We are analyzing https://link.springer.com/article/10.1186/s13073-023-01155-w.

Title:
The neuroimmune axis of Alzheimer’s disease | Genome Medicine
Description:
Alzheimer’s disease (AD) is a genetically complex and heterogeneous disorder with multifaceted neuropathological features, including β-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Over the past decade, emerging evidence has implicated both beneficial and pathological roles for innate immune genes and immune cells, including peripheral immune cells such as T cells, which can infiltrate the brain and either ameliorate or exacerbate AD neuropathogenesis. These findings support a neuroimmune axis of AD, in which the interplay of adaptive and innate immune systems inside and outside the brain critically impacts the etiology and pathogenesis of AD. In this review, we discuss the complexities of AD neuropathology at the levels of genetics and cellular physiology, highlighting immune signaling pathways and genes associated with AD risk and interactions among both innate and adaptive immune cells in the AD brain. We emphasize the role of peripheral immune cells in AD and the mechanisms by which immune cells, such as T cells and monocytes, influence AD neuropathology, including microglial clearance of amyloid-β peptide, the key component of β-amyloid plaque cores, pro-inflammatory and cytotoxic activity of microglia, astrogliosis, and their interactions with the brain vasculature. Finally, we review the challenges and outlook for establishing immune-based therapies for treating and preventing AD.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

google, scholar, article, cas, disease, cells, alzheimers, immune, brain, cell, nat, microglia, role, risk, peripheral, microglial, system, studies, pathology, cognitive, βamyloid, activation, med, aging, neurodegenerative, patients, neuroinflammation, genes, mouse, including, diseases, immunol, sci, progression, increased, amyloid, dementia, human, alzheimer, heterogeneity, therapeutic, development, model, function, infiltration, models, innate, immunity, mice, gene,

Topics {✒️}

genome-wide meta-analysis identifies bone-marrow-derived cells contribute astrocyte-targeted gene delivery tnfr2-expressing cd4+foxp3+ regulatory abnormal proteostasis—β-amyloid aggregation long-term apoe ε2 overexpression pro-inflammatory microglial activation/neuroinflammation rho/rock signaling pathway myeloid-/leukocyte-related processes single-cell rna-sequencing genome-wide association study atp-binding cassette subfamily anti-amyloid monoclonal antibody restoring tgf-β+ microglia blood-brain barrier leakage β-amyloid deposition begins brain-wide glymphatic enhancement clear aggregated amyloid-β42 clear aggregated amyloid-beta42 genome-wide associations studies generating ipsc-derived microglia myeloid-specific genetic ablation anna maaser-hecker & rudolph single-cell eqtl analysis β-amyloid plaque cores ifn-i-dependent manner ephrin-eph receptor interactions virus vector-based knockdown blood-brain barrier disruption antigen-presenting cells promotes extracellular β-amyloid plaques targeting abnormal proteostasis—plaques single-cell peripheral immunoprofiling stage-wise fashion leading synapse-related gene expression potent γ-secretase modulator slp-76-related adaptor expressed pro-inflammatory glial activation immature antigen-presenting cells complement c3-dependent adherence increased long-term risk β-amyloid deposition long app-ps1 transgenic mice pro-inflammatory conditions compared blood–brain barrier breakdown blood-brain barrier breakdown target γ-secretase enzyme target β-amyloid plaques increased β-amyloid deposits hospital-treated infectious diseases

Questions {❓}

CD8+ T cell-mediated mechanisms contribute to the progression of neurocognitive impairment in both multiple sclerosis and Alzheimer’s disease?
Could Alzheimer’s disease originate in the periphery and if so how so?
Heterogeneity of Alzheimer’s disease: consequence for drug trials?
Tau and neuroinflammation: what impact for Alzheimer’s disease and tauopathies?

Schema {🗺️}

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         headline:The neuroimmune axis of Alzheimer’s disease
         description:Alzheimer’s disease (AD) is a genetically complex and heterogeneous disorder with multifaceted neuropathological features, including β-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Over the past decade, emerging evidence has implicated both beneficial and pathological roles for innate immune genes and immune cells, including peripheral immune cells such as T cells, which can infiltrate the brain and either ameliorate or exacerbate AD neuropathogenesis. These findings support a neuroimmune axis of AD, in which the interplay of adaptive and innate immune systems inside and outside the brain critically impacts the etiology and pathogenesis of AD. In this review, we discuss the complexities of AD neuropathology at the levels of genetics and cellular physiology, highlighting immune signaling pathways and genes associated with AD risk and interactions among both innate and adaptive immune cells in the AD brain. We emphasize the role of peripheral immune cells in AD and the mechanisms by which immune cells, such as T cells and monocytes, influence AD neuropathology, including microglial clearance of amyloid-β peptide, the key component of β-amyloid plaque cores, pro-inflammatory and cytotoxic activity of microglia, astrogliosis, and their interactions with the brain vasculature. Finally, we review the challenges and outlook for establishing immune-based therapies for treating and preventing AD.
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      headline:The neuroimmune axis of Alzheimer’s disease
      description:Alzheimer’s disease (AD) is a genetically complex and heterogeneous disorder with multifaceted neuropathological features, including β-amyloid plaques, neurofibrillary tangles, and neuroinflammation. Over the past decade, emerging evidence has implicated both beneficial and pathological roles for innate immune genes and immune cells, including peripheral immune cells such as T cells, which can infiltrate the brain and either ameliorate or exacerbate AD neuropathogenesis. These findings support a neuroimmune axis of AD, in which the interplay of adaptive and innate immune systems inside and outside the brain critically impacts the etiology and pathogenesis of AD. In this review, we discuss the complexities of AD neuropathology at the levels of genetics and cellular physiology, highlighting immune signaling pathways and genes associated with AD risk and interactions among both innate and adaptive immune cells in the AD brain. We emphasize the role of peripheral immune cells in AD and the mechanisms by which immune cells, such as T cells and monocytes, influence AD neuropathology, including microglial clearance of amyloid-β peptide, the key component of β-amyloid plaque cores, pro-inflammatory and cytotoxic activity of microglia, astrogliosis, and their interactions with the brain vasculature. Finally, we review the challenges and outlook for establishing immune-based therapies for treating and preventing AD.
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         Heterogeneity
         Immune system
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         Human Genetics
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         Medicine/Public Health
         general
         Cancer Research
         Systems Biology
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