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  1. Article ; Online: FDA Approval of Aduhelm Paves a New Path for Alzheimer's Disease.

    Tanzi, Rudolph E

    ACS chemical neuroscience

    2021  Volume 12, Issue 15, Page(s) 2714–2715

    MeSH term(s) Alzheimer Disease/drug therapy ; Drug Approval ; Humans ; United States ; United States Food and Drug Administration
    Language English
    Publishing date 2021-07-14
    Publishing country United States
    Document type Editorial
    ISSN 1948-7193
    ISSN (online) 1948-7193
    DOI 10.1021/acschemneuro.1c00394
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  2. Article ; Online: Adult neurogenesis in Alzheimer's disease.

    Choi, Se Hoon / Tanzi, Rudolph E

    Hippocampus

    2023  Volume 33, Issue 4, Page(s) 307–321

    Abstract: Alzheimer's disease (AD) is the most common form of age-related dementia, characterized by progressive memory loss and cognitive disturbances. The hippocampus, where adult hippocampal neurogenesis (AHN), a relatively novel form of brain plasticity that ... ...

    Abstract Alzheimer's disease (AD) is the most common form of age-related dementia, characterized by progressive memory loss and cognitive disturbances. The hippocampus, where adult hippocampal neurogenesis (AHN), a relatively novel form of brain plasticity that refers to the birth of new neurons, occurs, is one of the first brain regions to be affected in AD patients. Recent studies showed that AHN persists throughout life in humans, but it drops sharply in AD patients. Next questions to consider would be whether AHN impairment is a contributing factor to learning and memory impairment in AD and whether restoring AHN could ameliorate or delay cognitive dysfunction. Here, we outline and discuss the current knowledge about the state of AHN in AD patients, AHN impairment as a potentially relevant mechanism underlying memory deficits in AD, therapeutic potential of activating AHN in AD, and the mechanisms of AHN impairment in AD.
    MeSH term(s) Humans ; Adult ; Alzheimer Disease ; Learning/physiology ; Hippocampus/physiology ; Neurons/physiology ; Neurogenesis/physiology ; Memory Disorders
    Language English
    Publishing date 2023-02-07
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1074352-2
    ISSN 1098-1063 ; 1050-9631
    ISSN (online) 1098-1063
    ISSN 1050-9631
    DOI 10.1002/hipo.23504
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  3. Article ; Online: The neuroimmune axis of Alzheimer's disease.

    Jorfi, Mehdi / Maaser-Hecker, Anna / Tanzi, Rudolph E

    Genome medicine

    2023  Volume 15, Issue 1, Page(s) 6

    Abstract: 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 ...

    Abstract 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.
    MeSH term(s) Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Neuroimmunomodulation ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Microglia/metabolism ; Nervous System Diseases
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2023-01-26
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2484394-5
    ISSN 1756-994X ; 1756-994X
    ISSN (online) 1756-994X
    ISSN 1756-994X
    DOI 10.1186/s13073-023-01155-w
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  4. Article ; Online: The role of innate immune genes in Alzheimer's disease.

    Griciuc, Ana / Tanzi, Rudolph E

    Current opinion in neurology

    2021  Volume 34, Issue 2, Page(s) 228–236

    Abstract: Purpose of review: The aim of this study was to provide an update on the role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease, with an emphasis on microglial receptors CD33 and TREM2.: Recent findings: ... ...

    Abstract Purpose of review: The aim of this study was to provide an update on the role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease, with an emphasis on microglial receptors CD33 and TREM2.
    Recent findings: Genome-wide association studies (GWAS) have identified many Alzheimer's disease risk genes related to immune response and microglia including the phagocytic receptors CD33 and TREM2. Recent GWAS and pathway analyses emphasize the crucial role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease. Disease-associated microglia have been characterized by TREM2-dependent upregulation of phagocytic and lipid metabolism genes. Impaired microglial phagocytosis results in amyloid beta (Aβ) accumulation leading to neuroinflammation that is the primary cause of neurodegeneration. CD33 and TREM2 modulate neuroinflammation in Alzheimer's disease and have emerged as therapeutic targets in Alzheimer's disease. Progress has been made to inhibit CD33 by gene therapy, small molecules or immunotherapy, and to increase TREM2 activity by immunotherapy. Finally, mAbs against CD33 and TREM2 have entered clinical trials and may reduce neuroinflammation in Alzheimer's disease brain.
    Summary: Targeting neuroinflammation via CD33 inhibition and/or TREM2 activation may have important implications for neurodegeneration in Alzheimer's disease and may be an addition to monoclonal anti-Aβ antibody treatments that remove plaques without reducing neuroinflammation.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/therapy ; Amyloid beta-Peptides ; Genome-Wide Association Study ; Humans ; Immunity, Innate/genetics ; Membrane Glycoproteins/genetics ; Plaque, Amyloid ; Receptors, Immunologic/genetics
    Chemical Substances Amyloid beta-Peptides ; Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human
    Language English
    Publishing date 2021-01-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1182686-1
    ISSN 1473-6551 ; 1350-7540
    ISSN (online) 1473-6551
    ISSN 1350-7540
    DOI 10.1097/WCO.0000000000000911
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  5. Article ; Online: Correction: Palmitoylated APP Forms Dimers, Cleaved by BACE1.

    Bhattacharyya, Raja / Fenn, Rebecca H / Barren, Cory / Tanzi, Rudolph E / Kovacs, Dora M

    PloS one

    2024  Volume 19, Issue 2, Page(s) e0299972

    Abstract: This corrects the article DOI: 10.1371/journal.pone.0166400.]. ...

    Abstract [This corrects the article DOI: 10.1371/journal.pone.0166400.].
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0299972
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  6. Article: Literatur. Das heilende Selbst

    Chopra, Deepak / Tanzi, Rudolph E.

    Osteopathische Medizin

    2022  Volume 23, Issue 3, Page(s) 41

    Language German
    Document type Article
    ZDB-ID 2041875-9
    ISSN 1615-9071
    Database Current Contents Medicine

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    Zs.A 5417: Show issues Location:
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  7. Article ; Online: Genomic mechanisms in Alzheimer's disease.

    Bertram, Lars / Tanzi, Rudolph E

    Brain pathology (Zurich, Switzerland)

    2020  Volume 30, Issue 5, Page(s) 966–977

    Abstract: Alzheimer's disease (AD) is the most common neurodegenerative disease and, owing to its increasing prevalence, represents one of the leading public health problems in aging populations. The molecular causes underlying the onset and progression of AD are ... ...

    Abstract Alzheimer's disease (AD) is the most common neurodegenerative disease and, owing to its increasing prevalence, represents one of the leading public health problems in aging populations. The molecular causes underlying the onset and progression of AD are manifold and hitherto still incompletely understood. Research over nearly four decades has clearly delineated genetics to play a crucial role in AD susceptibility, likely in concert with non-genetic factors. The field has gained considerable momentum and novel insights over the past 10 years owing to the advent and application of high-throughput genomics technologies in datasets of increasing size. In this contribution to the Mini-Symposium on the Molecular Etiology of Alzheimer's Disease, we review the current status of genomics research in AD. To this end, we scrutinize and discuss the main findings from the two largest and most current genome-wide association studies (GWAS) in the field, that is, the papers published by Jansen et al (Nat Genet 51:404-413) and Kunkle et al (Nat Genet 51:414-430). Particular focus is laid on genomics findings overlapping across both studies and on the novel insights they provide in terms of improving our understanding of the "genomic mechanisms" underlying this devastating disease.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Genetic Predisposition to Disease ; Genome-Wide Association Study/methods ; Genomics/methods ; Humans ; Neurodegenerative Diseases/genetics
    Language English
    Publishing date 2020-07-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.12882
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  8. Article ; Online: TREM2 and Risk of Alzheimer's Disease--Friend or Foe?

    Tanzi, Rudolph E

    The New England journal of medicine

    2015  Volume 372, Issue 26, Page(s) 2564–2565

    MeSH term(s) Alzheimer Disease/etiology ; Animals ; Disease Models, Animal ; Gene Expression ; Humans ; Macrophages/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mutation ; Plaque, Amyloid/etiology ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism
    Chemical Substances Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human
    Language English
    Publishing date 2015-06-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcibr1503954
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  9. Article ; Online: Alzheimer disease risk genes: 29 and counting.

    Bertram, Lars / Tanzi, Rudolph E

    Nature reviews. Neurology

    2019  Volume 15, Issue 4, Page(s) 191–192

    MeSH term(s) Alzheimer Disease/genetics ; Genetic Predisposition to Disease/genetics ; Humans
    Language English
    Publishing date 2019-02-27
    Publishing country England
    Document type Journal Article
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-019-0158-4
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  10. Article ; Online: Is Alzheimer's Disease a Neurogenesis Disorder?

    Choi, Se Hoon / Tanzi, Rudolph E

    Cell stem cell

    2019  Volume 25, Issue 1, Page(s) 7–8

    Abstract: The existence of adult hippocampal neurogenesis (AHN) in humans has been controversial. However, recent reports have detected AHN in aged adults and patients with mild cognitive impairment and Alzheimer's disease (AD), suggesting that therapies aimed at ... ...

    Abstract The existence of adult hippocampal neurogenesis (AHN) in humans has been controversial. However, recent reports have detected AHN in aged adults and patients with mild cognitive impairment and Alzheimer's disease (AD), suggesting that therapies aimed at promoting AHN may be useful for the prevention and treatment of AD.
    MeSH term(s) Adult ; Alzheimer Disease ; Healthy Volunteers ; Hippocampus ; Humans ; Middle Aged ; Neurogenesis
    Language English
    Publishing date 2019-07-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2019.06.001
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