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Sharma, Hari Shanker
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Publications (10 of 241) Show all publications
Huang, H., Young, W., Skaper, S., Chen, L., Moviglia, G., Saberi, H., . . . Feng, S. (2020). Clinical Neurorestorative Therapeutic Guidelines for Spinal Cord Injury (IANR/CANR version 2019). JOURNAL OF ORTHOPAEDIC TRANSLATION, 20, 14-24
Open this publication in new window or tab >>Clinical Neurorestorative Therapeutic Guidelines for Spinal Cord Injury (IANR/CANR version 2019)
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2020 (English)In: JOURNAL OF ORTHOPAEDIC TRANSLATION, ISSN 2214-031X, Vol. 20, p. 14-24Article, review/survey (Refereed) Published
Abstract [en]

Functional restoration after spinal cord injury (SCI) is one of the most challenging tasks in neurological clinical practice. With a view to exploring effective neurorestorative methods in the acute, subacute, and chronic phases of SCI, "Clinical Therapeutic Guidelines of Neurorestoration for Spinal Cord Injury (China Version 2016)" was first proposed in 2016 by the Chinese Association of Neurorestoratology (CANR). Given the rapid advances in this field in recent years, the International Association of Neurorestoratology (IANR) and CANR formed and approved the "Clinical Neurorestorative Therapeutic Guidelines for Spinal Cord Injury (IANR/CANR version 2019)". These guidelines mainly introduce restoring damaged neurological structure and functions by varying neurorestorative strategies in acute, subacute, and chronic phases of SCI. These guidelines can provide a neurorestorative therapeutic standard or reference for clinicians and researchers in clinical practice to maximally restore functions of patients with SCI and improve their quality of life. The translational potential of this article: This guideline provided comprehensive management strategies for SCI, which contains the evaluation and diagnosis, pre-hospital first aid, treatments, rehabilitation training, and complications management. Nowadays, amounts of neurorestorative strategies have been demonstrated to be benefit in promoting the functional recovery and improving the quality of life for SCI patients by clinical trials. Also, the positive results of preclinical research provided lots of new neurorestorative strategies for SCI treatment. These promising neurorestorative strategies are worthy of translation in the future and can promote the advancement of SCI treatments.

Place, publisher, year, edition, pages
ELSEVIER, 2020
Keywords
Cell therapy, Clinical therapeutic guideline, Neurorehabilitation, Neurorestoration, Neurotization, Spinal cord injury
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-407114 (URN)10.1016/j.jot.2019.10.006 (DOI)000511146000004 ()31908929 (PubMedID)
Available from: 2020-03-19 Created: 2020-03-19 Last updated: 2020-03-19Bibliographically approved
Huang, H., Sharma, H. S., Chen, L., Saberi, H. & Mao, G. (2019). 2018 Yearbook of Neurorestoratology. JOURNAL OF NEURORESTORATOLOGY, 7, 8-17
Open this publication in new window or tab >>2018 Yearbook of Neurorestoratology
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2019 (English)In: JOURNAL OF NEURORESTORATOLOGY, ISSN 2324-2426, Vol. 7, p. 8-17Article, review/survey (Refereed) Published
Abstract [en]

The Neurorestoratology discipline is getting worldwide attention from the clinicians, basic scientists, students and policy makers alike. Accordingly, this year too, the discipline has made profound advances and great achievements for the benefit of the mankind. In this report, of the 2018 Neurorestoratology Yearbook, salient features of new developments are summarized. This Yearbook consists 3 key themes namely (i) the new findings on pathogenesis of neurological diseases or degeneration; (ii) the new mechanisms of neurorestorative aspects; and (iii) the achievements and progresses made in the clinical field of neurorestorative therapies. The new trend has emerged in clinical studies that are based on greater levels of evidence-based medical practices both in clinical therapies and clinical trials based on standard designs.

Place, publisher, year, edition, pages
TSINGHUA UNIV PRESS, 2019
Keywords
yearbook, neurorestoratology, pathogenesis, diseases and damage to the nervous system, neurorestorative mechanisms, neurorestorative therapies
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-391434 (URN)10.26599/JNR.2019.9040003 (DOI)000477737400001 ()
Available from: 2019-10-08 Created: 2019-10-08 Last updated: 2019-10-08Bibliographically approved
Sharma, A., Castellani, R. J., Smith, M. A., Muresanu, D. F., Dey, P. K. & Sharma, H. S. (2019). 5-Hydroxytryptophan: A precursor of serotonin influences regional blood-brain barrier breakdown, cerebral blood flow, brain edema formation, and neuropathology. In: Sharma, HS Sharma, A (Ed.), New Therapeutic Strategies for Brain Edema and Cell Injury: (pp. 1-44). Elsevier
Open this publication in new window or tab >>5-Hydroxytryptophan: A precursor of serotonin influences regional blood-brain barrier breakdown, cerebral blood flow, brain edema formation, and neuropathology
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2019 (English)In: New Therapeutic Strategies for Brain Edema and Cell Injury / [ed] Sharma, HS Sharma, A, Elsevier, 2019, p. 1-44Chapter in book (Refereed)
Abstract [en]

5-Hydroxytryptophan (5-HTP), a precursor of serotonin, is therapeutically used for several psychiatric disorders such as anxiety and depression in the clinic. However, severe side effects, including abnormal mental functions, behavioral disturbances and intolerance are associated with this treatment. 5-HTP-induced elevation of plasma and brain serotonin levels may affect blood-brain barrier (BBB) breakdown, edema formation and regional cerebral blood flow (CBF) disturbances. Breakdown of BBB to serum proteins leads to vasogenic brain edema formation and cellular injuries. However, 5-HTP-neurotoxicity is still not well known. In this investigations 5-HTP induced elevation of endogenous plasma and brain serotonin levels and its effect on BBB breakdown, edema formation neuronal injuries was examined in a rat model. Furthermore, potential role of oxidative stress and nitric oxide (NO) was evaluated. In addition, several neurochemical agents such as p-CPA (5-HT synthesis inhibitor) indomethacin (prostaglandin synthase inhibitor), diazepam (ant stress drug), cyproheptadine, ketanserin (5-HT2 receptor antagonists) and vinblastine (inhibitor of microtubule function) were examined on 5-HT neurotoxicity. Our observations suggest that 4h after 5-HTP administrations, the endogenous serotonin levels increased by fourfold (150mg/kg) in the plasma and brain associated with profound hyperthermia (+3.86 +/- 0.24 degrees C, oxidative stress and NO upregulation. Breakdown of the BBB to Evans blue albumin (EBA) in 8 brain regions and to ([131])Iodine in 14 brain regions was observed. The CBF exhibited marked reduction in all the brain regions examined. Brain edema and cellular injuries are present in the areas associated with BBB disruption. Drug treatments reduced the BBB breakdown, edema formation NO production and brain pathology. These observations are the first to point out that 5-HTP-neurotoxicity caused by BBB breakdown, edema formation and NO production is instrumental in causing adverse mental and behavioral abnormalities, not reported earlier.

Place, publisher, year, edition, pages
Elsevier, 2019
Series
International Review of Neurobiology, ISSN 0074-7742 ; 146
National Category
Neurology Neurosciences
Identifiers
urn:nbn:se:uu:diva-401922 (URN)10.1016/bs.irn.2019.06.005 (DOI)000501592100002 ()31349924 (PubMedID)978-0-12-816754-0 (ISBN)
Funder
Swedish Research Council, 2710NIH (National Institute of Health), R01 AG028679AstraZenecaGöran Gustafsson Foundation for Research in Natural Sciences and Medicine
Available from: 2020-01-13 Created: 2020-01-13 Last updated: 2020-01-13Bibliographically approved
Sharma, H. S., Muresanu, D. F., Nozari, A., Castellani, R. J., Dey, P. K., Wiklund, L. & Sharma, A. (2019). Anesthetics influence concussive head injury induced blood-brain barrier breakdown, brain edema formation, cerebral blood flow, serotonin levels, brain pathology and functional outcome. In: Sharma, HS Sharma, A (Ed.), New Therapeutic Strategies for Brain Edema and Cell Injury: (pp. 45-81). Elsevier
Open this publication in new window or tab >>Anesthetics influence concussive head injury induced blood-brain barrier breakdown, brain edema formation, cerebral blood flow, serotonin levels, brain pathology and functional outcome
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2019 (English)In: New Therapeutic Strategies for Brain Edema and Cell Injury / [ed] Sharma, HS Sharma, A, Elsevier, 2019, p. 45-81Chapter in book (Refereed)
Abstract [en]

Several lines of evidences show that anesthetics influence neurotoxicity and neuroprotection. The possibility that different anesthetic agents potentially influence the pathophysiological and functional outcome following neurotrauma was examined in a rat model of concussive head injury (CHI). The CHI was produced by an impact of 0.224N on the right parietal bone by dropping a weight of 114.6g from a 20cm height under different anesthetic agents, e.g., inhaled ether anesthesia or intraperitoneally administered ketamine, pentobarbital, equithesin or urethane anesthesia. Five hour CHI resulted in profound volume swelling and brain edema formation in both hemispheres showing disruption of the blood-brain barrier (BBB) to Evans blue and radio-iodine. A marked decrease in the cortical CBF and a profound increase in plasma or brain serotonin levels were seen at this time. Neuronal damages were present in several parts of the brain. These pathological changes were most marked in CHI under ether anesthesia followed by ketamine (35mg/kg, i.p.), pentobarbital (50 mg/kg, i.p.), equithesin (3 mL/kg, i.p.) and urethane (1 g/kg, i.p.). The functional outcome on Rota Rod performances or grid walking tests was also most adversely affected after CHI under ether anesthesia followed by pentobarbital, equithesin and ketamine. Interestingly, the plasma and brain serotonin levels strongly correlated with the development of brain edema in head injured animals in relation to different anesthetic agents used. These observations suggest that anesthetic agents are detrimental to functional and pathological outcomes in CHI probably through influencing the circulating plasma and brain serotonin levels, not reported earlier. Whether anesthetics could also affect the efficacy of different neuroprotective agents in CNS injuries is a new subject that is currently being examined in our laboratory.

Place, publisher, year, edition, pages
Elsevier, 2019
Series
International Review of Neurobiology, ISSN 0074-7742 ; 146
National Category
Anesthesiology and Intensive Care Neurosciences
Identifiers
urn:nbn:se:uu:diva-401923 (URN)10.1016/bs.irn.2019.06.006 (DOI)000501592100003 ()31349932 (PubMedID)978-0-12-816754-0 (ISBN)
Funder
Swedish Research Council, 2710Göran Gustafsson Foundation for Research in Natural Sciences and MedicineAstraZenecaNIH (National Institute of Health), R01 AG028679
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
Chen, H., Tan, Q., Xie, C., Li, C., Chen, Y., Deng, Y., . . . Sharma, H. S. (2019). Application of olfactory ensheathing cells in clinical treatment of spinal cord injury: meta-analysis and prospect. JOURNAL OF NEURORESTORATOLOGY, 7(2), 70-81
Open this publication in new window or tab >>Application of olfactory ensheathing cells in clinical treatment of spinal cord injury: meta-analysis and prospect
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2019 (English)In: JOURNAL OF NEURORESTORATOLOGY, ISSN 2324-2426, Vol. 7, no 2, p. 70-81Article in journal (Refereed) Published
Abstract [en]

Background:

A number of clinical trials of olfactory ensheathing cells (OECs) for the treatment of chronic spinal cord injury (SCI) have been carried out all over the world. However, their safety and efficacy have not been basically evaluated. Moreover, there are no uniform standards laid out for the use of optimal source, transplantation method and the dosage of OECs.

Objective:

This study evaluated the source, dose, and route of transplantation of OECs for the treatment of chronic SCI.

Methods:

PubMed, Cochrane Library, EMBASE, CNKI, and Wanfang Data were searched for the clinical studies of OECs in the treatment of chronic SCI on July 2018.

Results:

A total of 30 articles on OECs transplantation for chronic SCI were selected for comprehensive evaluation of OECs sources, doses, and transplantation methods. The efficacy of OECs in the treatment of chronic SCI was evaluated using Review Manager 5.3.

Conclusion:

Fetal OECs are the primary source of cells for the treatment of chronic SCI in OECs, with standardized cell-culture and quality-control processes. Fetal OECs can significantly improve the neurological function of patients with chronic SCI. It is an ideal cell therapy for neurorestoration. However to explore more precise and minimally invasive treatment options are required in the future.

Keywords
olfactory ensheathing cell (OEC), spinal cord injury (SCI), meta-analysis
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-396558 (URN)10.26599/JNR.2019.9040008 (DOI)000489629300003 ()
Available from: 2019-11-06 Created: 2019-11-06 Last updated: 2019-11-06Bibliographically approved
Muresanu, D. F., Sharma, A., Patnaik, R., Menon, P. K., Mössler, H. & Sharma, H. S. (2019). Exacerbation of blood-brain barrier breakdown, edema formation, nitric oxide synthase upregulation and brain pathology after heat stroke in diabetic and hypertensive rats. Potential neuroprotection with cerebrolysin treatment. In: Sharma, HS Sharma, A (Ed.), New Therapeutic Strategies for Brain Edema and Cell Injury: (pp. 83-102). Elsevier
Open this publication in new window or tab >>Exacerbation of blood-brain barrier breakdown, edema formation, nitric oxide synthase upregulation and brain pathology after heat stroke in diabetic and hypertensive rats. Potential neuroprotection with cerebrolysin treatment
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2019 (English)In: New Therapeutic Strategies for Brain Edema and Cell Injury / [ed] Sharma, HS Sharma, A, Elsevier, 2019, p. 83-102Chapter in book (Refereed)
Abstract [en]

There is a growing trend of hypertension among military and civilian populations due to lifetime stressful situations. If hypertension is uncontrolled it leads to development of diabetes and serious neurological complications. Most of the World populations live in temperate zone across the World. Thus, a possibility exists that these hypertensive and diabetic people may have external heat as potential risk factors for brain damage. We have seen brain edema and brain damage following exposure to heat stress at 38 degrees C for 4h. A possibility exists that heat exposure in diabetic-hypertensive (DBHY) cases exacerbates exacerbation of brain pathology and edema formation. This hypothesis is examined in a rat model. The role of nitric oxide (NO) in exacerbation of HS-induced brain pathology was also evaluated using nitric oxide synthase (NOS) immunoreactivity. Hypertensive rats (produced by two-kidney one clip (2K1C) method) were made diabetic with streptozotocine (50 mg/kg, i.p./day for 3 days) treatment. After 6 weeks, DBHY rats show 20-30 mM/L Blood Glucose and hypertension (180-200 mmHg). Subjection of these rats to 4h HS resulted in six- to eightfold higher BBB breakdown, brain edema formation and brain pathology. At this time, neuronal or inducible NOS expression was four- to sixfold higher in DBHY rats compared to controls. Interestingly, iNOS expression was higher than nNOS in DBHY rats. Cerebrolysin in high doses (10-mL/kg, i.v. instead of 5-mL/kg) induced significant neuroprotection and downregulation of nNOS and iNOS in DBHY animals whereas normal animals need only 5-mL/kg doses for this purpose. Our observations demonstrate that co-morbidly factors exacerbate brain damage in HS through NOS expression and require double dose of cerebrolysin for neuroprotection as compared to normal rats, not reported earlier.

Place, publisher, year, edition, pages
Elsevier, 2019
Series
International Review of Neurobiology, ISSN 0074-7742 ; 146
National Category
Neurology Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:uu:diva-401921 (URN)10.1016/bs.irn.2019.06.007 (DOI)000501592100004 ()31349933 (PubMedID)978-0-12-816754-0 (ISBN)
Funder
Swedish Research Council, 2710Göran Gustafsson Foundation for Research in Natural Sciences and MedicineAstraZeneca
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
Kiyatkin, E. A. & Sharma, H. S. (2019). Leakage of the blood-brain barrier followed by vasogenic edema as the ultimate cause of death induced by acute methamphetamine overdose. In: Sharma, HS Sharma, A (Ed.), New Therapeutic Strategies for Brain Edema and Cell Injury: (pp. 189-207). Elsevier
Open this publication in new window or tab >>Leakage of the blood-brain barrier followed by vasogenic edema as the ultimate cause of death induced by acute methamphetamine overdose
2019 (English)In: New Therapeutic Strategies for Brain Edema and Cell Injury / [ed] Sharma, HS Sharma, A, Elsevier, 2019, p. 189-207Chapter in book (Refereed)
Abstract [en]

Methamphetamine (METH) is a potent CNS stimulant that is widely used as a recreational drug. Due to its ability to increase bodily heat production and diminish heat loss due to peripheral vasoconstriction, METH is able to increase brain and body temperature. The hyperthermic effects of METH are potentiated when the drug is used under conditions of psycho-physiological activation and in warm ambient temperatures. In this short review, we present and discuss our data on the effects of METH on brain temperature and a number of neural parameters that characterize permeability of the blood-brain barrier (albumin immunoreactivity), glial activity (GFAP immunoreactivity), brain tissue water content, and structural abnormalities of brain cells. We demonstrate that the extent of these neural alterations strongly depends on METH-induced brain temperature elevation and they all dramatically increase following exposure to METH in warm (29 degrees C) vs. standard (23 degrees C) ambient temperatures. Based on these data weconsider possible pathophysiological mechanisms underlying acute METH toxicity, suggesting the critical role of drug-induced brain hyperthermia, temperature-dependent leakage of the blood-brain barrier (BBB), and the development of vasogenic edema that could finally result in decompensation of vital functions and death.

Place, publisher, year, edition, pages
Elsevier, 2019
Series
International Review of Neurobiology, ISSN 0074-7742 ; 146
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-401925 (URN)10.1016/bs.irn.2019.06.010 (DOI)000501592100007 ()31349927 (PubMedID)978-0-12-816754-0 (ISBN)
Funder
NIH (National Institute of Health)
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
Ozkizilcik, A., Sharma, A., Vicente Lafuente, J., Muresanu, D. F., Castellani, R. J., Nozari, A., . . . Sharma, H. S. (2019). Nanodelivery of cerebrolysin reduces pathophysiology of Parkinson's disease. In: Sharma, A Sharma, HS (Ed.), NANONEUROPROTECTION AND NANONEUROTOXICOLOGY: (pp. 201-246). ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
Open this publication in new window or tab >>Nanodelivery of cerebrolysin reduces pathophysiology of Parkinson's disease
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2019 (English)In: NANONEUROPROTECTION AND NANONEUROTOXICOLOGY / [ed] Sharma, A Sharma, HS, ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD , 2019, p. 201-246Chapter in book (Refereed)
Abstract [en]

Parkinson's disease (PD) is affecting >10 million people worldwide for which no suitable cure has been developed so far. Roughly, about two people per thousand populations are affected with PD like symptoms especially over the age of 50. About 1% of the populations above 60 years suffer from PD-like disease. The prevalence of the disease is increasing over the years, and future projections by 2020 could be 12-14 millions people affected by the disease. Thus, exploration of suitable therapeutic measures is the need of the hour to enhance quality of the life of PD patients. PD induced brain pathology includes loss of dopaminergic neurons in the substantia niagra that could later extends to other cortical regions causing loss of voluntary motor control. Deposition of alpha-synuclein in the brain further leads to neurodegeneration. However, the exact cause of PD is still unknown. It appears that breakdown of the blood-brain barrier (BBB) and leakage of serum component into the brain could lead to neurodegeneration in PD. Thus, novel treatment strategies that are able to restore BBB breakdown and enhance neuronal plasticity and neuroregeneration in PD could be effective in future therapy. With the advancement of nanotechnology, it is worthwhile to understand the role of nanodelivery of selected agents in PD to enhance neuroprotection. In this review new role of BBB, brain edema, and neuropathology in PD is discussed. In addition, superior neuroprotection induced by nanowired delivery of a multimodal drug cerebrolysin in PD is summarized based on our own investigations.

Place, publisher, year, edition, pages
ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD, 2019
Series
Progress in Brain Research, ISSN 0079-6123 ; 245
Keywords
Parkinson's disease, Blood-brain barrier, Brain edema, Alpha-synuclein, Cerebrolysin, Nanowired delivery
National Category
Neurology Neurosciences
Identifiers
urn:nbn:se:uu:diva-401953 (URN)10.1016/bs.pbr.2019.03.014 (DOI)000500699500007 ()30961868 (PubMedID)978-0-444-64208-0 (ISBN)
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
Sharma, A. & Sharma, H. S. (2019). Nanoneuroprotection and Nanoneurotoxicology. In: Sharma, A Sharma, HS (Ed.), NANONEUROPROTECTION AND NANONEUROTOXICOLOGY: (pp. XIII-XVI). ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
Open this publication in new window or tab >>Nanoneuroprotection and Nanoneurotoxicology
2019 (English)In: NANONEUROPROTECTION AND NANONEUROTOXICOLOGY / [ed] Sharma, A Sharma, HS, ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD , 2019, p. XIII-XVIChapter in book (Refereed)
Place, publisher, year, edition, pages
ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD, 2019
Series
Progress in Brain Research, ISSN 0079-6123 ; 245
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-401948 (URN)000500699500001 ()30961874 (PubMedID)978-0-444-64208-0 (ISBN)
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
Sharma, H. S., Muresanu, D. F., Castellani, R. J., Nozari, A., Vicente Lafuente, J., Tian, Z. R., . . . Sharma, A. (2019). Nanowired delivery of cerebrolysin with neprilysin and p-Tau antibodies induces superior neuroprotection in Alzheimer's disease. In: Sharma, A Sharma, HS (Ed.), NANONEUROPROTECTION AND NANONEUROTOXICOLOGY: (pp. 145-200). ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD
Open this publication in new window or tab >>Nanowired delivery of cerebrolysin with neprilysin and p-Tau antibodies induces superior neuroprotection in Alzheimer's disease
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2019 (English)In: NANONEUROPROTECTION AND NANONEUROTOXICOLOGY / [ed] Sharma, A Sharma, HS, ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD , 2019, p. 145-200Chapter in book (Refereed)
Abstract [en]

Alzheimer's disease (AD) is estimated to be afflicting over 55 millions of individual worldwide in 2018-19 for which no suitable clinical therapeutic measures have been developed so far. Thus, there is an urgent need to explore novel therapeutic strategies using nanodelivery of drugs and agents either alone or in combination for superior neuroprotection in AD and enhanced quality of life of the affected individuals. There are reports that AD is often associated with diminished neurotrophic factors and neprilysin together with enhancement of phosphorylated Tau (p-Tau) within the brain and in the cerebrospinal fluid (CSF). Thus, studies aiming to enhance neurotrophic factors and neprilysin together with neutralizing p-Tau within the central nervous system (CNS) may alleviate brain pathology in AD. In this review these strategies are discussed using nanotechnological approaches largely based on our own investigations in relation to current literature in the field.

Place, publisher, year, edition, pages
ACADEMIC PRESS LTD-ELSEVIER SCIENCE LTD, 2019
Series
Progress in Brain Research, ISSN 0079-6123 ; 245
Keywords
Alzheimer's disease, Neurotrophic factors, Cerebrolysin, Antibodies, Phosphorylated Tau protein, Brain pathology, Blood-brain barrier, Brain edema, Nanowired delivery
National Category
Neurology Neurosciences
Identifiers
urn:nbn:se:uu:diva-401956 (URN)10.1016/bs.pbr.2019.03.009 (DOI)000500699500006 ()30961867 (PubMedID)978-0-444-64208-0 (ISBN)
Available from: 2020-01-10 Created: 2020-01-10 Last updated: 2020-01-10Bibliographically approved
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