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Article ; Online: Role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury.

Mi, Zhiping / Graham, Steven H

2023 Volume 86, Page(s) 101856

Abstract: UCHL1 is a multifunctional protein expressed at high concentrations in neurons in the brain and spinal cord. UCHL1 plays important roles in regulating the level of cellular free ubiquitin and redox state as well as the degradation of select proteins. ... ...

Abstract	UCHL1 is a multifunctional protein expressed at high concentrations in neurons in the brain and spinal cord. UCHL1 plays important roles in regulating the level of cellular free ubiquitin and redox state as well as the degradation of select proteins. This review focuses on the potential role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury and recovery. Subjects addressed in the review include 1) Normal physiological functions of UCHL1. 2) Posttranslational modification sites and splice variants that alter the function of UCHL1 and mouse models with mutations and deletions of UCHL1. 3) The hypothesized role and pathogenic mechanisms of UCHL1 in neurodegenerative diseases and brain injury. 4) Potential therapeutic strategies targeting UCHL1 in these disorders.
MeSH term(s)	Mice ; Animals ; Humans ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism ; Neurons/metabolism ; Ubiquitin/metabolism ; Brain/metabolism ; Brain Injuries/genetics ; Brain Injuries/metabolism
Chemical Substances	Ubiquitin Thiolesterase (EC 3.4.19.12) ; Ubiquitin ; UCHL1 protein, human ; Uchl1 protein, mouse (EC 3.4.19.12)
Language	English
Publishing date	2023-01-19
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2023.101856
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Article: Sexual Dimorphism in the Limb Bones of Asiatic Toad (

Yan, Chengzhi / Ma, Hui / Yang, Yuejun / Mi, Zhiping

Animals : an open access journal from MDPI

2023 Volume 13, Issue 16

Abstract: Sexual dimorphism is often considered to be the result of differences in the intensity of sexual selection between sexes. From this point of view, the sexual dimorphism of the limb bones of ... ...

Abstract	Sexual dimorphism is often considered to be the result of differences in the intensity of sexual selection between sexes. From this point of view, the sexual dimorphism of the limb bones of the
Language	English
Publishing date	2023-08-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606558-7
ISSN	2076-2615
ISSN	2076-2615
DOI	10.3390/ani13162638
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Article ; Online: Metabolic Adaption of Flexor Carpi Radialis to Amplexus Behavior in Asiatic Toads (

Yan, Chengzhi / Ma, Hui / Yang, Yuejun / Mi, Zhiping

International journal of molecular sciences

2023 Volume 24, Issue 12

Abstract: Amplexus is a type of mating behavior among toads that is essential for successful external fertilization. Most studies have primarily focused on the behavioral diversity of amplexus, and less is known regarding the metabolic changes occurring in ... ...

Abstract	Amplexus is a type of mating behavior among toads that is essential for successful external fertilization. Most studies have primarily focused on the behavioral diversity of amplexus, and less is known regarding the metabolic changes occurring in amplectant males. The aim of this study was to compare the metabolic profiles of amplectant Asiatic toad (
MeSH term(s)	Animals ; Male ; Adaptation, Physiological ; Amino Acids/analysis ; Amino Acids/metabolism ; Bufonidae/metabolism ; Carbohydrate Metabolism ; Carbohydrates/analysis ; Energy Metabolism ; Forelimb ; Lipid Metabolism ; Metabolome ; Muscle, Skeletal/metabolism ; Sexual Behavior, Animal
Chemical Substances	Amino Acids ; Carbohydrates
Language	English
Publishing date	2023-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241210174
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Article ; Online: Sexual Dimorphism in the Limb Bones of Asiatic Toad (Bufo gargarizans) in Relation to Sexual Selection

Yan, Chengzhi / Ma, Hui / Yang, Yuejun / Mi, Zhiping

Animals. 2023 Aug. 16, v. 13, no. 16

2023

Abstract	Sexual dimorphism is often considered to be the result of differences in the intensity of sexual selection between sexes. From this point of view, the sexual dimorphism of the limb bones of the Bufo gargarizans in southwest China was studied. Results showed that the fore- and hindlimb skeletons of this species were sexually dimorphic in anatomy. The humerus, radioulna, and total lengths of the forelimb skeleton of males were substantially longer than those of females, but the hand length of males was smaller than that of females. Several other features of males, such as deltoid and medial crest areas and humerus and radioulnar weights, were also significantly larger than those of females. The femoris, tibiofibula, talus–calcaneus, and foot lengths; total hindlimb skeleton length; and femoral upper crest areas of males were significantly greater than those of females. However, no significant intersexual difference in femoris and tibiofibular weights was observed. These findings suggested that robust forelimb bones and long hindlimb bones could contribute to the mating success of males; if so, sexual selection promotes the evolution of sexual size and shape dimorphism in the limb bones of the B. gargarizans.
Keywords	Bufo ; hindlimbs ; humerus ; sexual dimorphism ; sexual selection ; skeleton ; toads ; China
Language	English
Dates of publication	2023-0816
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2606558-7
ISSN	2076-2615
ISSN	2076-2615
DOI	10.3390/ani13162638
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Article ; Online: Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders.

Ikonomovic, Milos D / Mi, Zhiping / Abrahamson, Eric E

Ageing research reviews

2017 Volume 34, Page(s) 51–63

Abstract: Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer's disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The ... ...

Abstract	Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer's disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The hallmark pathology of AD consists of pathological aggregates of amyloid-β (Aβ) peptides and tau proteins. These molecules are also involved in neuropathology of several other chronic neurodegenerative diseases, and are under intense investigation in the aftermath of TBI as potential contributors to the risk for developing AD and chronic traumatic encephalopathy (CTE). The pathology of TBI is complex and dependent on injury severity, age-at-injury, and length of time between injury and neuropathological evaluation. In addition, the mechanisms influencing pathology and recovery after TBI likely involve genetic/epigenetic factors as well as additional disorders or comorbid states related to age and central and peripheral vascular health. In this regard, dysfunction of the aging neurovascular system could be an important link between TBI and chronic neurodegenerative diseases, either as a precipitating event or related to accumulation of AD-like pathology which is amplified in the context of aging. Thus with advanced age and vascular dysfunction, TBI can trigger self-propagating cycles of neuronal injury, pathological protein aggregation, and synaptic loss resulting in chronic neurodegenerative disease. In this review we discuss evidence supporting TBI and aging as dual, interacting risk factors for AD, and the role of Aβ and cerebral vascular dysfunction in this relationship. Evidence is discussed that Aβ is involved in cyto- and synapto-toxicity after severe TBI, and that its chronic effects are potentiated by aging and impaired cerebral vascular function. From a therapeutic perspective, we emphasize that in the fields of TBI- and aging-related neurodegeneration protective strategies should include preservation of neurovascular function.
MeSH term(s)	Aging/pathology ; Aging/physiology ; Aging/psychology ; Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Brain/blood supply ; Brain/metabolism ; Brain/physiopathology ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/pathology ; Humans ; Neurovascular Coupling/physiology ; Risk Factors ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; tau Proteins
Language	English
Publishing date	2017-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2016.11.003
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Article ; Online: Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice.

Mi, Zhiping / Ma, Jie / Zeh, Dennis J / Rose, Marie E / Henchir, Jeremy J / Liu, Hao / Ma, Xiecheng / Cao, Guodong / Dixon, C Edward / Graham, Steven H

Experimental neurology

2023 Volume 373, Page(s) 114650

Abstract: Traumatic brain injury (TBI) is often associated with axonal injury that leads to significant motor and cognitive deficits. Ubiquitin carboxy terminal hydrolase L1 (UCHL1) is highly expressed in neurons and loss of its activity plays an important role in ...

Abstract	Traumatic brain injury (TBI) is often associated with axonal injury that leads to significant motor and cognitive deficits. Ubiquitin carboxy terminal hydrolase L1 (UCHL1) is highly expressed in neurons and loss of its activity plays an important role in the pathogenesis of TBI. Fusion protein was constructed containing wild type (WT) UCHL1 and the HIV trans-activator of transcription capsid protein transduction domain (TAT-UCHL1) that facilitates transport of the protein into neurons after systemic administration. Additional mutant proteins bearing cysteine to alanine UCHL1 mutations at cysteine 152 (C152A TAT-UCHL1) that prevents nitric oxide and reactive lipid binding of C152, and at cysteine 220 (C220A TAT-UCHL1) that inhibits farnesylation of the C220 site were also constructed. WT, C152A, and C220A TAT-UCHL1 proteins administered to mice systemically after controlled cortical impact (CCI) were detectable in brain at 1 h, 4 h and 24 h after CCI by immunoblot. Mice treated with C152A or WT TAT-UCHL1 decreased axonal injury detected by NF200 immunohistochemistry 24 h after CCI, but C220A TAT-UCHL1 treatment had no significant effect. Further study indicated that WT TAT-UCHL1 treatment administered 24 h after CCI alleviated axonal injury as detected by SMI32 immunoreactivity 7 d after CCI, improved motor and cognitive deficits, reduced accumulation of total and K48-linked poly-Ub proteins, and attenuated the increase of the autophagy marker Beclin-1. These results suggest that UCHL1 activity contributes to the pathogenesis of white matter injury, and that restoration of UCHL1 activity by systemic treatment with WT TAT-UCHL1 after CCI may improve motor and cognitive deficits. These results also suggest that farnesylation of the C220 site may be required for the protective effects of UCHL1.
MeSH term(s)	Mice ; Animals ; Ubiquitin Thiolesterase/genetics ; Gene Products, tat/therapeutic use ; Cysteine ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries, Traumatic/pathology ; Axons/pathology
Chemical Substances	Ubiquitin Thiolesterase (EC 3.4.19.12) ; Gene Products, tat ; Cysteine (K848JZ4886)
Language	English
Publishing date	2023-12-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2023.114650
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Article ; Online: Vesicular Glutamate Transporter Changes in the Cortical Default Mode Network During the Clinical and Pathological Progression of Alzheimer's Disease.

Mi, Zhiping / Abrahamson, Eric E / Ryu, Angela Y / Malek-Ahmadi, Michael / Kofler, Julia K / Fish, Kenneth N / Sweet, Robert A / Villemagne, Victor L / Schneider, Julie A / Mufson, Elliott J / Ikonomovic, Milos D

Journal of Alzheimer's disease : JAD

2023 Volume 94, Issue 1, Page(s) 227–246

Abstract: Background: Altered glutamatergic neurotransmission may contribute to impaired default mode network (DMN) function in Alzheimer's disease (AD). Among the DMN hub regions, frontal cortex (FC) was suggested to undergo a glutamatergic plasticity response ... ...

Abstract	Background: Altered glutamatergic neurotransmission may contribute to impaired default mode network (DMN) function in Alzheimer's disease (AD). Among the DMN hub regions, frontal cortex (FC) was suggested to undergo a glutamatergic plasticity response in prodromal AD, while the status of glutamatergic synapses in the precuneus (PreC) during clinical-neuropathological AD progression is not known. Objective: To quantify vesicular glutamate transporter VGluT1- and VGluT2-containing synaptic terminals in PreC and FC across clinical stages of AD. Methods: Unbiased sampling and quantitative confocal immunofluorescence of cortical VGluT1- and VGluT2-immunoreactive profiles and spinophilin-labeled dendritic spines were performed in cases with no cognitive impairment (NCI), mild cognitive impairment (MCI), mild-moderate AD (mAD), or moderate-severe AD (sAD). Results: In both regions, loss of VGluT1-positive profile density was seen in sAD compared to NCI, MCI, and mAD. VGluT1-positive profile intensity in PreC did not differ across groups, while in FC it was greater in MCI, mAD, and sAD compared to NCI. VGluT2 measures were stable in PreC while FC had greater VGluT2-positive profile density in MCI compared to sAD, but not NCI or mAD. Spinophilin measures in PreC were lower in mAD and sAD compared to NCI, while in FC they were stable across groups. Lower VGluT1 and spinophilin measures in PreC, but not FC, correlated with greater neuropathology. Conclusion: Frank loss of VGluT1 in advanced AD relative to NCI occurs in both DMN regions. In FC, an upregulation of VGluT1 protein content in remaining glutamatergic terminals may contribute to this region's plasticity response in AD.
MeSH term(s)	Humans ; Alzheimer Disease/pathology ; Vesicular Glutamate Transport Proteins/metabolism ; Default Mode Network ; Vesicular Glutamate Transport Protein 2/metabolism ; Presynaptic Terminals/metabolism ; Vesicular Glutamate Transport Protein 1/metabolism
Chemical Substances	Vesicular Glutamate Transport Proteins ; Vesicular Glutamate Transport Protein 2 ; Vesicular Glutamate Transport Protein 1
Language	English
Publishing date	2023-05-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-221063
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Article ; Online: Abolishing UCHL1's hydrolase activity exacerbates TBI-induced axonal injury and neuronal death in mice.

Mi, Zhiping / Liu, Hao / Rose, Marie E / Ma, Xiecheng / Reay, Daniel P / Ma, Jie / Henchir, Jeremy / Dixon, C Edward / Graham, Steven H

Experimental neurology

2020 Volume 336, Page(s) 113524

Abstract: Ubiquitin (Ub) C-terminal hydrolase L1 (UCHL1) is a multifunctional protein that is expressed in neurons throughout brain at high levels. UCHL1 deletion is associated with axonal degeneration, progressive sensory motor ataxia, and premature death in mice. ...

Abstract	Ubiquitin (Ub) C-terminal hydrolase L1 (UCHL1) is a multifunctional protein that is expressed in neurons throughout brain at high levels. UCHL1 deletion is associated with axonal degeneration, progressive sensory motor ataxia, and premature death in mice. UCHL1 has been hypothesized to play a role in the pathogenesis of neurodegenerative diseases and recovery after neuronal injury. UCHL1 hydrolyzes Ub from polyubiquitinated (poly-Ub) proteins, but also may ligate Ub to select neuronal proteins, and interact with cytoskeletal proteins. These and other mechanisms have been hypothesized to underlie UCHL1's role in neurodegeneration and response to brain injury. A UCHL1 knockin mouse containing a C90A mutation (C90A) devoid of hydrolase activity was constructed. The C90A mouse did not develop the sensory and motor deficits, degeneration of the gracile nucleus and tract, or premature death as seen in UCHL1 deficient mice. C90A and wild type (WT) mice were subjected to the controlled cortical impact (CCI) model of traumatic brain injury (TBI), and cell death, axonal injury and behavioral outcome were assessed. C90A mice exhibited decreased spared tissue volume, greater loss of CA1 hippocampal neurons and greater axonal injury as detected using anti-amyloid precursor protein (APP) antibody and anti- non-phosphorylated neurofilament H (SMI-32) antibody immunohistochemistry after CCI compared to WT controls. Poly-Ub proteins and Beclin-1 were elevated after CCI in C90A mice compared to WT controls. Vestibular motor deficits assessed using the beam balance test resolved by day 5 after CCI in WT mice but not in C90A mice. These results suggest that the hydrolase activity of UCHL1 does not account for the progressive neurodegeneration and premature death seen in mice that do not express full length UCHL1. The hydrolase activity of UCHL1 contributes to the function of the ubiquitin proteasome pathway (UPP), ameliorates activation of autophagy, and improves motor recovery after CCI. Thus, UCHL1 hydrolase activity plays an important role in acute injury response after TBI.
MeSH term(s)	Amyloid beta-Protein Precursor/antagonists & inhibitors ; Animals ; Autophagy ; Axons/pathology ; Beclin-1/metabolism ; Brain Injuries, Traumatic/genetics ; Brain Injuries, Traumatic/pathology ; Brain Injuries, Traumatic/psychology ; CA1 Region, Hippocampal/pathology ; Cell Death/drug effects ; Cell Death/genetics ; Gene Knock-In Techniques ; Mice ; Mutation/genetics ; Neurons/pathology ; Psychomotor Performance ; Signal Transduction/genetics ; Ubiquitin Thiolesterase/genetics ; Ubiquitination
Chemical Substances	APP protein, mouse ; Amyloid beta-Protein Precursor ; Beclin-1 ; Becn1 protein, mouse ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Uchl1 protein, mouse (EC 3.4.19.12)
Language	English
Publishing date	2020-11-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2020.113524
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Article ; Online: Mutation of a Ubiquitin Carboxy Terminal Hydrolase L1 Lipid Binding Site Alleviates Cell Death, Axonal Injury, and Behavioral Deficits After Traumatic Brain Injury in Mice.

Mi, Zhiping / Liu, Hao / Rose, Marie E / Ma, Jie / Reay, Daniel P / Ma, Xiecheng / Henchir, Jeremy J / Dixon, C Edward / Graham, Steven H

Neuroscience

2021 Volume 475, Page(s) 127–136

Abstract: Ubiquitin carboxy terminal hydrolase L1 (UCHL1) is a protein highly expressed in neurons that may play important roles in the ubiquitin proteasome pathway (UPP) in neurons, axonal integrity, and motor function after traumatic brain injury (TBI). Binding ... ...

Abstract	Ubiquitin carboxy terminal hydrolase L1 (UCHL1) is a protein highly expressed in neurons that may play important roles in the ubiquitin proteasome pathway (UPP) in neurons, axonal integrity, and motor function after traumatic brain injury (TBI). Binding of reactive lipid species to cysteine 152 of UCHL1 results in unfolding, aggregation, and inactivation of the enzyme. To test the role of this mechanism in TBI, mice bearing a cysteine to alanine mutation at site 152 (C152A mice) that renders UCHL1 resistant to inactivation by reactive lipids were subjected to the controlled cortical impact model (CCI) of TBI and compared to wild type (WT) controls. Alterations in protein ubiquitination and activation of autophagy pathway markers in traumatized brain were detected by immunoblotting. Cell death and axonal injury were determined by histological assessment and anti-amyloid precursor protein (APP) immunohistochemistry. Behavioral outcomes were determined using the beam balance and Morris water maze tests. C152A mice had reduced accumulation of ubiquitinated proteins, decreased activation of the autophagy markers Beclin-1 and LC3B, a decreased number of abnormal axons, decreased CA1 cell death, and improved motor and cognitive function compared to WT controls after CCI; no significant change in spared tissue volume was observed. These results suggest that binding of lipid substrates to cysteine 152 of UCHL1 is important in the pathogenesis of injury and recovery after TBI and may be a novel target for future therapeutic approaches.
MeSH term(s)	Animals ; Axons/metabolism ; Binding Sites ; Brain Injuries, Traumatic ; Cell Death ; Lipids ; Mice ; Mutation/genetics ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	Lipids ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Uchl1 protein, mouse (EC 3.4.19.12)
Language	English
Publishing date	2021-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2021.09.001
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Article ; Online: Immunohistochemical analysis of hippocampal butyrylcholinesterase: Implications for regional vulnerability in Alzheimer's disease.

Mizukami, Katsuyoshi / Akatsu, Hiroyasu / Abrahamson, Eric E / Mi, Zhiping / Ikonomovic, Milos D

Neuropathology : official journal of the Japanese Society of Neuropathology

2016 Volume 36, Issue 2, Page(s) 135–145

Abstract: Studies of acetylcholine degrading enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in Alzheimer's disease (AD) have suggested their potential role in the development of fibrillar amyloid-β (Aβ) plaques (amyloid plaques). A recent ... ...

Abstract	Studies of acetylcholine degrading enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in Alzheimer's disease (AD) have suggested their potential role in the development of fibrillar amyloid-β (Aβ) plaques (amyloid plaques). A recent genome-wide association study analysis identified a novel association between genetic variations in the BCHE locus and amyloid burden. We studied BChE immunoreactivity in hippocampal tissue sections from AD and control cases, and examined its relationship with amyloid plaques, neurofibrillary tangles (NFT), dystrophic neurites (DN) and neuropil threads (NT). Compared to controls, AD cases had greater BChE immunoreactivity in hippocampal neurons and neuropils in CA2/3, but not in the CA1, CA4 and dentate gyrus. The majority of amyloid plaques (> 80%, using a pan-amyloid marker X-34) contained discrete neuritic clusters which were dual-labeled with antibodies against BChE and phosphorylated tau (clone AT8). There was no association between overall regional BChE immunoreaction intensity and amyloid plaque burden. In contrast to previous reports, BChE was localized in only a fraction (~10%) of classic NFT (positive for X-34). A similar proportion of BChE-immunoreactive pyramidal cells were AT8 immunoreactive. Greater NFT and DN loads were associated with greater BChE immunoreaction intensity in CA2/3, but not in CA1, CA4 and dentate gyrus. Our results demonstrate that in AD hippocampus, BChE accumulates in neurons and plaque-associated neuritic clusters, but only in a small proportion of NFT. The association between greater neurofibrillary pathology burden and markedly increased BChE immunoreactivity, observed selectively in CA2/3 region, could reflect a novel compensatory mechanism. Since CA2/3 is generally considered more resistant to AD pathology, BChE upregulation could impact the cholinergic modulation of glutamate neurotransmission to prevent/reduce neuronal excitotoxicity in AD hippocampus.
MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/enzymology ; Alzheimer Disease/pathology ; Butyrylcholinesterase/analysis ; Butyrylcholinesterase/biosynthesis ; Female ; Hippocampus/enzymology ; Hippocampus/pathology ; Humans ; Immunohistochemistry ; Male ; Neurofibrillary Tangles/enzymology ; Neurofibrillary Tangles/pathology ; Neurons/enzymology ; Neurons/pathology ; Neuropil Threads/enzymology ; Neuropil Threads/pathology ; Plaque, Amyloid/enzymology ; Plaque, Amyloid/pathology
Chemical Substances	Butyrylcholinesterase (EC 3.1.1.8)
Language	English
Publishing date	2016-04
Publishing country	Australia
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483794-8
ISSN	1440-1789 ; 0919-6544
ISSN (online)	1440-1789
ISSN	0919-6544
DOI	10.1111/neup.12241
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