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     <title><![CDATA[NUST Institutions Library Catalogue Search for 'an:&quot;122351&quot;']]></title>
     <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?q=ccl=an%3A%22122351%22&amp;format=rss</link>
     <atom:link rel="self" type="application/rss+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?q=ccl=an%3A%22122351%22&amp;sort_by=relevance_dsc&amp;format=atom"/>
     <description><![CDATA[ Search results for 'an:&quot;122351&quot;' at NUST Institutions Library Catalogue]]></description>
     <opensearch:totalResults>20</opensearch:totalResults>
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       <opensearch:itemsPerPage>50</opensearch:itemsPerPage>
     
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Dysfunctional Glucose Metabolism and Progression of Alzheimer's disease. /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608852</link>
        
       <description><![CDATA[









	   <p>By Awan ,Mawara Farooq . 
	   
                        . 71p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608852">Place Hold on <em>Dysfunctional Glucose Metabolism and Progression of Alzheimer's disease. /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608852</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Role of PARK7 and Linked Parkinsonism in Pakistani Population /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608853</link>
        
       <description><![CDATA[









	   <p>By  MALIK ,NIMRA MEHMOOD. 
	   
                        . 101p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608853">Place Hold on <em>Role of PARK7 and Linked Parkinsonism in Pakistani Population /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608853</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    ANALYSIS OF EAE MODEL FOR THE DEVELOPMENT OF THERAPIES OF MULTIPLE SCLEROSIS THROUGH BIOINFORMATIC TOOLS /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608872</link>
        
       <description><![CDATA[









	   <p>By Zeb ,Maria . 
	   
                        . 91p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608872">Place Hold on <em>ANALYSIS OF EAE MODEL FOR THE DEVELOPMENT OF THERAPIES OF MULTIPLE SCLEROSIS THROUGH BIOINFORMATIC TOOLS /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608872</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Identification and Characterization of Cathepsins in Parkinsonism /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608873</link>
        
       <description><![CDATA[









	   <p>By Fatima ,Shehzadi Irum . 
	   
                        . 122p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608873">Place Hold on <em>Identification and Characterization of Cathepsins in Parkinsonism /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608873</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Characterization of Rab32 and HMGB1 involved in the disease course of Experimental Autoimmune Encephalomyelitis, An animal model of Multiple Sclerosis. /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608884</link>
        
       <description><![CDATA[









	   <p>By Shafique ,Tayyaba . 
	   
                        . 74p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608884">Place Hold on <em>Characterization of Rab32 and HMGB1 involved in the disease course of Experimental Autoimmune Encephalomyelitis, An animal model of Multiple Sclerosis. /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608884</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Identification of Compounds from Nigella Sativa as Potential drug for Alzheimer Disease: Bioinformatics Approach /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608885</link>
        
       <description><![CDATA[









	   <p>By Rahman ,Sania . 
	   
                        . 53p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608885">Place Hold on <em>Identification of Compounds from Nigella Sativa as Potential drug for Alzheimer Disease: Bioinformatics Approach /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608885</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Identification of Protein Signatures for AD and MCI in Body Fluids (Blood and CSF) /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608886</link>
        
       <description><![CDATA[









	   <p>By Baseer ,Javaria . 
	   
                        . 90p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608886">Place Hold on <em>Identification of Protein Signatures for AD and MCI in Body Fluids (Blood and CSF) /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608886</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Functional Characterization Of Risk Factor Involved In Mptp-Induced Parkinsonism In Mice /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608901</link>
        
       <description><![CDATA[









	   <p>By Jatala, Faria Hasan . 
	   
                        . 72p.
                        , The second-most prevalent neurological disease in the world, Parkinson's disease (PD) affects
roughly 4 million people. The death and loss of dopaminergic neurons in the substantia nigra
compacta (SNpc) is the primary pathogenic characteristic of PD. Motor abnormalities include limb
stiffness, tremor, and bradykinesia are the major features of PD. Although levodopa (L-DOPA) is
the gold standard medication, but it has clear negative effects when taken over an extended period.
Therefore, it is vital that novel medicines and ideal therapeutic agents be discovered. Parkinson's
disease remains an unsolved clinical problem, as currently authorized PD therapies offer relatively
modest therapeutic benefits. New therapeutic approaches that not only alleviate symptoms in the
short term but also stop the disease from getting worse are desperately needed. For this purpose,
mice model is utilized for PD induction by MPTP neurotoxin for functional characterization of
proteomic factor GFAP as a risk factor in an effort to enhance the efficacy of the treatment of PD.
In future, by targeting pathway of GFAP level in substantia nigra with some targeted drug will
eventually lead to innovative therapeutic approach for PD patients.
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608901">Place Hold on <em>Functional Characterization Of Risk Factor Involved In Mptp-Induced Parkinsonism In Mice /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608901</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Identification and Characterization of Risk Factors in Alzheimer’s Disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608910</link>
        
       <description><![CDATA[









	   <p>By  Munawar ,Sabahat. 
	   
                        . 83p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608910">Place Hold on <em>Identification and Characterization of Risk Factors in Alzheimer’s Disease /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608910</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Proteome Wide Alterations and Impact of Identified Risk Factors on the Progression of Parkinson´s Disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608919</link>
        
       <description><![CDATA[









	   <p>By Fatima , Rizwana . 
	   
                        . 90p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608919">Place Hold on <em>Proteome Wide Alterations and Impact of Identified Risk Factors on the Progression of Parkinson´s Disease /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608919</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Assessment of Protein Aggregation in Aging Retina as an Early Retinal Biomarker /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608929</link>
        
       <description><![CDATA[









	   <p>By  Mehtab, Sameen. 
	   
                        . 49p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608929">Place Hold on <em>Assessment of Protein Aggregation in Aging Retina as an Early Retinal Biomarker /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608929</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    In silico Characterization of Prion Proteins and interactive association with Amyloid beta as novel therapeutic trends for Alzheimer’s Disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608930</link>
        
       <description><![CDATA[









	   <p>By Jamshaid ,Zanib . 
	   
                        . 62p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=608930">Place Hold on <em>In silico Characterization of Prion Proteins and interactive association with Amyloid beta as novel therapeutic trends for Alzheimer’s Disease /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=608930</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    COVID-19 (6LU7) predictive binding association with Aβ oligomers and possible link to Alzheimer's disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=609040</link>
        
       <description><![CDATA[









	   <p>By Khan, Areej Sohail . 
	   
                        . 74p.
                        , The high rise pandemic of Coronavirus Disease 2019 (COVID-19) makes the world
face medical challenges associated with multifaceted nature of its pathology. SARSCoV-2 affects several organs and systems as it enters the host’s body one of which
is the brain. Over 80 million humans around the globe, including those with
neurodegenerative disease (NDD), have been diagnosed with coronavirus disease
2019 (COVID-19) to date. COVID-19 affects the brain in many ways including
direct infection of neural cells with SARS-CoV-2, severe systemic inflammation that
floods the brain with pro-inflammatory agents leading to damaging cells and leading
to symptoms presenting cognitive impairment. COVID-19 positive patients
showcase neurological symptoms leading to the belief that coronavirus disease plays
a role in neurodegenerative diseases. The most common NDD, Alzheimer’s disease
(AD) is characterized by its multifactorial nature leading to research on risk factors
that emphasizes on the inflammation of toxicity and mutual death of cells due to
amyloid beta and its conformers, namely monomeric and oligomeric forms.
Amyloid beta oligomers initiate toxicity and neural death of cells in AD. The main
aim of this study is to decipher the interactive association between toxic forms of
amyloid beta oligomer against COVID-19 main protease. We used PDB and
Pubchem for library retrieval that was loaded in to discovery studio to extract the
active binding site of main protease of SARS-CoV-2 and prepare ligands for
docking. Furthermore, we utilized PyRx for docking to investigating binding
energies of conformations attained, the best affinity ligands were formed into a
complex by the use of Pymol that were than visualized using Discovery studio where
2D interactions were also observed that later were further analyzed using Ligplot+
to get an insight on bond length and strength along with bond types. Aβ oligomer
31-35 binds actively to the active site of M-pro of SARS-CoV-2 at a high affinity
rate of -6.3kcal/mol. 6LU7 complex with amyloid 31-35 (Complex 1) when docked
XII
with the receptor of apoptotic pathway showed enhanced predictive association.
Bioinformatics tools in this research substantiated the important interactive partners
amongst amyloid oligomers to COVID-19 highlighting that SARS-Cov-2 may play
a role in apoptotic demise of cells ultimately leading to neurodegeneration.
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=609040">Place Hold on <em>COVID-19 (6LU7) predictive binding association with Aβ oligomers and possible link to Alzheimer's disease /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=609040</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Investigating the Protective Effects of Phototherapy and various drugs in Alzheimer Disease /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612160</link>
        
       <description><![CDATA[









	   <p>By Tanveer ,Laila . 
	   
                        . 86p. ;
                        
                         30cm.. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=612160">Place Hold on <em>Investigating the Protective Effects of Phototherapy and various drugs in Alzheimer Disease /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612160</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Exploring Psoriasis Treatment Efficacy and Cognitive Impairment in a Murine Model /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612432</link>
        
       <description><![CDATA[









	   <p>By Durr E Shahwar. 
	   
                        . 98p.
                        , Psoriasis is a chronic, immune-mediated skin disease characterized by increased
proliferation of keratinocytes and immune dysfunction, which results in symptoms of
erythema and scaling and discomfort. This condition is always accompanied with
systemic co-morbidities, such as cognitive impairment that worsens the prognosis.
Corticosteroids and biologic agents are available, but these therapies are often linked with
a variety of adverse effects. This study also presents a new topical gel formulation used to
address both cutaneous and systemic effects of psoriasis symptoms, by combining
curcumin, chamomile extract, and salicylic acid loaded into polymeric nanoparticles.
Polymeric nanoparticles were synthesized, characterized and employed as carriers to
encapsulate the active compounds of the drug. The drug loaded nanoparticles were
characterized for particle size, zeta potential, drug release efficiency and other desirable
parameters to guarantee efficient delivery and controlled release at the site of action. This
formulation was tested in an IMQ-induced psoriasis mouse model where it provided
substantial therapeutic improvement by decreasing skin scaling, thickness, and
inflammation. Furthermore, a decrease in the inflammation was observed, by decreased
serum CRP levels in the blood serum of treated mice. Behavioural tests also revealed that
memory of mice treated with drug-loaded polymeric nanoparticles was better as
compared to the untreated group of mice. This implies that the formulation not only
targets the skin but also has neuro-protective effects addressing cognitive defects
resulting from psoriasis. The histopathological examination of the hippocampus area after
the therapy showed decreased neuroinflammation and reduced cell apoptosis, further
validating the neuroprotective potentials of the formulation. These findings suggest this
novel topical gel formulation as a non-invasive treatment option with reduced systemic
inflammation &amp; enhanced neuroprotection. The collective antioxidant, anti-inflammatory
and keratolytic properties of all active compounds encapsulated and delivered via
polymeric nanoparticles, provides a holistic approach in managing cutaneous and
systemic manifestations of psoriasis, making this topical formulation a promising and
more efficient alternative to conventional therapies.
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=612432">Place Hold on <em>Exploring Psoriasis Treatment Efficacy and Cognitive Impairment in a Murine Model /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612432</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Unlocking Neurogenesis: PRGF Regenerative Therapy and the role of Tau Protein in Neurodegenerative Disease Models /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612947</link>
        
       <description><![CDATA[









	   <p>By Salih, Aqsa. 
	   
                        . 71p.
                        , Alzheimer's disease (AD) is a neurological condition characterized by persistent
cognitive impairment with few treatment options available. Platelet-rich plasma
(PRP) and platelet-rich growth factors (PRGF), produced from human blood, have
shown promise in treating a variety of neurological disorders. However, their use in
Alzheimer's disease is underexplored, particularly in chemically produced models.
This study looks at the therapeutic potential of PRGF and PRP in a chemically
induced Alzheimer's mouse model using aluminum chloride (AlCl3), with a
particular emphasis on the novel use of intranasal PRGF administration. This study
to explore and compare the effects of PRGF and PRP in an Alzheimer's disease
chemical model. Behavioral assessments were performed to evaluate cognitive
deficits, memory retention, and spatial learning. The Y-maze and Elevated Plus
Maze (EPM) tests demonstrated significant cognitive improvements in the PRGFtreated mice. PRGF administration resulted in enhanced memory performance and
cognitive flexibility, with higher number of alterations and entries to novel arm.
Additionally, PRGF-treated mice exhibited reduced anxiety-like behavior in the
EPM. These findings suggest that PRGF treatment significantly improves cognitive
abilities and memory retention however do not fully restore and cannot be used
confidently in treatment. Histological analysis of the frontal cortex, cerebral cortex,
hippocampus, dentate gyrus (DG) region, and liver was conducted following
behavioral assessments to There were no significant improvements in cellular
integrity observed in either the PRGF or PRP treated groups, indicating less to no
neuroprotection and potential reversal of AlCl3-induced damage. 
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=612947">Place Hold on <em>Unlocking Neurogenesis: PRGF Regenerative Therapy and the role of Tau Protein in Neurodegenerative Disease Models /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612947</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Characterization of Blood-Derived Exosomes for Diagnostics Insights in Neurological Diseases /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612948</link>
        
       <description><![CDATA[









	   <p>By Tahir, Javaria . 
	   
                        . 87p.
                        , Exosomes, nanosized extracellular vesicles, are emerging as potential non-invasive
biomarkers for diagnosing neurological disorders. In this study, we explored the isolation
and characterization of blood-derived exosomes to assess their diagnostic relevance.
Blood samples were collected from two groups: a control group of individuals without
neurological disorders and a patient group diagnosed with various neurological
conditions. Plasma was extracted using differential centrifugation to remove cellular
debris, apoptotic bodies, and larger vesicles. Exosomes were isolated from the plasma
using a polymer-based precipitation method optimized with PEG-6000 to achieve high
yield and purity. The isolated exosomes were then characterized using Scanning Electron
Microscopy (SEM) to verify their morphology and methylene blue staining to confirm
their extracellular vesicular nature. After staining, RNA was extracted from the exosomes
using TRIzol, followed by cDNA synthesis to analyze the molecular profile. Gel
electrophoresis was performed to assess the quality of the cDNA, and RT-PCR was
conducted to detect biomarkers associated with neurological disorders. These molecular
analyses provided insights into the differences between the control and diseased groups,
highlighting potential biomarkers for disease diagnosis. The results of this study promise
valuable insights into the potential properties of blood-derived exosomes in advancing
non-invasive diagnostics for neurological diseases by contributing to early detection
strategies and paving the way for improved patient care through innovative diagnostic
tools.
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=612948">Place Hold on <em>Characterization of Blood-Derived Exosomes for Diagnostics Insights in Neurological Diseases /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=612948</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Exploring the Neuroprotective Effects of Indole Propionate and Shikonin in STZ-Induced Diabetic Rats: A Novel Therapeutic Strategy for Cognitive Impairment in Type 2 Diabetes Mellitus /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=613677</link>
        
       <description><![CDATA[









	   <p>By Asif, Muhammad . 
	   
                        . 91p.
                        , The chronic metabolic disorder known as diabetes mellitus severely deteriorates memory
function and learning while damaging hippocampal tissue. Given that impaired
hippocampal insulin signaling leads to memory deficits, insulin resistance and
hyperinsulinemia are considered critical links between type 2 diabetes mellitus (T2DM)
and AD. This study utilized streptozotocin (STZ)-induced diabetic rat model to evaluate
the therapeutic potential of indole propionate (IPA) and Shikonin as treatments for
cognitive impairment. Male albino rats were divided into seven groups, three control
groups receiving ddH₂O, IPA, and Shikonin, respectively, and four experimental groups
treated with a high-fat diet and intraperitoneal (IP) injections of STZ (25 mg/kg) to
induce diabetes. Following disease induction, diabetic rats were treated with IPA (40
mg/kg), Shikonin (10 mg/kg), and metformin (200 mg/kg) for 28 days. The study
measured three critical parameters which included body weight assessment together with
blood glucose levels and evaluation of hippocampal and cortical gene expression analysis
related to cognitive impairment. Real-time quantitative PCR (RT-qPCR) was utilized to
evaluate mRNA expression levels of genes implicated in these deficits. Our findings
demonstrate that the elevated expression of Tau and APP in diabetic rats was
substantially reduced with IPA treatment (p &lt; 0.0001). Additionally, PDIA3 (ERp57), an
endoplasmic reticulum (ER)-resident chaperone, was significantly downregulated in the
T2DM group but restored with IPA treatment. Dysregulated expression of the
mitochondrial chaperone Hsp60 was also improved with both IPA and Shikonin. Insulindegrading enzyme (IDE), a key protein linking T2DM and AD, showed substantial
restoration in the T2DM+IPA-treated group. IPA and Shikonin treatments improved the
body weight and blood glucose levels of diabetic rats who experienced notable decreases
in both parameters initially. The results of the study demonstrate how IPA and Shikonin
show promise as treatments for reducing cognitive problems in diabetes patients.
However, the clinical deployment of these compounds needs confirmation through
additional studies at the cellular and molecular levels
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=613677">Place Hold on <em>Exploring the Neuroprotective Effects of Indole Propionate and Shikonin in STZ-Induced Diabetic Rats: A Novel Therapeutic Strategy for Cognitive Impairment in Type 2 Diabetes Mellitus /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=613677</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Exploring the Neuroprotective Effects of Indole Propionate and Shikonin in STZ-Induced Diabetic Rats: A Novel Therapeutic Strategy for Cognitive Impairment in Type 2 Diabetes Mellitus /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=613794</link>
        
       <description><![CDATA[









	   <p>By  Asif, Muhammad. 
	   
                        . 91p.
                        , The chronic metabolic disorder known as diabetes mellitus severely deteriorates memory
function and learning while damaging hippocampal tissue. Given that impaired
hippocampal insulin signaling leads to memory deficits, insulin resistance and
hyperinsulinemia are considered critical links between type 2 diabetes mellitus (T2DM)
and AD. This study utilized streptozotocin (STZ)-induced diabetic rat model to evaluate
the therapeutic potential of indole propionate (IPA) and Shikonin as treatments for
cognitive impairment. Male albino rats were divided into seven groups, three control
groups receiving ddH₂O, IPA, and Shikonin, respectively, and four experimental groups
treated with a high-fat diet and intraperitoneal (IP) injections of STZ (25 mg/kg) to
induce diabetes. Following disease induction, diabetic rats were treated with IPA (40
mg/kg), Shikonin (10 mg/kg), and metformin (200 mg/kg) for 28 days. The study
measured three critical parameters which included body weight assessment together with
blood glucose levels and evaluation of hippocampal and cortical gene expression analysis
related to cognitive impairment. Real-time quantitative PCR (RT-qPCR) was utilized to
evaluate mRNA expression levels of genes implicated in these deficits. Our findings
demonstrate that the elevated expression of Tau and APP in diabetic rats was
substantially reduced with IPA treatment (p &lt; 0.0001). Additionally, PDIA3 (ERp57), an
endoplasmic reticulum (ER)-resident chaperone, was significantly downregulated in the
T2DM group but restored with IPA treatment. Dysregulated expression of the
mitochondrial chaperone Hsp60 was also improved with both IPA and Shikonin. Insulindegrading enzyme (IDE), a key protein linking T2DM and AD, showed substantial
restoration in the T2DM+IPA-treated group. IPA and Shikonin treatments improved the
body weight and blood glucose levels of diabetic rats who experienced notable decreases
in both parameters initially. The results of the study demonstrate how IPA and Shikonin
show promise as treatments for reducing cognitive problems in diabetes patients.
However, the clinical deployment of these compounds needs confirmation through
additional studies at the cellular and molecular levels.
                         30CM. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=613794">Place Hold on <em>Exploring the Neuroprotective Effects of Indole Propionate and Shikonin in STZ-Induced Diabetic Rats: A Novel Therapeutic Strategy for Cognitive Impairment in Type 2 Diabetes Mellitus /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=613794</guid>
     </item>
	 
     <atom:link rel="search" type="application/opensearchdescription+xml" href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-search.pl?&amp;sort_by=&amp;format=opensearchdescription"/>
     <opensearch:Query role="request" searchTerms="" startPage="" />
     <item>
       <title>
    Psoriasis &amp; Neuroinflammation: Exploring Cytokine Release in Barrier and Metabolic Organs /






</title>
       <dc:identifier>ISBN:</dc:identifier>
        
        <link>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=616895</link>
        
       <description><![CDATA[









	   <p>By Perveen, Anita . 
	   
                        . 99p.
                        , Psoriasis is a chronic systemic inflammatory disease with its effects beyond skin. One
major comorbidity reported to be highly prevalent in psoriatic patients is cognitive
impairment. Moreover, overexpression of pro-inflammatory cytokines plays a central role
in development and progression of psoriasis and neuroinflammation. This study aims to
explore the role of inflammatory cytokines in neurodegeneration and disease progression
in psoriatic patients. Furthermore, it assesses the therapeutic effect of curcumin-chamomile
based plant extract loaded onto PVA nanoparticles via wet lab and bioinformatics tools.
Curcumin and Chamomile Plant extract-based drug was designed and loaded with Nanoparticles to use as treatment. The drug was tested on various parameters to check its toxicity
and reactivity before using in-vivo. Psoriatic animal model was designed by imiquimod
(IMQ) application on male BALB/c mice. The complete In-Vivo study from disease
induction to treatment followed by collection of cortex, hippocampus, Eyes, Skin and Liver
was done which were later used for gene expression analysis. Protein hallmarks of
neurodegeneration; α-Syn, and inflammatory cytokines like IL‐1β, TNF‐α, PEBP-1 and
HSP-90AB1 were measured at transcriptional level in cortex, hippocampus, Eyes, Skin
and Liver. Disease induction using IMQ resulted in excessive production of keratinocytes.
Pro-inflammatory cytokines were over-expressed whereas α-Syn showed a moderate
increase in hippocampus, eyes, cortex, liver and skin. Both treatment groups showed a
significant decline in α-Syn and normalization and downregulation of pro-inflammatory
cytokines. Molecular docking revealed potential interactions between proteins and
cytokines, and proteins and phytochemicals exhibiting potential roles in alleviating the
disease pathology. Pathway enrichment analysis was carried out to understand the
underlying mechanisms involved in disease progression and roles of these proteins. The
increased expression of inflammatory markers causes neuroinflammation and contribute to
depression and cognitive impairment, which can be reversed using the novel designed drug.
In psoriatic conditions, elevated levels of inflammatory cytokines cause chronic
inflammation, which trigger neuroinflammatory transcription factors. The Curcuminchamomile based novel drug encapsulated with nanoparticles comes as a new promising
approach to cure neurodegenerative diseases, and the comorbidities arising from psoriasis. 
                         30cm. 
                        
       </p>

<p><a href="http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-reserve.pl?biblionumber=616895">Place Hold on <em>Psoriasis &amp; Neuroinflammation: Exploring Cytokine Release in Barrier and Metabolic Organs /</em></a></p>

						]]></description>
       <guid>http://catalogue.nust.edu.pk:8081/cgi-bin/koha/opac-detail.pl?biblionumber=616895</guid>
     </item>
	 
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