Young Blood Plasma Administration to Fight Alzheimer's Disease?

被引:8
作者
Aicardi, Giorgio [1 ,2 ]
机构
[1] Univ Bologna, Dept Life Qual Studies, Via San Donato 19-2, I-40127 Bologna, Italy
[2] Univ Bologna, Interdept Ctr Luigi Galvani Integrated Study Biop, Bologna, Italy
关键词
Alzheimer's disease; young plasma administration; heterochronic parabiosis; transgenic mouse; learning and memory; synaptophysin; HIPPOCAMPAL CA1 REGION; PROTEIN-KINASE CASCADE; MOUSE MODEL; GROWTH-HORMONE; SYNAPTIC PLASTICITY; COGNITIVE FUNCTION; BRAIN; ACTIVATION; EXPRESSION; IMPAIRMENTS;
D O I
10.1089/rej.2017.1940
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Despite decades of intensive research, no drugs can cure or even stabilize Alzheimer's disease (AD). Current pharmacological treatments only partially mask the symptoms while the disease progresses within the brain. Finding a preventive measure or a cure for people with AD is indeed a worldwide urgent priority. A recent interesting study by T. Wyss-Coray's research group provides the first evidence that exposure to young blood or plasma can reverse some AD-related molecular and behavioral alterations. Heterochronic parabiosis (shared blood circulation) of AD transgenic mice with young healthy mice did not reduce amyloidosis and microglial activation in AD mice, but reversed the loss of synaptophysin and calbindin (critical synaptic proteins, indicators of cognitive decline in AD) in the dentate gyrus, and the abnormal expression, in the hippocampus, of many genes involved in key neuronal signaling pathways. Moreover, repeated intravenous administration of plasma from young healthy mice to AD mice reversed the excessive phosphorylation of hippocampal extracellular signal-regulated kinase (ERK), and improved spatial working memory and associative memory. Although observations in mouse models of AD might not necessarily extrapolate to humans, this preclinical study provides the first demonstration that young plasma has potential therapeutic properties, by ameliorating aspects of the disease that are present in AD patients. Clinical trials are already under way. If young plasma transfusion will be effective in AD patients, it will be important to identify the key factors responsible for the positive effects, as they might lead to the development of molecule interventions with a better efficacy/risk profile.
引用
收藏
页码:178 / 181
页数:4
相关论文
共 41 条
[1]   New Hope from an Old Drug: Fighting Alzheimer's Disease with the Cancer Drug Bexarotene (Targretin)? [J].
Aicardi, Giorgio .
REJUVENATION RESEARCH, 2013, 16 (06) :524-528
[2]   Serum TNF-alpha levels are increased and correlate negatively with free IGF-I in Alzheimer disease [J].
Alvarez, Anton ;
Cacabelos, Ramon ;
Sanpedro, Carolina ;
Garcia-Fantini, Manuel ;
Aleixandre, Manuel .
NEUROBIOLOGY OF AGING, 2007, 28 (04) :533-536
[3]  
Alzheimer's A, 2014, ALZHEIMERS DEMENT, V2014, pe47, DOI [DOI 10.1016/J.JALZ.2010.01.009, DOI 10.1016/J.JALZ.2015.02.003]
[4]  
[Anonymous], 2015, ALZHEIMERS DIS INT W
[5]   Effects of Growth Hormone-Releasing Hormone on Cognitive Function in Adults With Mild Cognitive Impairment and Healthy Older Adults Results of a Controlled Trial [J].
Baker, Laura D. ;
Barsness, Suzanne M. ;
Borson, Soo ;
Merriam, George R. ;
Friedman, Seth D. ;
Craft, Suzanne ;
Vitiello, Michael V. .
ARCHIVES OF NEUROLOGY, 2012, 69 (11) :1420-1429
[6]   Early Selective Vulnerability of Synapses and Synaptic Mitochondria in the Hippocampal CA1 Region of the Tg2576 Mouse Model of Alzheimer's Disease [J].
Balietti, Marta ;
Giorgetti, Belinda ;
Casoli, Tiziana ;
Solazzi, Moreno ;
Tamagnini, Francesco ;
Burattini, Costanza ;
Aicardi, Giorgio ;
Fattoretti, Patrizia .
JOURNAL OF ALZHEIMERS DISEASE, 2013, 34 (04) :887-896
[7]   Impairments of Synaptic Plasticity in Aged Animals and in Animal Models of Alzheimer's Disease [J].
Balietti, Marta ;
Tamagnini, Francesco ;
Fattoretti, Patrizia ;
Burattini, Costanza ;
Casoli, Tiziana ;
Platano, Daniela ;
Lattanzio, Fabrizia ;
Aicardi, Giorgio .
REJUVENATION RESEARCH, 2012, 15 (02) :235-238
[8]   Serum insulin-like growth factor I regulates brain amyloid-levels [J].
Carro, E ;
Trejo, JL ;
Gomez-Isla, T ;
LeRoith, D ;
Torres-Aleman, I .
NATURE MEDICINE, 2002, 8 (12) :1390-1397
[9]   Drug development in Alzheimer's disease: the path to 2025 [J].
Cummings, Jeffrey ;
Aisen, Paul S. ;
DuBois, Bruno ;
Froelich, Lutz ;
Jack, Clifford R., Jr. ;
Jones, Roy W. ;
Morris, John C. ;
Raskin, Joel ;
Dowsett, Sherie A. ;
Scheltens, Philip .
ALZHEIMERS RESEARCH & THERAPY, 2016, 8
[10]   β-amyloid activates the mitogen-activated protein kinase cascade via hippocampal α7 nicotinic acetylcholine receptors:: In vitro and in vivo mechanisms related to Alzheimer's disease [J].
Dineley, KT ;
Westerman, M ;
Bui, D ;
Bell, K ;
Ashe, KH ;
Sweatt, JD .
JOURNAL OF NEUROSCIENCE, 2001, 21 (12) :4125-4133