Aging and disease

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01 May 2011. VOL 2, ISSUE 5 Previous Issue Next Issue

Immune Aging and Challenges for Immune Protection of the Graying Population
Abbe N. Vallejo

2011, 2 (5): 339-345

PDF (349KB)
Age-related Dysregulation of Inflammation and Innate Immunity: Lessons Learned from Rodent Models
Aleah L. Brubaker, Jessica L. Palmer, Elizabeth J. Kovacs

2011, 2 (5): 346-360

PDF (528KB)
Aging Impairs Murine B Cell Differentiation and Function in Primary and Secondary Lymphoid Tissues
Daniela Frasca, Bonnie B Blomberg

2011, 2 (5): 361-373

PDF (473KB)
Age-related Deficiencies in Antigen-Specific CD4 T cell Responses: Lessons from Mouse Models
Laura Haynes, Julie S. Lefebvre

2011, 2 (5): 374-381

PDF (519KB)
Role of CD8 T Cell Replicative Senescence in Human Aging and in HIV-mediated Immunosenescence
Jeffrey N. Dock, Rita B. Effros

2011, 2 (5): 382-397

PDF (500KB)
Finding Balance: T cell Regulatory Receptor Expression during Aging
Mary M. Cavanagh, Qian Qi, Cornelia M. Weyand, Jörg J. Goronzy

2011, 2 (5): 398-413

PDF (862KB)
Senescence-accelerated Mice (SAMs) as a Model for Brain Aging and Immunosenescence
Atsuyoshi Shimada, Sanae Hasegawa-Ishii

2011, 2 (5): 414-435

PDF (922KB)
The Origin and Implication of Thymic Involution
Danielle Aw, Donald B. Palmer

2011, 2 (5): 437-443

PDF (337KB)

Cover Illustration

01 May 2011. Vol.2 No.5
The Senescence-Accelerated Mouse (SAM) represents a group of inbred mouse strains developed as a model for the study of human aging and age-related diseases. Senescence-prone (SAMP) strains exhibit an early onset of age-related decline in the peripheral immunity such as thymic involution, loss of CD4+ T cells, impaired helper T cell function, decreased antibody-forming capacity, dysfunction of antigen-presenting cells, decreased natural killer activity, increased auto-antibodies, and susceptibility to virus infection. Senescence-prone SAMP10 mice undergo age-related changes in the brain such as brain atrophy, shrinkage and loss of cortical neurons, retraction of cortical neuronal dendrites, loss of dendritic spines, loss of synapses, impaired learning and memory, depressive behavior, accumulation of neuronal DNA damage, neuronal ubiquitinated inclusions, reduced hippocampal cholinergic receptors, decreased neurotrophic factors, decreased hippocampal zinc and zinc transporters, increased sphyngomyelinase, and elevated oxidative-nitrative stress. Recent data indicating increased pro-inflammatory cytokines in the brain of SAMP10 mice are directing investigators toward an integration of immune and neural abnormalities to enhance understanding of the principles of brain aging. We highlight how mouse brain cells adopt cytokine-mediated responses and how SAMP10 mice are defective in these responses. SAMP10 model would be useful to study how age-related disturbances in peripheral immunity have an impact on dysregulation of brain tissue homeostasis, resulting in age-related neurodegeneration.

[Detail]

Cover Illustration

The Senescence-Accelerated Mouse (SAM) represents a group of inbred mouse strains developed as a model for the study of human aging and age-related diseases. Senescence-prone (SAMP) strains exhibit an early onset of age-related decline in the peripheral immunity such as thymic involution, loss of CD4+ T cells, impaired helper T cell function, decreased antibody-forming capacity, dysfunction of antigen-presenting cells, decreased natural killer activity, increased auto-antibodies, and susceptibility to virus infection. Senescence-prone SAMP10 mice undergo age-related changes in the brain such as brain atrophy, shrinkage and loss of cortical neurons, retraction of cortical neuronal dendrites, loss of dendritic spines, loss of synapses, impaired learning and memory, depressive behavior, accumulation of neuronal DNA damage, neuronal ubiquitinated inclusions, reduced hippocampal cholinergic receptors, decreased neurotrophic factors, decreased hippocampal zinc and zinc transporters, increased sphyngomyelinase, and elevated oxidative-nitrative stress. Recent data indicating increased pro-inflammatory cytokines in the brain of SAMP10 mice are directing investigators toward an integration of immune and neural abnormalities to enhance understanding of the principles of brain aging. We highlight how mouse brain cells adopt cytokine-mediated responses and how SAMP10 mice are defective in these responses. SAMP10 model would be useful to study how age-related disturbances in peripheral immunity have an impact on dysregulation of brain tissue homeostasis, resulting in age-related neurodegeneration.