UCC Research Profiles: barry.boland@ucc.ie, Pharmacology & Therapeutics

Contact Details

Lecturer In Pharmacology
Pharmacology & Therapeutics
Room 2.48
Department of Pharmacology and Therapeutics
Western Gateway Building
University College Cork
Co. Cork, Ireland

T: +353-21-4205977
E: barry.boland@ucc.ie

Biography

I received my B.Sc. degree in Pharmacology from University College Dublin in 1999 and a PhD in Physiology from Trinity College Dublin in 2003. During my PhD studies, I developed a keen interest in the role of dysfunctional catabolism in neurodegenerative diseases. As a Wellcome Trust postdoctoral fellow, I first trained with Dr. Ralph Nixon at the Nathan Kline Institute, New York University (2003-2005), with whom I identified hallmarks of impaired autophagic flux in neurons affected by Alzheimer's disease. I then trained with Prof. Frances Platt at the Pharmacology Dept., University of Oxford (2005-2007), where I characterised temporal impairments in endocytic and autophagic flux in mouse models of lysosomal storage diseases. In 2007, I returned to Ireland as a lecturer in Neuroscience at University College Dublin, and worked with Prof. Dominic Walsh as a Health Research Board postdoctoral fellow (2008-2012), where I developed expertise in the neuronal metabolism of amyloid precursor protein (APP). In early 2013, I became a lecturer in the Dept. of Pharmacology and Therapeutics at University College Cork, where I have established my own research group.

Research Interests

Inside all of our cells, waste products are packaged into acidic organelles known as lysosomes, which contain specialised enzymes that degrade cellular waste. Impaired processing (flux) of cellular waste through the endosomal-autophagic-lysosomal system of cells is a central feature of lysosomal storage diseases. Impaired lysosomal flux is evident in many neurodegenerative diseases across the entire age spectrum; from childhood neurodegenerative conditions that occur in lysosomal storage diseases, to late-onset conditions such as Alzheimer’s disease. Our goal is to identify cellular biomarkers of impaired lysosomal flux and develop therapies that can restore their function, thus enabling early diagnosis and new treatments for these diseases.

Research Grants

Project	Funding Body	Start Date	End Date	Award
Therapeutic targeting of impaired lysosomal flux in Alzheimer’s disease	Science Foundation Ireland	01-AUG-16	31-JUL-18	€201,112.00
Spedding Research Solutions"Nature of ALS"Dr B Boland [X]	Industry	01-AUG-15	31-AUG-17	€10,058.00
Biomarkers of Impaired Lysosomal Flux in Alzheimer's Disease.	Foreign Research Institute	01-MAR-14	28-FEB-17	€87,000.00
IN-BIND	Irish Research Council	01-MAR-14	08-MAY-15	€6,000.00
purchase of Transblot system.	Miscellaneous	01-SEP-13	30-SEP-14	€2,000.00

Publications

Peer Reviewed Journals

	Year	Publication
	(2016)	'Tetraspanin 3: A central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein' Seipold, Lisa; Damme, Markus; Prox, Johannes; Rabe, Björn; Kasparek, Petr; Sedlacek, Radislav; Altmeppen, Hermann; Willem, Michael; Boland, Barry; Glatzel, Markus; Saftig, Paul (2016) 'Tetraspanin 3: A central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein'. BBA Biochimica et Biophysica Acta, [CORA Link] [Details]
	(2015)	'Bridging the age spectrum of neurodegenerative storage diseases' Boland B., Platt F.M. (2015) 'Bridging the age spectrum of neurodegenerative storage diseases'. Best Practice & Research Clinical Endocrinology and Metabolism, 29 (2):127-143 [DOI] [Details]
	(2015)	'The familial British dementia mutation promotes formation of neurotoxic cystine cross-linked amyloid Bri (ABri) oligomers' Cantlon A, Sala Frigerio C, Freir DB, Boland B, Jin M, Walsh DM (2015) 'The familial British dementia mutation promotes formation of neurotoxic cystine cross-linked amyloid Bri (ABri) oligomers'. Journal of Biological Chemistry, [DOI] [Details]
	(2012)	'Role of aromatic side chains in amyloid-β-protein aggregation' Cukalevski R, Boland B, Frohm B, Thulin E, Walsh D, Linse S (2012) 'Role of aromatic side chains in amyloid-β-protein aggregation'. ACS Chemical Neuroscience, 3 (12):1008-1016 [DOI] [Details]
	(2012)	'The cell biology of disease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction' Platt FM, Boland B, van der Spoel AC (2012) 'The cell biology of disease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction'. The Journal of Cell Biology, 199 (5):723-734 [DOI] [Details]
	(2010)	'Amyloid β-protein aggregation produces highly reproducible kinetic data and occurs by a two-phase process' Hellstrand E, Boland B, Walsh DM, Linse S (2010) 'Amyloid β-protein aggregation produces highly reproducible kinetic data and occurs by a two-phase process'. ACS Chemical Neuroscience, 1 (1):13-18 [DOI] [Details]
	(2010)	'Macroautophagy is not directly involved in the metabolism of amyloid precursor protein' Boland B, Smith DA, Mooney D, Jung SS, Walsh DM, Platt FM (2010) 'Macroautophagy is not directly involved in the metabolism of amyloid precursor protein'. The Journal of Biological Chemistry, 285 (48):37415-37426 [DOI] [Details]
	(2009)	'gamma-secretase processing of APLP1 leads to the production of a p3-like peptide that does not aggregate and is not toxic to neurons' Minogue AM, Stubbs AK, Frigerio CS, Boland B, Fadeeva JV, Tang J, Selkoe DJ, Walsh DM (2009) 'gamma-secretase processing of APLP1 leads to the production of a p3-like peptide that does not aggregate and is not toxic to neurons'. Brain, 1262 :89-99 [DOI] [Details]
	(2008)	'Neurofilament tail phosphorylation: identity of the RT-97 phosphoepitope and regulation in neurons by cross-talk among proline-directed kinases' Veeranna, Lee JH, Pareek TK, Jaffee H, Boland B, Vinod KY, Amin N, Kulkarni AB, Pant HC, Nixon RA (2008) 'Neurofilament tail phosphorylation: identity of the RT-97 phosphoepitope and regulation in neurons by cross-talk among proline-directed kinases'. Journal of Neurochemistry, 107 (1):35-49 [DOI] [Details]
	(2008)	'Autophagy induction and autophagosome clearance in neurons: relationship to autophagic pathology in Alzheimer's disease' Boland B, Kumar A, Lee S, Platt FM, Wegiel J, Yu WH, Nixon RA (2008) 'Autophagy induction and autophagosome clearance in neurons: relationship to autophagic pathology in Alzheimer's disease'. The Journal of Neuroscience, 28 (27):6926-6937 [DOI] [Details]
	(2006)	'Neuronal macroautophagy: from development to degeneration' Boland B, Nixon RA (2006) 'Neuronal macroautophagy: from development to degeneration'. Molecular aspects of medicine, 27 (5-6):503-519 [DOI] [Details]
	(2004)	'Aβ-mediated activation of the apoptotic cascade in cultured cortical neurones: a role for cathepsin-L' Boland B, Campbell V (2004) 'Aβ-mediated activation of the apoptotic cascade in cultured cortical neurones: a role for cathepsin-L'. Neurobiology of Aging, 25 (1):83-91 [DOI] [Details]
	(2004)	'Calpain mediates calcium-induced activation of the ERK1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease' Veeranna, Kaji T, Boland B, Odrljin T, Mohan P, Basavarajappa BS, Peterhoff C, Cataldo A, Rudnicki A, Amin N, Li BS, Pant HC, Hungund BL, Arancio O, Nixon RA (2004) 'Calpain mediates calcium-induced activation of the ERK1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease'. American Journal of Pathology, 165 (3):795-805 [DOI] [Details]
	(2003)	'β-Amyloid (1-40)-induced apoptosis of cultured cortical neurones involves calpain-mediated cleavage of poly-ADP-ribose polymerase' Boland B, Campbell V (2003) 'β-Amyloid (1-40)-induced apoptosis of cultured cortical neurones involves calpain-mediated cleavage of poly-ADP-ribose polymerase'. Neurobiology of Aging, 24 (1):179-186 [DOI] [Details]
	(2002)	'Apoptotic changes in the aged brain are triggered by interleukin-1β-induced activation of p38 and reversed by treatment with eicosapentaenoic acid' Martin DS, Lonergan PE, Boland B, Fogarty MP, Brady M, Horrobin DF, Campbell VA, Lynch MA (2002) 'Apoptotic changes in the aged brain are triggered by interleukin-1β-induced activation of p38 and reversed by treatment with eicosapentaenoic acid'. The Journal of Biological Chemistry, 277 (37):34239-34246 [DOI] [Details]
	(2001)	'Δ9-Tetrahydrocannabinol induces the apoptotic pathway in cultured cortical neurones via activation of the CB1 receptor' Downer, E., Boland, B., Fogarty, M. and Campbell, V. (2001) 'Δ9-Tetrahydrocannabinol induces the apoptotic pathway in cultured cortical neurones via activation of the CB1 receptor'. Neuroreport, 12 (18):3973-8-3978 [DOI] [Details]

Professional Activities

Honours and Awards

	Year	Title	Awarding Body
	2009	Peter Carlton Jones Memorial Award	Niemann Pick Disease Group UK

Professional Associations

	Association	Function	From / To
	Irish Network for Biomarkers in Neurodegeneration (IN-BIND)	Support translational biomaker research for neurodegenerative diseases in Ireland and abroad	01-AUG-12 /

Committees

	Committee	Function	From / To
	Brain Tumour Ireland	Scientific Advisor	2017 /

Outreach Activities

	Description
	2016: Organised a 1-day event in UCC for Brain Awareness Week

	Name	Institute	Country
	Dr. Cora O'Neill	Dept. of Biochemistry, University College Cork	IRELAND
	Prof. William Molloy	St. Finbarr's Hospital Cork and The Centre for Gerontology and Rehabilitation (UCC)	IRELAND