Literature DB >> 26402018

Garrison Institute on Aging: A New Hope for Elderly Individuals and Patients with Alzheimer's Disease.

P Hemachandra Reddy1,2, Joan Blackmon2, Veronica Molinar-Lopez2, Clay Ament2, Maria Manczak1, Ramesh Kandimalla1, Xianglin Yin1, Akhilesh Pandey1, Chandra Sekhar Kuruva1, Rui Wang1, David Fry1, Carrah Osborn1, Kathleen Stonum1, Kandi Quesada1, Ruben Gonzales1, Annette Boles2.   

Abstract

The Garrison Institute on Aging (GIA) is an established institute within Texas Tech University Health Sciences Center, whose mission is to promote healthy aging through cutting-edge research on Alzheimer's disease (AD) and other diseases of aging through innovative educational opportunities for students, clinicians, researchers, health care professionals, and the public. The GIA has multiple programs, including both research and education on healthy aging and AD, community outreach, caregiving, the Retired Senior Volunteer Program, Healthy Lubbock, the GIA Brain Bank, healthy aging seminars, research seminars, and collaborations and scholarships. The GIA programs connect basic and clinical researchers and health care professionals, and provide a unique environment to help our growing elderly population and patients with AD and their families.

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Mesh：

Year:  2015        PMID： 26402018      PMCID： PMC5343754          DOI： 10.3233/JAD-150490

Source DB:  PubMed          Journal:  J Alzheimers Dis        ISSN： 1387-2877            Impact factor:   4.472


  16 in total

Review 1.  Increased mitochondrial fission and neuronal dysfunction in Huntington's disease: implications for molecular inhibitors of excessive mitochondrial fission.

Authors:  P Hemachandra Reddy
Journal:  Drug Discov Today       Date:  2014-03-28       Impact factor: 7.851

Review 2.  Inhibitors of mitochondrial fission as a therapeutic strategy for diseases with oxidative stress and mitochondrial dysfunction.

Authors:  P Hemachandra Reddy
Journal:  J Alzheimers Dis       Date:  2014       Impact factor: 4.472

Review 3.  Mutant huntingtin, abnormal mitochondrial dynamics, defective axonal transport of mitochondria, and selective synaptic degeneration in Huntington's disease.

Authors:  P Hemachandra Reddy; Ulziibat P Shirendeb
Journal:  Biochim Biophys Acta       Date:  2011-11-04

4.  Mitochondria-targeted catalase reduces abnormal APP processing, amyloid β production and BACE1 in a mouse model of Alzheimer's disease: implications for neuroprotection and lifespan extension.

Authors:  Peizhong Mao; Maria Manczak; Marcus J Calkins; Quang Truong; Tejaswini P Reddy; Arubala P Reddy; Ulziibat Shirendeb; Herng-Hsiang Lo; Peter S Rabinovitch; P Hemachandra Reddy
Journal:  Hum Mol Genet       Date:  2012-04-05       Impact factor: 6.150

5.  Mutant huntingtin's interaction with mitochondrial protein Drp1 impairs mitochondrial biogenesis and causes defective axonal transport and synaptic degeneration in Huntington's disease.

Authors:  Ulziibat P Shirendeb; Marcus J Calkins; Maria Manczak; Vishwanath Anekonda; Brett Dufour; Jodi L McBride; Peizhong Mao; P Hemachandra Reddy
Journal:  Hum Mol Genet       Date:  2011-10-13       Impact factor: 6.150

6.  Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease.

Authors:  P Hemachandra Reddy; Shannon McWeeney; Byung S Park; Maria Manczak; Ramana V Gutala; Dara Partovi; Youngsin Jung; Vincent Yau; Robert Searles; Motomi Mori; Joseph Quinn
Journal:  Hum Mol Genet       Date:  2004-04-28       Impact factor: 6.150

Review 7.  Mitochondrial structural and functional dynamics in Huntington's disease.

Authors:  P Hemachandra Reddy; Peizhong Mao; Maria Manczak
Journal:  Brain Res Rev       Date:  2009-04-24

8.  Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's disease.

Authors:  Maria Manczak; P Hemachandra Reddy
Journal:  Hum Mol Genet       Date:  2012-08-27       Impact factor: 6.150

9.  Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression.

Authors:  Maria Manczak; Thimmappa S Anekonda; Edward Henson; Byung S Park; Joseph Quinn; P Hemachandra Reddy
Journal:  Hum Mol Genet       Date:  2006-03-21       Impact factor: 6.150

10.  MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.

Authors:  Peizhong Mao; Maria Manczak; Ulziibat P Shirendeb; P Hemachandra Reddy
Journal:  Biochim Biophys Acta       Date:  2013-09-19
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  1 in total

Review 1.  Garrison Institute on Aging-Lubbock Retired and Senior Volunteer Program (RSVP) Provides Services to South Plains, Texas.

Authors:  Joan Blackmon; Annette N Boles; P Hemachandra Reddy
Journal:  Front Aging Neurosci       Date:  2015-12-08       Impact factor: 5.750
  1 in total

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