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Neurodegeneration

MRC London Neurodegenerative Diseases Brain Bank

The Brain Bank was established in 1989 with the aim of providing high quality, clinically and neuropathologically well-characterised human brain and spinal cord tissue to the neuroscience community. The Brain Bank is partially funded by the Medical Research Council (MRC) and is part of the Basic and Clinical Neuroscience department at the Institute of Psychiatry, Psychology and Neuroscience (IoPPN) and the Department of Clinical Neuropathology at King’s College Hospital.

Braintissue

Image shows Tau pathology within the hippocampus (identified by the AT8 antibody against PHF Tau).

 

Brain Bank Team
Prof Safa Al-Sarraj   Director of Brain Bank and Head of Clinical Neuropathology department.
Dr Istvan Bodi     Consultant Neuropathologist
Dr Andrew King    Consultant Neuropathologist
Dr Miren Aizpurua    M.D Neuropath SpR
Dr Claire Troakes   Brain Bank Coordinator
Sashika Selvackadunco  Brain Bank Research Worker
Shalmai Jones Research Technician for Brains for Dementia Research

 

Objectives for the MRC Brainbank

Facilitate brain donation through an ethically approved programme of informed consent for cohort studies and ad-hoc donations.

Provide pathological diagnosis to the relatives of brain donors according to the best national and international protocols.

Dissemination of high quality brain tissue to neuroscience research.

Maintain an ’open door’ policy for responding to requests without prejudice.

Ensure optimum donor care and retain contact with donor families, informing them about diagnosis and progress in research.

Disseminate and promote knowledge of brain banking through scientific meetings, public engagements and newsletters.

Provide teaching, training information and educational resources for neuroscientists.

Facilitate collaboration between basic research scientists, pathologists and clinicians.

Maintain gold standards of excellence in brain banking for the archiving and storage of frozen and formalin fixed tissue.

Participate in ethical training and consultation and implement the most recent ethical guidelines for donor recruitment through informed consent.

Neuroscience Research

Clinically and neuropathologically well characterised brain tissue is one of the most important resources for neurodegeneration research. It is especially valuable since for many psychiatric and neurological disorders there are, as yet, no suitable animal models. The Brain Bank focuses on neurodegenerative diseases including Alzheimer’s Disease (AD), Frontotemperal dementias (FTD) and Motor Neurone Disease (MND) but we also hold a number of other disease collections including various movement disorders, HIV, Autism and Schizophrenia (see poster for examples of holdings). We also provide control brain and spinal cord tissue for comparative purposes and for basic neuroscience research. All information on tissue availability is stored on an easily accessible and frequently updated database.Standardised dissection protocols are followed and material is available for research in frozen and/or formalin-fixed form.

Poster: MRC London Brain Bank: a resource for neurodegeneration research

Requests for Tissue

The Brain Bank endeavours to provide suitable material to bona fide research groups, both at the local, national and international level. In order to consider a request, the Brain Bank requires details of the nature of the project for which tissue is to be used.

From 1st January 2016, and in line with a sustainable future for brain banking, The Medical Research Council (MRC) and associated charities have introduced a cost recovery scheme for the provision of tissue. The tariff will partially subsidise the costs of retrieval, assessment and archiving of the brain tissue.  The MRC will continue to contribute substantially to the remaining costs for the foreseeable future.

If you are intending to use human tissue in future projects please remember to include these costs in any upcoming grant applications.  Exceptions may be made for pilot studies and if yours falls into this category that should be noted in your application to the tissue bank.

For further information and consultation on tariffs please contact the brain bank by e-mail brainbank@kcl.ac.uk  or phone on 020 7848 0290.

Tissue Request form

Tissue Request form guidance notes

Make a Donation

There is a real need for brain donation in order to carry out vital research for a variety of neurological and psychiatric disorders. For comparative purposes, there is an equally great need for brain tissue donated from healthy individuals who do not have a neurological or psychiatric condition (known as control tissue). All donations are gratefully received. Donor details are held in confidence and the Brain Bank operates under the regulation of the Human Tissue Authority. A donor information pack is available on request.

Making a brain donation for scientific research - Frequently Asked Questions

Public Engagement

One of the main objectives of the Brain Bank is to disseminate and promote knowledge of brain banking and brain research through public engagement. The Brain Bank has been present in several initiatives, some of these include:

  • Brain Awareness Week. An international celebration of the brain for people of all ages, disseminating information about brain anatomy, functions, medical conditions and brain research. See Dr Claire Troakes (Brain Bank coordinator) in this video.
  • Alzheimer’s Disease Open Day , celebrated annually at the IoPPN. The Open Day brings together researchers, patients and carers to offer a unique insight into the disease.
  • Pint of Science brings scientists to local venues to engage the general public in an informal and approachable manner.
Brains for Dementia Research

The London Neurodegenerative Diseases Brain Bank is also part of a new initative - Brains for Dementia Research. Brain tissue from regularly assessed individuals provides the very best resource for scientists working on understanding dementia. Linking progression of memory impairment with what is seen in the brain itself and comparing with normal brain tissue is essential to developing more effective treatments.

Brains for Dementia Research is a network between 6 centres (based in London, Oxford, Bristol, Newcastle, Manchester and Cardiff universities) funded jointly by the Alzheimer’s Research Trust and Alzheimer’s Society. It invites people diagnosed with a memory impairment (or dementia), and those who do not have a memory impairment (normal controls) to participate in monitoring of memory, thinking and behavior every one to two years prior to brain donation.

If you are interested in finding out more please

Tel: 0191 208 2109

Email: BDRCoordinatingcentre@ncl.ac.uk

or visit www.brainsfordementiaresearch.org.uk/
MRC UK Brain Banks Network

The brain bank is also part of the newly created MRC UK Brain Banks Network. The UK Brain Banks Network will provide high quality brain tissue to scientists and clinicians to carry out cutting edge neurosciences research, and will support major initiatives on research into neurological disorders, including the aims of the Ministerial Action Group on Dementia Research.

https://mrc.ukri.org/research/facilities-and-resources-for-researchers/brain-banks

Contact Us

For further information please contact the brain bank

Tel: 020 7848 0290

Email: brain.bank@kcl.ac.uk

Address: London Neurodegenerative Diseases Brain Bank, Box PO65, Institute of Psychiatry, King's College London, De Crespigny Park, London, SE5 8AF

To contact us regarding a donation, please call 020 7848 0290 during office hours (9am-5pm Monday-Friday)

To contact us regarding a donation outside normal working hours, please call 0207 848 0003 and leave a contact name and number for our on-call staff to get in touch. 

Please continue to make usual arrangements until our on-call staff are able to contact you.

Publications

[1-65] Publications acknowledging LND Brain Bank 2016-2019

1.            Aman, Y., et al., Reduced thermal sensitivity and increased opioidergic tone in the TASTPM mouse model of Alzheimer's disease. Pain, 2016. 157(10): p. 2285-96.

2.            Baek, J.H., et al., Unfolded protein response is activated in Lewy body dementias. Neuropathol Appl Neurobiol, 2016. 42(4): p. 352-65.

3.            Bereczki, E., et al., Synaptic proteins predict cognitive decline in Alzheimer's disease and Lewy body dementia. Alzheimers Dement, 2016. 12(11): p. 1149-1158.

4.            Bondulich, M.K., et al., Tauopathy induced by low level expression of a human brain-derived tau fragment in mice is rescued by phenylbutyrate. Brain, 2016. 139(Pt 8): p. 2290-306.

5.            Bukar Maina, M., Y.K. Al-Hilaly, and L.C. Serpell, Nuclear Tau and Its Potential Role in Alzheimer's Disease. Biomolecules, 2016. 6(1): p. 9.

6.            Davidson, Y., et al., Neurodegeneration in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9orf72 is linked to TDP-43 pathology and not associated with aggregated forms of dipeptide repeat proteins. Neuropathol Appl Neurobiol, 2016. 42(3): p. 242-54.

7.            Duarte, R.R., et al., Genome-wide significant schizophrenia risk variation on chromosome 10q24 is associated with altered cis-regulation of BORCS7, AS3MT, and NT5C2 in the human brain. Am J Med Genet B Neuropsychiatr Genet, 2016. 171(6): p. 806-14.

8.            Gami-Patel, P., et al., The presence of heterogeneous nuclear ribonucleoproteins in frontotemporal lobar degeneration with FUS-positive inclusions. Neurobiol Aging, 2016. 46: p. 192-203.

9.            Guerreiro, R., et al., Genome-wide analysis of genetic correlation in dementia with Lewy bodies, Parkinson's and Alzheimer's diseases. Neurobiol Aging, 2016. 38: p. 214 e7-10.

10.          Hannon, E., et al., Methylation QTLs in the developing brain and their enrichment in schizophrenia risk loci. Nat Neurosci, 2016. 19(1): p. 48-54.

11.          Kenna, K.P., et al., NEK1 variants confer susceptibility to amyotrophic lateral sclerosis. Nat Genet, 2016. 48(9): p. 1037-42.

12.          Koss, D.J., et al., Soluble pre-fibrillar tau and beta-amyloid species emerge in early human Alzheimer's disease and track disease progression and cognitive decline. Acta Neuropathol, 2016. 132(6): p. 875-895.

13.          Kovacs, G.G., et al., Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy. Acta Neuropathol, 2016. 131(1): p. 87-102.

14.          Kun-Rodrigues, C., et al., Analysis of C9orf72 repeat expansions in a large international cohort of dementia with Lewy bodies. Neurobiol Aging, 2016.

15.          Kurbatskaya, K., et al., Upregulation of calpain activity precedes tau phosphorylation and loss of synaptic proteins in Alzheimer's disease brain. Acta Neuropathol Commun, 2016. 4: p. 34.

16.          Lau, D.H., et al., Critical residues involved in tau binding to fyn: implications for tau phosphorylation in Alzheimer's disease. Acta Neuropathol Commun, 2016. 4(1): p. 49.

17.          Ling, H., et al., Astrogliopathy predominates the earliest stage of corticobasal degeneration pathology. Brain, 2016. 139(Pt 12): p. 3237-3252.

18.          Lunnon, K., et al., Variation in 5-hydroxymethylcytosine across human cortex and cerebellum. Genome Biol, 2016. 17: p. 27.

19.          Marzi, S.J., et al., Tissue-specific patterns of allelically-skewed DNA methylation. Epigenetics, 2016. 11(1): p. 24-35.

20.          Mirza, A., et al., The Identification of Aluminum in Human Brain Tissue Using Lumogallion and Fluorescence Microscopy. J Alzheimers Dis, 2016. 54(4): p. 1333-1338.

21.          Niblock, M., et al., Lack of association between TDP-43 pathology and tau mis-splicing in Alzheimer's disease. Neurobiol Aging, 2016. 37: p. 45-6.

22.          Niblock, M., et al., Retention of hexanucleotide repeat-containing intron in C9orf72 mRNA: implications for the pathogenesis of ALS/FTD. Acta Neuropathol Commun, 2016. 4: p. 18.

23.          Robinson, A.C., et al., Extended post-mortem delay times should not be viewed as a deterrent to the scientific investigation of human brain tissue: a study from the Brains for Dementia Research Network Neuropathology Study Group, UK. Acta Neuropathol, 2016. 132(5): p. 753-755.

24.          Salta, E., et al., miR-132 loss de-represses ITPKB and aggravates amyloid and TAU pathology in Alzheimer's brain. EMBO Mol Med, 2016. 8(9): p. 1005-18.

25.          Sassi, C., et al., ABCA7 p.G215S as potential protective factor for Alzheimer's disease. Neurobiol Aging, 2016. 46: p. 235 e1-9.

26.          Sassi, C., et al., Influence of Coding Variability in APP-Abeta Metabolism Genes in Sporadic Alzheimer's Disease. PLoS One, 2016. 11(6): p. e0150079.

27.          Smethurst, P., et al., In vitro prion-like behaviour of TDP-43 in ALS. Neurobiol Dis, 2016. 96: p. 236-247.

28.          Tiwari, S.S., et al., Alzheimer-related decrease in CYFIP2 links amyloid production to tau hyperphosphorylation and memory loss. Brain, 2016. 139(Pt 10): p. 2751-2765.

29.          Troakes, C., et al., Clusterin expression is upregulated following acute head injury and localizes to astrocytes in old head injury. Neuropathology, 2016.

30.          Vidal, B., et al., Agonist and antagonist bind differently to 5-HT1A receptors during Alzheimer's disease: A post-mortem study with PET radiopharmaceuticals. Neuropharmacology, 2016. 109: p. 88-95.

31.          Alghamdi, A., et al., Reduction of RPT6/S8 (a Proteasome Component) and Proteasome Activity in the Cortex is Associated with Cognitive Impairment in Lewy Body Dementia. J Alzheimers Dis, 2017. 57(2): p. 373-386.

32.          Chong, J.R., et al., Increased Transforming Growth Factor beta2 in the Neocortex of Alzheimer's Disease and Dementia with Lewy Bodies is Correlated with Disease Severity and Soluble Abeta42 Load. J Alzheimers Dis, 2017. 56(1): p. 157-166.

33.          Ditsworth, D., et al., Mutant TDP-43 within motor neurons drives disease onset but not progression in amyotrophic lateral sclerosis. Acta Neuropathol, 2017. 133(6): p. 907-922.

34.          Farg, M.A., et al., The DNA damage response (DDR) is induced by the C9orf72 repeat expansion in Amyotrophic Lateral Sclerosis. Hum Mol Genet, 2017.

35.          Hoglinger, G.U., et al., Clinical diagnosis of progressive supranuclear palsy: The movement disorder society criteria. Mov Disord, 2017. 32(6): p. 853-864.

36.          Keogh, M.J., et al., Genetic compendium of 1511 human brains available through the UK Medical Research Council Brain Banks Network Resource. Genome Res, 2017. 27(1): p. 165-173.

37.          King, A., et al., Unusual neuropathological features and increased brain aluminium in a resident of Camelford, UK. Neuropathol Appl Neurobiol, 2017. 43(6): p. 537-541.

38.          Koss, D.J. and B. Platt, Alzheimer's disease pathology and the unfolded protein response: prospective pathways and therapeutic targets. Behav Pharmacol, 2017. 28(2 and 3 - Special Issue): p. 161-178.

39.          Kun-Rodrigues, C., et al., Analysis of C9orf72 repeat expansions in a large international cohort of dementia with Lewy bodies. Neurobiol Aging, 2017. 49: p. 214 e13-214 e15.

40.          Lee, Y.B., et al., C9orf72 poly GA RAN-translated protein plays a key role in amyotrophic lateral sclerosis via aggregation and toxicity. Hum Mol Genet, 2017. 26(24): p. 4765-4777.

41.          Mirza, A., et al., Aluminium in brain tissue in familial Alzheimer's disease. J Trace Elem Med Biol, 2017. 40: p. 30-36.

42.          Moncini, S., et al., The miR-15/107 Family of microRNA Genes Regulates CDK5R1/p35 with Implications for Alzheimer's Disease Pathogenesis. Mol Neurobiol, 2017. 54(6): p. 4329-4342.

43.          Respondek, G., et al., Which ante mortem clinical features predict progressive supranuclear palsy pathology? Mov Disord, 2017. 32(7): p. 995-1005.

44.          Sinclair, L.I. and S. Love, Effect of APOE Genotype on Synaptic Proteins in Earlier Adult Life. J Alzheimers Dis, 2017. 59(3): p. 1123-1137.

45.          Smith, B.N., et al., Mutations in the vesicular trafficking protein annexin A11 are associated with amyotrophic lateral sclerosis. Sci Transl Med, 2017. 9(388).

46.          Sproviero, W., et al., ATXN2 trinucleotide repeat length correlates with risk of ALS. Neurobiol Aging, 2017. 51: p. 178 e1-178 e9.

47.          Trist, B.G., et al., Amyotrophic lateral sclerosis-like superoxide dismutase 1 proteinopathy is associated with neuronal loss in Parkinson's disease brain. Acta Neuropathol, 2017. 134(1): p. 113-127.

48.          Troakes, C., et al., Clusterin expression is upregulated following acute head injury and localizes to astrocytes in old head injury. Neuropathology, 2017. 37(1): p. 12-24.

49.          Viana, J., et al., Schizophrenia-associated methylomic variation: molecular signatures of disease and polygenic risk burden across multiple brain regions. Hum Mol Genet, 2017. 26(1): p. 210-225.

50.          Wei, W., et al., Mitochondrial DNA point mutations and relative copy number in 1363 disease and control human brains. Acta Neuropathol Commun, 2017. 5(1): p. 13.

51.          Guerreiro, R., et al., Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study. Lancet Neurol, 2018. 17(1): p. 64-74.

52.          Keogh, M.J., et al., Oligogenic genetic variation of neurodegenerative disease genes in 980 postmortem human brains. J Neurol Neurosurg Psychiatry, 2018. 89(8): p. 813-816.

53.          Kun-Rodrigues, C., et al., A comprehensive screening of copy number variability in dementia with Lewy bodies. Neurobiol Aging, 2018.

54.          Marzi, S.J., et al., A histone acetylome-wide association study of Alzheimer's disease identifies disease-associated H3K27ac differences in the entorhinal cortex. Nat Neurosci, 2018. 21(11): p. 1618-1627.

55.          Murray, C.E., et al., APOE epsilon4 is also required in TREM2 R47H variant carriers for Alzheimer's disease to develop. Neuropathol Appl Neurobiol, 2018.

56.          Navarrete, F., et al., Cannabinoid CB1 and CB2 Receptors, and Monoacylglycerol Lipase Gene Expression Alterations in the Basal Ganglia of Patients with Parkinson's Disease. Neurotherapeutics, 2018. 15(2): p. 459-469.

57.          Nicolas, A., et al., Genome-wide Analyses Identify KIF5A as a Novel ALS Gene. Neuron, 2018. 97(6): p. 1268-1283 e6.

58.          Pottier, C., et al., Potential genetic modifiers of disease risk and age at onset in patients with frontotemporal lobar degeneration and GRN mutations: a genome-wide association study. Lancet Neurol, 2018. 17(6): p. 548-558.

59.          Sassi, C., et al., Mendelian adult-onset leukodystrophy genes in Alzheimer's disease: critical influence of CSF1R and NOTCH3. Neurobiol Aging, 2018. 66: p. 179 e17-179 e29.

60.          Smith, R.G., et al., Elevated DNA methylation across a 48-kb region spanning the HOXA gene cluster is associated with Alzheimer's disease neuropathology. Alzheimers Dement, 2018. 14(12): p. 1580-1588.

61.          Solomon, D.A., et al., A feedback loop between dipeptide-repeat protein, TDP-43 and karyopherin-alpha mediates C9orf72-related neurodegeneration. Brain, 2018. 141(10): p. 2908-2924.

62.          Wei, W., et al., Frequency and signature of somatic variants in 1461 human brain exomes. Genet Med, 2018.

63.          Ashton, N.J., et al., Increased plasma neurofilament light chain concentration correlates with severity of post-mortem neurofibrillary tangle pathology and neurodegeneration. Acta Neuropathol Commun, 2019. 7(1): p. 5.

64.          Gkazi, S.A., et al., Striking phenotypic variation in a family with the P506S UBQLN2 mutation including amyotrophic lateral sclerosis, spastic paraplegia, and frontotemporal dementia. Neurobiol Aging, 2019. 73: p. 229 e5-229 e9.

65.          Smith, A.R., et al., A cross-brain regions study of ANK1 DNA methylation in different neurodegenerative diseases. Neurobiol Aging, 2019. 74: p. 70-76.

 

 

 

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