Macrophages in the Brain: Friends or Enemies?

Physiology ◽  
1994 ◽  
Vol 9 (2) ◽  
pp. 80-84 ◽  
Author(s):  
D Piani ◽  
DB Constam ◽  
K Frei ◽  
A Fontana
Keyword(s):  
Central Nervous System ◽  
Host Defense ◽  
The Body ◽  
Defense System ◽  
Tissue Destruction ◽  
Brain Macrophages ◽  
Host Defense System ◽  
The Central Nervous System ◽  
The Brain ◽  
Macrophage Lineage

Cells of the macrophage lineage are ubiquitously distributed in the body, including the central nervous system. They represent an essential host defense system to protect from infections. However, recent evidence indicates that brain macrophages may also be responsible for tissue destruction, including loss of neurons and demyelination.

scholarly journals Immune cells and CNS physiology: Microglia and beyond

2018 ◽  
Vol 216 (1) ◽  
pp. 60-70 ◽  
Author(s):  
Geoffrey T. Norris ◽  
Jonathan Kipnis
Keyword(s):  
Central Nervous System ◽  
Immune Cells ◽  
Brain Function ◽  
Brain Parenchyma ◽  
The Body ◽  
Immune Repertoire ◽  
Perivascular Macrophages ◽  
The Central Nervous System ◽  
Cns Immunity ◽  
The Brain

Recent advances have directed our knowledge of the immune system from a narrative of “self” versus “nonself” to one in which immune function is critical for homeostasis of organs throughout the body. This is also the case with respect to the central nervous system (CNS). CNS immunity exists in a segregated state, with a marked partition occurring between the brain parenchyma and meningeal spaces. While the brain parenchyma is patrolled by perivascular macrophages and microglia, the meningeal spaces are supplied with a diverse immune repertoire. In this review, we posit that such partition allows for neuro–immune crosstalk to be properly tuned. Convention may imply that meningeal immunity is an ominous threat to brain function; however, recent studies have shown that its presence may instead be a steady hand directing the CNS to optimal performance.

The Pathogenesis of Somatic Disease in Mental Defectives

1951 ◽  
Vol 97 (409) ◽  
pp. 792-800 ◽  
Author(s):  
L. Crome
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Scientific Basis ◽  
The Body ◽  
Normal Person ◽  
Somatic Disease ◽  
The Central Nervous System ◽  
Mental Defectives ◽  
The Brain

The problems of the interdependence and unity of the brain and body have been put on a scientific basis by Pavlov and his successors. Bykov (1947) has, for example, been able to demonstrate that the cortex plays a leading part in the regulation of somatic processes, such as secretion of urine, blood pressure, peristalsis and metabolism. It is therefore reasonable to argue that lesions of the central nervous system will be reflected in the pathogenesis and course of morbid processes in the body. It does not follow, however, that this influence will necessarily be in the direction of greater lability, more rapid pathogenesis or more extensive destruction. The outstanding feature of the central nervous system is its plasticity and power of compensation. It is therefore possible and probable that those parts of the nervous system which remain intact will take over and compensate for the function of the lost ones. Emotion may, for example, lead to polyuria, but it does not follow that urinary secretion will be impaired in a leucotomized patient. The brain may well play an important part in the infective processes of a normal person, but the defence against infection in a microcephalic idiot may remain perfectly adequate, and may even be more effective than in a normal person, provided that the mechanism of the immunity and phagocytosis had been more fully mobilized in the course of his previous life.

scholarly journals Modern aspects of neuropathogenesis and neurological manifestations of COVID-19

2021 ◽  
Vol 17 (2) ◽  
pp. 6-15
Author(s):  
L.A. Dziak ◽  
O.S. Tsurkalenko ◽  
K.V. Chekha ◽  
V.M. Suk
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Psychiatric Symptoms ◽  
Clinical Manifestations ◽  
The Body ◽  
Altered Level ◽  
Wide Range ◽  
The Central Nervous System ◽  
The Brain

Coronavirus infection is a systemic pathology resulting in impairment of the nervous system. The involvement of the central nervous system in COVID-19 is diverse by clinical manifestations and main mechanisms. The mechanisms of interrelations between SARS-CoV-2 and the nervous system include a direct virus-induced lesion of the central nervous system, inflammatory-mediated impairment, thrombus burden, and impairment caused by hypoxia and homeostasis. Due to the multi-factor mechanisms (viral, immune, hypoxic, hypercoagulation), the SARS-CoV-2 infection can cause a wide range of neurological disorders involving both the central and peripheral nervous system and end organs. Dizziness, headache, altered level of consciousness, acute cerebrovascular diseases, hypogeusia, hyposmia, peripheral neuropathies, sleep disorders, delirium, neuralgia, myalgia are the most common signs. The structural and functional changes in various organs and systems and many neurological symptoms are determined to persist after COVID-19. Regardless of the numerous clinical reports about the neurological and psychiatric symptoms of COVID-19 as before it is difficult to determine if they are associated with the direct or indirect impact of viral infection or they are secondary to hypoxia, sepsis, cytokine reaction, and multiple organ failure. Penetrated the brain, COVID-19 can impact the other organs and systems and the body in general. Given the mechanisms of impairment, the survivors after COVID-19 with the infection penetrated the brain are more susceptible to more serious diseases such as Parkinson’s disease, cognitive decline, multiple sclerosis, and other autoimmune diseases. Given the multi-factor pathogenesis of COVID-19 resulting in long-term persistence of the clinical symptoms due to impaired neuroplasticity and neurogenesis followed by cholinergic deficiency, the usage of Neuroxon® 1000 mg a day with twice-day dosing for 30 days. Also, a long-term follow-up and control over the COVID-19 patients are recommended for the prophylaxis, timely determination, and correction of long-term complications.

scholarly journals Several forms of callitachykinins are distributed in the central nervous system and intestine of the blowfly Calliphora vomitoria.

1995 ◽  
Vol 198 (12) ◽  
pp. 2527-2536
Author(s):  
D R Nässel ◽  
M Y Kim ◽  
C T Lundquist
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
High Performance ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Additional Material ◽  
Immunoreactive Material ◽  
The Central Nervous System ◽  
Entire Central Nervous System ◽  
The Brain

We have examined the distribution of two tachykinin-related neuropeptides, callitachykinin I and II (CavTK-I and CavTK-II), isolated from whole-animal extracts of the blowfly Calliphora vomitoria. Extracts of dissected brains, thoracic-abdominal ganglia and midguts of adult blowflies and the entire central nervous system of larval flies were analysed by high performance liquid chromatography (HPLC) combined with enzyme-linked immunosorbent assay (ELISA) for the presence of CavTKs. To identify the two neuropeptides by HPLC, we used the retention times of synthetic CavTK-I and II as reference and detection with an antiserum raised to locustatachykinin II (shown here to recognise both CavTK-I and II). The brain contains only two immunoreactive components, and these have exactly the same retention times as CavTK-I and II. The thoracic-abdominal ganglia and midgut contain immunoreactive material eluting like CavTK-I and II as well as additional material eluting later. The larval central nervous system (CNS) contains material eluting like CavTK-I and II as well as a component that elutes earlier. We conclude that CavTK-I and II are present in all assayed tissues and that additional, hitherto uncharacterised, forms of tachykinin-immunoreactive material may be present in the body ganglia and midgut as well as in the larval CNS. An antiserum was raised to CavTK-II for immunocytochemistry. This antiserum, which was found to be specific for CavTK-II in ELISA, labelled all the neurones and midgut endocrine cells previously shown to react with the less selective locustatachykinin antisera. It is not clear, however, whether CavTK-I and II are colocalised in all LomTK-immunoreactive cells since there is no unambiguous probe for CavTK-I.

Influence of Starvation on Absorption, Distribution, and Action of Barbital in Mice and Rats

1974 ◽  
Vol 52 (6) ◽  
pp. 1192-1200 ◽  
Author(s):  
J. Brodeur ◽  
S. Lalonde ◽  
J. Leroux
Keyword(s):  
Central Nervous System ◽  
Early Phase ◽  
The Body ◽  
Total Blood ◽  
Blood Concentrations ◽  
Influence Of Food ◽  
The Central Nervous System ◽  
Righting Reflex ◽  
The Moment ◽  
The Brain

The influence of food deprivation on the disposition of barbital during the early phase following administration of the drug was studied in mice and rats. Starvation consisted of withholding solid food, but not water, for 24–72 h in mice, and 72 h in rats. The results show that starvation leads to higher blood concentrations of barbital given intraperitoneally (i.p.) and subcutaneously to mice and rats, and intramuscularly to rats. This effect was observed 2.5–10 min following the injection of the barbiturate. In mice, starvation significantly reduced the interval between injection of the drug and loss of the righting reflex, but it extended the duration of the sleeping period. When barbital was given intravenously, starvation no longer resulted in higher blood concentrations of the drug, although starved mice went to sleep more rapidly than fed controls. At the moment of loss of the righting reflex. starved mice had significantly lower concentrations of barbital in the brain than fed controls. The total blood and plasma volumes of starved animals were moderately increased when expressed as a percentage of the body weight. These results suggest that starvation might influence the early phase of barbital absorption following its parenteral administration. There is also an indication that starvation could induce a state of hypersensitivity of the central nervous system to barbital.

scholarly journals Brain-derived neurotrophic factor as a potential therapeutic tool in the treatment of nervous system disorders

2020 ◽  
Vol 74 ◽  
pp. 517-531
Author(s):  
Wioletta Kazana ◽  
Agnieszka Zabłocka
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurotrophic Factor ◽  
Intracellular Transport ◽  
Brain Derived Neurotrophic Factor ◽  
Nerve Cells ◽  
The Body ◽  
Bdnf Level ◽  
The Central Nervous System ◽  
The Brain

Brain-derived neurotrophic factor (BDNF) plays an important role in the proper functioning of the nervous system. It regulates the growth and survival of nerve cells, and is crucial in processes related to the memory, learning and synaptic plasticity. Abnormalities related to the distribution and secretion of BDNF protein accompany many diseases of the nervous system, in the course of which a significant decrease in BDNF level in the brain is observed. Impairments of BDNF transport may occur, for example, in the event of a single nucleotide polymorphism in the Bdnf (Val66Met) coding gene or due to the dysfunctions of the proteins involved in intracellular transport, such as huntingtin (HTT), huntingtin-associated protein 1 (HAP1), carboxypeptidase E (CPE) or sortilin 1 (SORT1). One of the therapeutic goals in the treatment of diseases of the central nervous system may be the regulation of expression and secretion of BDNF protein by nerve cells. Potential therapeutic strategies are based on direct injection of the protein into the specific region of the brain, the use of viral vectors expressing the Bdnf gene, transplantation of BDNF-producing cells, the use of substances of natural origin that stimulate the cells of the central nervous system for BDNF production, or the use of molecules activating the main receptor for BDNF – tyrosine receptor kinase B (TrkB). In addition, an appropriate lifestyle that promotes physical activity helps to increase BDNF level in the body. This paper summarizes the current knowledge about the biological role of BDNF protein and proteins involved in intracellular transport of this neurotrophin. Moreover, it presents contemporary research trends to develop therapeutic methods, leading to an increase in the level of BDNF protein in the brain.

scholarly journals Nanotherapeutics in Neuropathologies: Obstacles, Challenges and Recent Advancements in CNS Targeted Drug Delivery Systems

2020 ◽  
Vol 18 ◽  
Author(s):  
Vimal Patel ◽  
Vishal Chavda ◽  
Jigar Shah
Keyword(s):  
Drug Delivery ◽  
Central Nervous System ◽  
Nervous System ◽  
Targeted Drug Delivery ◽  
Drug Dose ◽  
The Body ◽  
Brain Drug Delivery ◽  
The Central Nervous System ◽  
Targeted Drug ◽  
The Brain

: Neurology and associated nanotherapeutics is a complex field in terms of therapeutics and neurological disorder complexity. Brain is an intricate appendage and requires more precise embattled treatment for the particular diseases and hence it’s a broad scale for developing more targeted drug deliveries. The brain is one of the most inaccessible tissues of the body due to the existence of the blood-brain barrier (BBB), thus delivery of drugs inside the brain is a striking dare and it is also tricky to treat central nervous system (CNS) complications pharmacologically. The therapeutic aspiration is to accomplish a lowest drug meditation in the brain tissues so as to gain favoured therapeutic results. To devastate this obstacle, nanotechnology is engaged in the field of targeted brain drug delivery and neuropathology targeting. These carriers hold myriad ability as they may augment the drug delivery into the brain by shielding them from degradation and prolonging their transmission in the blood, as well as promoting their transport through the BBB. Nanopharmaceuticals are quickly sprouting as new avenue that is engaged with the drug-loaded nanocarriers to demonstrate unique physicochemical properties and tiny size range for penetrating into the central nervous system. The enchantment behind their therapeutic achievement is the condensed drug dose and inferior toxicity, whereby restricting the therapeutic compound to the specific site. Therefore, in this article we have tried to recapitulate the advances the novel scopes for the brain targeted drug delivery for complex neurological disorders.

scholarly journals Repression of lysosomal transcription factors Tfeb and Tfe3 is essential for the development and function of microglia

2020 ◽  
Author(s):  
Harini Iyer ◽  
Kimberle Shen ◽  
Ana M. Meireles ◽  
William S. Talbot
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gtpase Activating Protein ◽  
Phagocytic Cells ◽  
Lysosomal Activity ◽  
Regulatory Circuit ◽  
The Central Nervous System ◽  
And Function ◽  
The Brain ◽  
Macrophage Lineage

SUMMARYAs the primary phagocytic cells of the central nervous system, microglia exquisitely regulate their lysosomal activity to facilitate brain development and homeostasis. However, mechanisms that coordinate lysosomal activity with microglia development, migration, and function remain unclear. Here we show that embryonic macrophages require the lysosomal GTPase RagA and the GTPase-activating protein Folliculin (Flcn) for colonization of the brain. Mutants lacking RagA and Flcn have nearly identical phenotypes, suggesting that RagA and Flcn act in concert in developing microglia. Furthermore, we demonstrate that RagA and Flcn repress the key lysosomal transcription factor Tfeb, and its homologs Tfe3a and Tfe3b, in macrophages. Accordingly, defects in rraga mutants can be restored by simultaneous mutations in tfeb, tfe3a, and tfe3b, and overexpression of tfe3b in the macrophage lineage recapitulates the major defects observed in rraga and flcn mutants. Collectively, our data define a lysosomal regulatory circuit that is essential for early development of microglia.

scholarly journals The microbiota protects from viral-induced neurologic damage through microglia-intrinsic TLR signaling

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
D Garrett Brown ◽  
Raymond Soto ◽  
Soumya Yandamuri ◽  
Colleen Stone ◽  
Laura Dickey ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oral Administration ◽  
Viral Replication ◽  
Viral Infection ◽  
Host Defense ◽  
Toll Like Receptor ◽  
Tlr Signaling ◽  
The Central Nervous System ◽  
The Brain

Symbiotic microbes impact the function and development of the central nervous system (CNS); however, little is known about the contribution of the microbiota during viral-induced neurologic damage. We identify that commensals aid in host defense following infection with a neurotropic virus through enhancing microglia function. Germfree mice or animals that receive antibiotics are unable to control viral replication within the brain leading to increased paralysis. Microglia derived from germfree or antibiotic-treated animals cannot stimulate viral-specific immunity and microglia depletion leads to worsened demyelination. Oral administration of toll-like receptor (TLR) ligands to virally infected germfree mice limits neurologic damage. Homeostatic activation of microglia is dependent on intrinsic signaling through TLR4, as disruption of TLR4 within microglia, but not the entire CNS (excluding microglia), leads to increased viral-induced clinical disease. This work demonstrates that gut immune-stimulatory products can influence microglia function to prevent CNS damage following viral infection.

The effect of undernutrition on the postnatal development of the brain and cord in pigs

1967 ◽  
Vol 166 (1005) ◽  
pp. 396-407 ◽  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Stem ◽  
The Body ◽  
Chronological Age ◽  
Absolute Amount ◽  
The Central Nervous System ◽  
One Year ◽  
The Brain

Sucking pigs about 2 weeks old were held back by undernutrition so that they weighed only 5 to 6 kg when they were a year of age. The brain and cord developed during this time to the size to be expected in a normal pig about 10 weeks old but, although they remained immature for their chronological age, the effect on the various constituents was not uniform. The accumulation of cholesterol was less retarded than that of DNA.P or the increase in brain weight. During rehabilitation on a highly satisfactory diet the final body w eight reached at 3 1/2 years was 80 % of that to be expected in an adult pig and was equivalent only to that of a normal pig two years old. The central nervous system grew to the appropriate size for the body. The percentage of cholesterol in the central nervous system rose during rehabilitation, but, particularly in the forebrain, brain stem and spinal cord, remained subnormal for the chronological age. The deficiency of DNA- P in the rehabilitated brain was even greater, and the absolute amount finally corresponded to that found in the brain of a norm alanimal only one year of age.

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