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  1. Article ; Online: The Cell Biology of LRRK2 in Parkinson's Disease.

    Usmani, Ahsan / Shavarebi, Farbod / Hiniker, Annie

    Molecular and cellular biology

    2021  Volume 41, Issue 5

    Abstract: Point mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson's disease (PD) and are implicated in a significant proportion of apparently sporadic PD cases. Clinically, LRRK2-driven PD is indistinguishable from ... ...

    Abstract Point mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson's disease (PD) and are implicated in a significant proportion of apparently sporadic PD cases. Clinically, LRRK2-driven PD is indistinguishable from sporadic PD, making it an attractive genetic model for the much more common sporadic PD. In this review, we highlight recent advances in understanding LRRK2's subcellular functions using LRRK2-driven PD models, while also considering some of the limitations of these model systems. Recent developments of particular importance include new evidence of key LRRK2 functions in the endolysosomal system and LRRK2's regulation of and by Rab GTPases. Additionally, LRRK2's interaction with the cytoskeleton allowed elucidation of the LRRK2 structure and appears relevant to LRRK2 protein degradation and LRRK2 inhibitor therapies. We further discuss how LRRK2's interactions with other PD-driving genes, such as the
    MeSH term(s) Cytoskeleton/metabolism ; Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Protein Serine-Threonine Kinases/metabolism ; rab GTP-Binding Proteins/metabolism
    Chemical Substances LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2021-04-22
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00660-20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The Cell Biology of LRRK2 in Parkinson's Disease

    Usmani, Ahsan / Shavarebi, Farbod / Hiniker, Annie

    Molecular and Cellular Biology. 2021 May 1, v. 41, no. 5 p.e00660-20-

    2021  

    Abstract: Point mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson’s disease (PD) and are implicated in a significant proportion of apparently sporadic PD cases. Clinically, LRRK2-driven PD is indistinguishable from ... ...

    Abstract Point mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of familial Parkinson’s disease (PD) and are implicated in a significant proportion of apparently sporadic PD cases. Clinically, LRRK2-driven PD is indistinguishable from sporadic PD, making it an attractive genetic model for the much more common sporadic PD. In this review, we highlight recent advances in understanding LRRK2's subcellular functions using LRRK2-driven PD models, while also considering some of the limitations of these model systems. Recent developments of particular importance include new evidence of key LRRK2 functions in the endolysosomal system and LRRK2’s regulation of and by Rab GTPases. Additionally, LRRK2's interaction with the cytoskeleton allowed elucidation of the LRRK2 structure and appears relevant to LRRK2 protein degradation and LRRK2 inhibitor therapies. We further discuss how LRRK2's interactions with other PD-driving genes, such as the VPS35, GBA1, and SNCA genes, may highlight cellular pathways more broadly disrupted in PD.
    Keywords Parkinson disease ; cytoskeleton ; genetic models ; guanosinetriphosphatase ; protein degradation ; LRRK2 ; Parkinson's disease ; endolysosome ; kinase ; microtubule
    Language English
    Dates of publication 2021-0501
    Publishing place Taylor & Francis
    Document type Article ; Online
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00660-20
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  3. Article ; Online: Skeletal myopathy in Pompe disease: a failure of satellite cell activation?

    Hiniker, Annie / Margeta, Marta

    Acta neuropathologica communications

    2018  Volume 6, Issue 1, Page(s) 133

    Language English
    Publishing date 2018-11-30
    Publishing country England
    Document type Letter
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-018-0638-6
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  4. Article ; Online: Age-at-Onset and

    Smirnov, Denis S / Galasko, Douglas / Hiniker, Annie / Edland, Steven D / Salmon, David P

    Neurology

    2021  Volume 96, Issue 18, Page(s) e2272–e2283

    Abstract: Objective: To characterize age-related clinical heterogeneity in Alzheimer disease (AD) and determine whether it is modified by : Methods: In this retrospective cohort study, regression and mixed effects models assessed effects of estimated age at ... ...

    Abstract Objective: To characterize age-related clinical heterogeneity in Alzheimer disease (AD) and determine whether it is modified by
    Methods: In this retrospective cohort study, regression and mixed effects models assessed effects of estimated age at onset,
    Results: A bimodal distribution of age at onset frequency in
    Conclusions: Early-onset sporadic AD is associated with a greater likelihood of an atypical, non-memory-dominant clinical presentation, especially in the absence of the
    MeSH term(s) Age of Onset ; Aged ; Aged, 80 and over ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Apolipoproteins E/genetics ; Female ; Genetic Heterogeneity ; Humans ; Male ; Middle Aged ; Retrospective Studies
    Chemical Substances Apolipoproteins E
    Language English
    Publishing date 2021-03-15
    Publishing country United States
    Document type Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 207147-2
    ISSN 1526-632X ; 0028-3878
    ISSN (online) 1526-632X
    ISSN 0028-3878
    DOI 10.1212/WNL.0000000000011772
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Selective tau seeding assays and isoform-specific antibodies define neuroanatomic distribution of progressive supranuclear palsy pathology arising in Alzheimer's disease.

    Coughlin, David G / Goodwill, Vanessa S / Standke, Heidi G / Kim, Yongya / Coley, Nicolas / Pizzo, Donald P / Galasko, Douglas / Kraus, Allison / Hiniker, Annie

    Acta neuropathologica

    2022  Volume 144, Issue 4, Page(s) 789–792

    MeSH term(s) Alzheimer Disease/pathology ; Carbolines ; Humans ; Protein Isoforms ; Supranuclear Palsy, Progressive/pathology ; tau Proteins
    Chemical Substances Carbolines ; Protein Isoforms ; tau Proteins
    Language English
    Publishing date 2022-08-18
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1079-0
    ISSN 1432-0533 ; 0001-6322
    ISSN (online) 1432-0533
    ISSN 0001-6322
    DOI 10.1007/s00401-022-02480-x
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  6. Article ; Online: PHGDH expression increases with progression of Alzheimer's disease pathology and symptoms.

    Chen, Xu / Calandrelli, Riccardo / Girardini, John / Yan, Zhangming / Tan, Zhiqun / Xu, Xiangmin / Hiniker, Annie / Zhong, Sheng

    Cell metabolism

    2022  Volume 34, Issue 5, Page(s) 651–653

    Abstract: Chen et al. reveal an increase of phosphoglycerate dehydrogenase (PHGDH) mRNA and protein levels in two mouse models and four human cohorts in Alzheimer's disease brains compared to age- and sex-matched control brains. The increase of PHGDH expression in ...

    Abstract Chen et al. reveal an increase of phosphoglycerate dehydrogenase (PHGDH) mRNA and protein levels in two mouse models and four human cohorts in Alzheimer's disease brains compared to age- and sex-matched control brains. The increase of PHGDH expression in human brain correlates with symptomatic development and disease pathology.
    MeSH term(s) Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Cell Line, Tumor ; Mice ; Phosphoglycerate Dehydrogenase/genetics ; Phosphoglycerate Dehydrogenase/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Serine/metabolism
    Chemical Substances RNA, Messenger ; Serine (452VLY9402) ; Phosphoglycerate Dehydrogenase (EC 1.1.1.95)
    Language English
    Publishing date 2022-05-04
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2022.02.008
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  7. Article ; Online: TDP-43 Pathology Exacerbates Cognitive Decline in Primary Age-Related Tauopathy.

    Smirnov, Denis S / Salmon, David P / Galasko, Douglas / Edland, Steven D / Pizzo, Donald P / Goodwill, Vanessa / Hiniker, Annie

    Annals of neurology

    2022  Volume 92, Issue 3, Page(s) 425–438

    Abstract: Objective: Primary age-related tauopathy (PART) refers to tau neurofibrillary tangles restricted largely to the medial temporal lobe in the absence of significant beta-amyloid plaques. PART has been associated with cognitive impairment, but ... ...

    Abstract Objective: Primary age-related tauopathy (PART) refers to tau neurofibrillary tangles restricted largely to the medial temporal lobe in the absence of significant beta-amyloid plaques. PART has been associated with cognitive impairment, but contributions from concomitant limbic age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) are underappreciated.
    Methods: We compare prevalence of LATE-NC and vascular copathologies in age- and Braak-matched patients with PART (n = 45, Braak stage I-IV, Thal phase 0-2) or early stage Alzheimer disease neuropathologic change (ADNC; n = 51, Braak I-IV, Thal 3-5), and examine their influence on clinical and cognitive decline.
    Results: Concomitant LATE-NC and vascular pathology were equally common, and cognition was equally impaired, in PART (Mini-Mental State Examination [MMSE] = 24.8 ± 6.9) and ADNC (MMSE = 24.2 ± 6.0). Patients with LATE-NC were more impaired than those without LATE-NC on the MMSE (by 5.8 points, 95% confidence interval [CI] = 3.0-8.6), Mattis Dementia Rating Scale (DRS; 17.5 points, 95% CI = 7.1-27.9), Clinical Dementia Rating, sum of boxes scale (CDR-sob; 5.2 points, 95% CI = 2.1-8.2), memory composite (0.8 standard deviations [SD], 95% CI = 0.1-1.6), and language composite (1.1 SD, 95% CI = 0.2-2.0), and more likely to receive a dementia diagnosis (odds ratio = 4.8, 95% CI = 1.5-18.0). Those with vascular pathology performed worse than those without on the DRS (by 10.2 points, 95% CI = 0.1-20.3) and executive composite (1.3 SD, 95% CI = 0.3-2.3). Cognition declined similarly in PART and ADNC over the 5 years preceding death; however, LATE-NC was associated with more rapid decline on the MMSE (β = 1.9, 95% CI = 0.9-3.0), DRS (β = 7.8, 95% CI = 3.4-12.7), CDR-sob (β = 1.9, 95% CI = 0.4-3.7), language composite (β = 0.5 SD, 95% CI = 0.1-0.8), and vascular pathology with more rapid decline on the DRS (β = 5.2, 95% CI = 0.6-10.2).
    Interpretation: LATE-NC, and to a lesser extent vascular copathology, exacerbate cognitive impairment and decline in PART and early stage ADNC. ANN NEUROL 2022;92:425-438.
    MeSH term(s) Alzheimer Disease/pathology ; Cognitive Dysfunction/pathology ; DNA-Binding Proteins ; Humans ; Neurofibrillary Tangles/pathology ; Plaque, Amyloid/pathology ; Tauopathies/pathology
    Chemical Substances DNA-Binding Proteins ; TARDBP protein, human
    Language English
    Publishing date 2022-07-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80362-5
    ISSN 1531-8249 ; 0364-5134
    ISSN (online) 1531-8249
    ISSN 0364-5134
    DOI 10.1002/ana.26438
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  8. Article ; Online: TDP43 pathology in chronic traumatic encephalopathy retinas.

    Phansalkar, Ragini / Goodwill, Vanessa S / Nirschl, Jeffrey J / De Lillo, Chiara / Choi, Jihee / Spurlock, Elizabeth / Coughlin, David G / Pizzo, Donald / Sigurdson, Christina J / Hiniker, Annie / Alvarez, Victor E / Mckee, Ann C / Lin, Jonathan H

    Acta neuropathologica communications

    2023  Volume 11, Issue 1, Page(s) 152

    Abstract: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive head trauma. Brain pathology in CTE is characterized by neuronal loss, gliosis, and a distinctive pattern of neuronal accumulation of hyper-phosphorylated ... ...

    Abstract Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive head trauma. Brain pathology in CTE is characterized by neuronal loss, gliosis, and a distinctive pattern of neuronal accumulation of hyper-phosphorylated tau (p-tau) and phospho-TDP43 (p-TDP43). Visual anomalies have been reported by patients with CTE, but the ocular pathology underlying these symptoms is unknown. We evaluated retinal pathology in post-mortem eyes collected from 8 contact sport athletes with brain autopsy-confirmed stage IV CTE and compared their findings to retinas from 8 control patients without CTE and with no known history of head injury. Pupil-optic nerve cross sections were prepared and stained with hematoxylin and eosin (H&E), p-tau, p-TDP43, and total TDP43 by immunohistochemistry. No significant retinal degeneration was observed in CTE eyes compared to control eyes by H&E. Strong cytoplasmic p-TDP43 and total TDP43 staining was found in 6/8 CTE eyes in a subset of inner nuclear layer interneurons (INL) of the retina, while only 1/8 control eyes showed similar p-TDP43 pathology. The morphology and location of these inner nuclear layer interneurons were most compatible with retinal horizontal cells, although other retinal cell types present in INL could not be ruled out. No p-tau pathology was observed in CTE or control retinas. These findings identify novel retinal TDP43 pathology in CTE retinas and support further investigation into the role of p-TDP43 in producing visual deficits in patients with CTE.
    MeSH term(s) Humans ; Chronic Traumatic Encephalopathy ; Neurodegenerative Diseases ; Retina ; Retinal Degeneration ; Brain ; Craniocerebral Trauma ; Eosine Yellowish-(YS)
    Chemical Substances Eosine Yellowish-(YS) (TDQ283MPCW)
    Language English
    Publishing date 2023-09-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-023-01650-6
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  9. Article ; Online: Bilateral Choroidal Metastases from Pancreatic Adenocarcinoma.

    Hiniker, Annie / Oakes, Scott A / Rao, Rajesh C

    Ophthalmology

    2017  Volume 124, Issue 12, Page(s) 1825

    Language English
    Publishing date 2017-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 392083-5
    ISSN 1549-4713 ; 0161-6420
    ISSN (online) 1549-4713
    ISSN 0161-6420
    DOI 10.1016/j.ophtha.2017.08.020
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  10. Article ; Online: Endogenous Rab38 regulates LRRK2's membrane recruitment and substrate Rab phosphorylation in melanocytes.

    Unapanta, Alexandra / Shavarebi, Farbod / Porath, Jacob / Shen, Yiyi / Balen, Carson / Nguyen, Albert / Tseng, Josh / Leong, Weng Si / Liu, Michelle / Lis, Pawel / Di Pietro, Santiago M / Hiniker, Annie

    The Journal of biological chemistry

    2023  Volume 299, Issue 10, Page(s) 105192

    Abstract: Point mutations in leucine-rich repeat kinase 2 (LRRK2) cause Parkinson's disease and augment LRRK2's kinase activity. However, cellular pathways that endogenously enhance LRRK2 kinase function have not been identified. While overexpressed Rab29 draws ... ...

    Abstract Point mutations in leucine-rich repeat kinase 2 (LRRK2) cause Parkinson's disease and augment LRRK2's kinase activity. However, cellular pathways that endogenously enhance LRRK2 kinase function have not been identified. While overexpressed Rab29 draws LRRK2 to Golgi membranes to increase LRRK2 kinase activity, there is little evidence that endogenous Rab29 performs this function under physiological conditions. Here, we identify Rab38 as a novel physiologic regulator of LRRK2 in melanocytes. In mouse melanocytes, which express high levels of Rab38, Rab32, and Rab29, knockdown (or CRISPR knockout) of Rab38, but not Rab32 or Rab29, decreases phosphorylation of multiple LRRK2 substrates, including Rab10 and Rab12, by both endogenous LRRK2 and exogenous Parkinson's disease-mutant LRRK2. In B16-F10 mouse melanoma cells, Rab38 drives LRRK2 membrane association and overexpressed kinase-active LRRK2 shows striking pericentriolar recruitment, which is dependent on the presence of endogenous Rab38 but not Rab32 or Rab29. Consistently, knockdown or mutation of BLOC-3, the guanine nucleotide exchange factor for Rab38 and Rab32, inhibits Rab38's regulation of LRRK2. Deletion or mutation of LRRK2's Rab38-binding site in the N-terminal armadillo domain decreases LRRK2 membrane association, pericentriolar recruitment, and ability to phosphorylate Rab10. In sum, our data identify Rab38 as a physiologic regulator of LRRK2 function and lend support to a model in which LRRK2 plays a central role in Rab GTPase coordination of vesicular trafficking.
    MeSH term(s) Animals ; Mice ; Golgi Apparatus/enzymology ; Golgi Apparatus/genetics ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Melanocytes/metabolism ; Mutation ; Parkinson Disease/metabolism ; Phosphorylation ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism ; HEK293 Cells ; Humans ; Gene Expression ; Protein Domains ; Protein Binding ; Intracellular Membranes/metabolism
    Chemical Substances Guanine Nucleotide Exchange Factors ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; rab GTP-Binding Proteins (EC 3.6.5.2) ; Rab38 protein, mouse (EC 3.6.1.-)
    Language English
    Publishing date 2023-08-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.105192
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