H, Lord A, Johansson AS, Almeida CG, Gellerfors P, Greengard P, Gouras GK, Lannfelt L, Nilsson LN. Amyloid-beta oligomers are inefficiently measured by enzyme-linked immunosorbent assay. Ann Neurol. 2005 Jul;58(1):147-50. (48 citations; IF = 10.746)
- Li F, Calingasan NY, Yu F, Mauck WM, Toidze M, Almeida CG, Takahashi RH, Carlson GA, Flint Beal M, Lin MT, Gouras GK. Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice.J Neurochem. 2004 Jun;89(5):1308-12. (110 citations; IF = 4.337)
- Takahashi RH, Almeida CG, Kearney PF, Yu F, Lin MT, Milner TA, Gouras GK. Oligomerization of Alzheimer's beta-amyloid within processes and synapses of cultured neurons and brain. J Neurosci. 2004 Apr 7;24(14):3592-9. (211 citations; IF = 7.271)
- Almeida CG, de Mendonca A., Cunha R.A., Ribeiro J.A. “Adenosine promotes neuronal recovery from reactive oxygen species induced lesion in rat hippocampal slices”. Neurosci Lett. 2003 339:127-30. (25 citations; IF = 2.055)
- Catarina Brito, ITQB
- Tiago Gil Oliveira, ICVS | 3B's
- Orfeu Flores, STAB Vida
- Henrique Girão, IBILI
A full-time position, initially for 6 months, renewable up to the end of the project is available for a highly motivated post-doc to join a multinational project to set-up a precise model of the human blood brain barrier in the research lab headed by Claudia Almeida. Selection will begin now until 15th of November to start in January 2018 but will continue until the right post-doc is found.
Dr. Claudia Almeida laboratory focuses on the dysfunction of intracellular trafficking in neuronal aging and neurodegenerative diseases. Dr. Almeida is seeking a highly talented and motivated postdoc, preferably with a PhD in neurosciences with expertise in cell biology, to work on the neurobiology part of NAB3, a collaborative project funded by JPND/H2020, aimed at combining different cellular types and organotypic brain slices or neuronal cultures to achieve a more precise in vitro model of the human blood-brain barrier in the Alzheimer’s disease state. The NAB3 project brings together expertise from across the continent and in a range of different fields, including genetic engineering, physiology, neurobiology, neuroanatomy and biochemistry. It is a coordinated effort with partners based in four European countries – France, Germany, Italy, and the Netherlands.
Key responsabilities and Requirements available here.
To apply, send your CV, a motivation letter and the name of 3 referees, to claudia.almeida(at)nms.unl.pt