Implantable brain computer interface: challenges to neurotechnology translation.

Abstract:

:This article reviews three concepts related to implantable brain computer interface (BCI) devices being designed for human use: neural signal extraction primarily for motor commands, signal insertion to restore sensation, and technological challenges that remain. A significant body of literature has occurred over the past four decades regarding motor cortex signal extraction for upper extremity movement or computer interface. However, little is discussed regarding postural or ambulation command signaling. Auditory prosthesis research continues to represent the majority of literature on BCI signal insertion. Significant hurdles continue in the technological translation of BCI implants. These include developing a stable neural interface, significantly increasing signal processing capabilities, and methods of data transfer throughout the human body. The past few years, however, have provided extraordinary human examples of BCI implant potential. Despite technological hurdles, proof-of-concept animal and human studies provide significant encouragement that BCI implants may well find their way into mainstream medical practice in the foreseeable future.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Konrad P,Shanks T

doi

10.1016/j.nbd.2009.12.007

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

369-75

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(09)00362-3

journal_volume

38

pub_type

杂志文章,评审
  • Alzheimer pathology disorganizes cortico-cortical circuitry: direct evidence from a transgenic animal model.

    abstract::It has been proposed that Alzheimer disease (AD) is associated with a "disconnection syndrome" due to the gradual loss of morphological and functional integrity of cortico-cortical pathways. This hypothesis derives from indirect neuropathological observations, but definitive evidence that AD primarily targets cortico-...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.01.008

    authors: Delatour B,Blanchard V,Pradier L,Duyckaerts C

    更新日期:2004-06-01 00:00:00

  • Cytokine profiling in the prefrontal cortex of Parkinson's Disease and Multiple System Atrophy patients.

    abstract::Parkinson's Disease (PD) and Multiple System Atrophy (MSA) are neurodegenerative diseases characterized neuropathologically by alpha-synuclein accumulation in brain cells. This accumulation is hypothesized to contribute to constitutive neuroinflammation, and to participate in the neurodegeneration. Cytokines, which ar...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2017.07.014

    authors: Rydbirk R,Elfving B,Andersen MD,Langbøl MA,Folke J,Winge K,Pakkenberg B,Brudek T,Aznar S

    更新日期:2017-10-01 00:00:00

  • Neuronal tissue-specific ribonucleoprotein complex formation on SOD1 mRNA: alterations by ALS SOD1 mutations.

    abstract::Amyotrophic lateral sclerosis (ALS) is a fatal disease of unknown etiology. Mutations in copper/zinc superoxide dismutase (SOD1) are the most commonly associated genetic abnormality. Given that SOD1 is ubiquitously expressed, the exclusive vulnerability of motor neurons is one of the most puzzling issues in ALS resear...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.03.007

    authors: Ge WW,Leystra-Lantz C,Sanelli TR,McLean J,Wen W,Strong W,Strong MJ

    更新日期:2006-08-01 00:00:00

  • Effects of exercise on gene-expression profile in the rat hippocampus.

    abstract::Exercise has beneficial effects on brain function, including the promotion of plasticity and the enhancement of learning and memory performance. Previously we found that exercise increases the expression of certain neurotrophic factors including brain derived neurotrophic factor in the rat hippocampus. To further expl...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.2001.0427

    authors: Tong L,Shen H,Perreau VM,Balazs R,Cotman CW

    更新日期:2001-12-01 00:00:00

  • Progressive neuroanatomical changes caused by Grin1 loss-of-function mutation.

    abstract::NMDA receptor dysfunction is central to the encephalopathies caused by missense mutations in the NMDA receptor subunit genes. Missense variants of GRIN1, GRIN2A, and GRIN2B cause similar syndromes with varying severity of intellectual impairment, autism, epilepsy, and motor dysfunction. To gain insight into possible b...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.104527

    authors: Intson K,van Eede MC,Islam R,Milenkovic M,Yan Y,Salahpour A,Henkelman RM,Ramsey AJ

    更新日期:2019-12-01 00:00:00

  • RIP3 participates in early brain injury after experimental subarachnoid hemorrhage in rats by inducing necroptosis.

    abstract::Necroptosis is a regulated form of necrosis that is mediated by a variety of proteins including tumor necrosis factor-α (TNF-α) and receptor-interacting proteins (RIPs). TNF-α, a critical inflammatory molecule, is one of the initiating signals in the necroptosis pathway, and RIP3 acts as a switch that commits the cell...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.05.004

    authors: Yuan S,Yu Z,Zhang Z,Zhang J,Zhang P,Li X,Li H,Shen H,Chen G

    更新日期:2019-09-01 00:00:00

  • Polyglutamine-induced neurodegeneration in SCA3 is not mitigated by non-expanded ataxin-3: conclusions from double-transgenic mouse models.

    abstract::A crucial question in polyQ-induced neurodegeneration is the influence of wild type protein on the formation of aggregates and toxicity. Recently it was shown that non-expanded ataxin-3 protein mitigated neurodegeneration in a Drosophila and mouse model of SCA3. We now explored the effects of overexpressing non-expand...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.01.005

    authors: Hübener J,Riess O

    更新日期:2010-04-01 00:00:00

  • Does gene deletion of AMPA GluA1 phenocopy features of schizoaffective disorder?

    abstract::Glutamatergic dysfunction is strongly implicated in schizophrenia and mood disorders. GluA1 knockout (KO) mice display schizophrenia- and depression-related abnormalities. Here, we asked whether GluA1 KO show mania-related abnormalities. KO were tested for behavior in approach/avoid conflict tests, responses to repeat...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.08.005

    authors: Fitzgerald PJ,Barkus C,Feyder M,Wiedholz LM,Chen YC,Karlsson RM,Machado-Vieira R,Graybeal C,Sharp T,Zarate C,Harvey-White J,Du J,Sprengel R,Gass P,Bannerman D,Holmes A

    更新日期:2010-12-01 00:00:00

  • Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation.

    abstract::The identification of novel molecular targets crucially involved in motor neuron degeneration/survival is a necessary step for the development of hopefully more effective therapeutic strategies for amyotrophic lateral sclerosis (ALS) patients. In this view, S1R, an endoplasmic reticulum (ER)-resident receptor with cha...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.10.010

    authors: Peviani M,Salvaneschi E,Bontempi L,Petese A,Manzo A,Rossi D,Salmona M,Collina S,Bigini P,Curti D

    更新日期:2014-02-01 00:00:00

  • Automated differentiation of pre-diagnosis Huntington's disease from healthy control individuals based on quadratic discriminant analysis of the basal ganglia: the IMAGE-HD study.

    abstract::We investigated two measures of neural integrity, T1-weighted volumetric measures and diffusion tensor imaging (DTI), and explored their combined potential to differentiate pre-diagnosis Huntington's disease (pre-HD) individuals from healthy controls. We applied quadratic discriminant analysis (QDA) to discriminate pr...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2012.10.001

    authors: Georgiou-Karistianis N,Gray MA,Domínguez D JF,Dymowski AR,Bohanna I,Johnston LA,Churchyard A,Chua P,Stout JC,Egan GF

    更新日期:2013-03-01 00:00:00

  • Comparisons of dual isogenic human iPSC pairs identify functional alterations directly caused by an epilepsy associated SCN1A mutation.

    abstract::Over 1250 mutations in SCN1A, the Nav1.1 voltage-gated sodium channel gene, are associated with seizure disorders including GEFS+. To evaluate how a specific mutation, independent of genetic background, causes seizure activity we generated two pairs of isogenic human iPSC lines by CRISPR/Cas9 gene editing. One pair is...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.104627

    authors: Xie Y,Ng NN,Safrina OS,Ramos CM,Ess KC,Schwartz PH,Smith MA,O'Dowd DK

    更新日期:2020-02-01 00:00:00

  • Metabolomics tools for identifying biomarkers for neuropsychiatric diseases.

    abstract::The repertoire of biochemicals (or small molecules) present in cells, tissue, and body fluids is known as the metabolome. Today, clinicians utilize only a very small part of the information contained in the metabolome, as revealed by the quantification of a limited set of analytes to gain information on human health. ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2009.02.019

    authors: Quinones MP,Kaddurah-Daouk R

    更新日期:2009-08-01 00:00:00

  • Degeneration of the nigrostriatal pathway and induction of motor deficit by tetrahydrobiopterin: an in vivo model relevant to Parkinson's disease.

    abstract::We determined whether the preferential toxicity of tetrahydrobiopterin (BH4) on dopamine-producing cells, which we have previously observed in vitro, might also occur in vivo and generate characteristics associated with Parkinson's disease. Intrastriatal BH4 injection caused a loss of tyrosine hydroxylase immunoreacti...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/s0969-9961(03)00037-8

    authors: Kim SW,Jang YJ,Chang JW,Hwang O

    更新日期:2003-07-01 00:00:00

  • TAT-Bcl-x(L) improves survival of neuronal precursor cells in the lesioned striatum after focal cerebral ischemia.

    abstract::Cerebral ischemia activates endogenous neurogenesis in the subventricular zone (SVZ) and the dentate gyrus. Consecutively, SVZ-derived neural precursors migrate towards ischemic lesions. However, functional relevance of activated neurogenesis is limited by poor survival of new-born precursors. We therefore employed th...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2008.12.013

    authors: Doeppner TR,Dietz GP,El Aanbouri M,Gerber J,Witte OW,Bähr M,Weise J

    更新日期:2009-04-01 00:00:00

  • DLK-dependent signaling is important for somal but not axonal degeneration of retinal ganglion cells following axonal injury.

    abstract::Injury to retinal ganglion cell (RGC) axons triggers rapid activation of Jun N-terminal kinase (JNK) signaling, a major prodeath pathway in injured RGCs. Of the multiple kinases that can activate JNK, dual leucine kinase (Dlk) is known to regulate both apoptosis and Wallerian degeneration triggered by axonal insult. H...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2014.05.015

    authors: Fernandes KA,Harder JM,John SW,Shrager P,Libby RT

    更新日期:2014-09-01 00:00:00

  • Implications of gut microbiota dysbiosis and metabolic changes in prion disease.

    abstract::Evidence of the gut microbiota influencing neurodegenerative diseases has been reported for several neural diseases. However, there is little insight regarding the relationship between the gut microbiota and prion disease. Here, using fecal samples of 12 prion-infected mice and 25 healthy controls, we analyzed the str...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.104704

    authors: Yang D,Zhao D,Shah SZA,Wu W,Lai M,Zhang X,Li J,Guan Z,Zhao H,Li W,Gao H,Zhou X,Yang L

    更新日期:2020-02-01 00:00:00

  • Mitochondrial dysfunction, peroxidation damage and changes in glutathione metabolism in PARK6.

    abstract::Oxidative stress and protein aggregation are biochemical hallmarks of Parkinson's disease (PD), a frequent sporadic late-onset degenerative disorder particularly of dopaminergic neurons in the substantia nigra, resulting in impaired spontaneous movement. PARK6 is a rare autosomal-recessively inherited disorder, mimick...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.10.007

    authors: Hoepken HH,Gispert S,Morales B,Wingerter O,Del Turco D,Mülsch A,Nussbaum RL,Müller K,Dröse S,Brandt U,Deller T,Wirth B,Kudin AP,Kunz WS,Auburger G

    更新日期:2007-02-01 00:00:00

  • Forebrain knock-out of torsinA reduces striatal free-water and impairs whole-brain functional connectivity in a symptomatic mouse model of DYT1 dystonia.

    abstract::Multiple lines of evidence implicate striatal dysfunction in the pathogenesis of dystonia, including in DYT1, a common inherited form of the disease. The impact of striatal dysfunction on connected motor circuits and their interaction with other brain regions is poorly understood. Conditional knock-out (cKO) of the DY...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2017.06.015

    authors: DeSimone JC,Pappas SS,Febo M,Burciu RG,Shukla P,Colon-Perez LM,Dauer WT,Vaillancourt DE

    更新日期:2017-10-01 00:00:00

  • Dystonia and levodopa-induced dyskinesias in Parkinson's disease: Is there a connection?

    abstract::Dystonia and levodopa-induced dyskinesia (LID) are both hyperkinetic movement disorders. Dystonia arises most often spontaneously, although it may be seen after stroke, injury, or as a result of genetic causes. LID is associated with Parkinson's disease (PD), emerging as a consequence of chronic therapy with levodopa,...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2019.104579

    authors: Calabresi P,Standaert DG

    更新日期:2019-12-01 00:00:00

  • Hereditary deficiencies in complement C5 are associated with intensified neurodegenerative responses that implicate new roles for the C-system in neuronal and astrocytic functions.

    abstract::Possible roles of the complement (C) system in the normal and injured brain were explored with inbred mice that carried a frameshift mutation in the C5 gene. A congenic pair was used: the C5-sufficient (C5+) B10.D2/nSnJ strain with the functional allele (Hc1) from the C57BL/10J donor strain was compared with the C5-de...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.1996.0020

    authors: Pasinetti GM,Tocco G,Sakhi S,Musleh WD,DeSimoni MG,Mascarucci P,Schreiber S,Baudry M,Finch CE

    更新日期:1996-01-01 00:00:00

  • Delayed administration of high dose human immunoglobulin G enhances recovery after traumatic cervical spinal cord injury by modulation of neuroinflammation and protection of the blood spinal cord barrier.

    abstract:BACKGROUND/INTRODUCTION:The neuroinflammatory response plays a major role in the secondary injury cascade after traumatic spinal cord injury (SCI). To date, systemic anti-inflammatory medications such as methylprednisolone sodium succinate (MPSS) have shown promise in SCI. However, systemic immunosuppression can have d...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.105187

    authors: Chio JCT,Wang J,Surendran V,Li L,Zavvarian MM,Pieczonka K,Fehlings MG

    更新日期:2021-01-01 00:00:00

  • Effect of a paraneoplastic cerebellar degeneration-associated neural protein on B-myb promoter activity.

    abstract::In this study, we have shown that a paraneoplastic cerebellar degeneration (PCD)-associated antigen, pcd17, binds to a cell cycle-related protein, MRG15. MRG15 derepresses the E2F-responsive B-myb promoter. The pcd17 antigen inhibits the derepression of the B-myb transcriptional activity by MRG15, and, as a result, pc...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2003.11.003

    authors: Sakai K,Kitagawa Y,Saiki S,Saiki M,Hirose G

    更新日期:2004-04-01 00:00:00

  • High-fructose intake as risk factor for neurodegeneration: Key role for carboxy methyllysine accumulation in mice hippocampal neurons.

    abstract::Several studies indicate the involvement of advanced glycation end-products (AGEs) in neurodegenerative diseases. Moreover, the rising consumption of fructose in industrialized countries has been related to cognitive impairment, but the impact of fructose-derived AGEs on hippocampus has never been investigated. The pr...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2016.02.005

    authors: Mastrocola R,Nigro D,Cento AS,Chiazza F,Collino M,Aragno M

    更新日期:2016-05-01 00:00:00

  • The role of copper in neurodegenerative disease.

    abstract::Copper is an essential trace metal which plays a fundamental role in the biochemistry of the human nervous system. Menkes disease and Wilson disease are inherited disorders of copper metabolism and the dramatic neurodegenerative phenotypes of these two diseases underscore the essential nature of copper in nervous syst...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1006/nbdi.1999.0250

    authors: Waggoner DJ,Bartnikas TB,Gitlin JD

    更新日期:1999-08-01 00:00:00

  • Neuromodulation targets pathological not physiological beta bursts during gait in Parkinson's disease.

    abstract::Freezing of gait (FOG) is a devastating axial motor symptom in Parkinson's disease (PD) leading to falls, institutionalization, and even death. The response of FOG to dopaminergic medication and deep brain stimulation (DBS) is complex, variable, and yet to be optimized. Fundamental gaps in the knowledge of the underly...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.09.004

    authors: Anidi C,O'Day JJ,Anderson RW,Afzal MF,Syrkin-Nikolau J,Velisar A,Bronte-Stewart HM

    更新日期:2018-12-01 00:00:00

  • Insights into Abeta and presenilin from a canine model of human brain aging.

    abstract::In this review, we describe insights into beta-amyloid (Abeta) production using aged dogs as a model of human brain aging. The advantage of using dogs is that they naturally accumulate Abeta neuropathology with age. In parallel, dogs also develop age-associated learning and memory impairments. Thus, dogs can complemen...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1006/nbdi.2002.0476

    authors: Head E,Torp R

    更新日期:2002-02-01 00:00:00

  • Recombinant Adeno Associated Viral (AAV) vector type 9 delivery of Ex1-Q138-mutant huntingtin in the rat striatum as a short-time model for in vivo studies in drug discovery.

    abstract::Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by dyskinesia, cognitive impairment and emotional disturbances, presenting progressive neurodegeneration in the striatum and intracellular mutant Huntingtin (mHTT) aggregates in various areas of the brain. Recombinant Adeno Associated V...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2015.11.019

    authors: Ceccarelli I,Fiengo P,Remelli R,Miragliotta V,Rossini L,Biotti I,Cappelli A,Petricca L,La Rosa S,Caricasole A,Pollio G,Scali C

    更新日期:2016-02-01 00:00:00

  • Redox regulation of autophagy in healthy brain and neurodegeneration.

    abstract::Autophagy and redox biochemistry are two major sub disciplines of cell biology which are both coming to be appreciated for their paramount importance in the etiology of neurodegenerative diseases including Alzheimer's disease (AD). Thus far, however, there has been relatively little exploration of the interface betwee...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2015.03.002

    authors: Hensley K,Harris-White ME

    更新日期:2015-12-01 00:00:00

  • Increased neuronal glutathione and neuroprotection in GTRAP3-18-deficient mice.

    abstract::Glutathione (GSH) is an important neuroprotective molecule in the brain. The strategy to increase neuronal GSH level is a promising approach to the treatment of neurodegenerative diseases. However, the regulatory mechanism by which neuron-specific GSH synthesis is facilitated remains elusive. Glutamate transporter-ass...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2011.12.016

    authors: Aoyama K,Wang F,Matsumura N,Kiyonari H,Shioi G,Tanaka K,Kinoshita C,Kikuchi-Utsumi K,Watabe M,Nakaki T

    更新日期:2012-03-01 00:00:00

  • Bri2-23 is a potential cerebrospinal fluid biomarker in multiple sclerosis.

    abstract::To identify potential multiple sclerosis (MS)-specific biomarkers, we used a proteomic approach to screen cerebrospinal fluid (CSF) from 40 MS patients and 13 controls. We identified seven proteins (Beta-2-microglobulin, Bri2-23, Fetuin-A, Kallikrein-6, Plasminogen, Ribonuclease-1, and Transferrin) that had significan...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.06.007

    authors: Harris VK,Diamanduros A,Good P,Zakin E,Chalivendra V,Sadiq SA

    更新日期:2010-10-01 00:00:00