Dr. Atoossa Fahimi, MD, PsyM - Stanford University School of Medicine - Postdoc Fellow/ Research Associate

Dr. Atoossa Fahimi

MD, PsyM

Stanford University School of Medicine

Postdoc Fellow/ Research Associate

Palo Alto, CA | United States

Main Specialties: Neurology

Additional Specialties: Psychiatry-Neuroscience

Dr. Atoossa Fahimi, MD, PsyM - Stanford University School of Medicine - Postdoc Fellow/ Research Associate

Dr. Atoossa Fahimi

MD, PsyM

Introduction

Primary Affiliation: Stanford University School of Medicine - Palo Alto, CA , United States

Specialties:

Additional Specialties:

Publications

7Publications

42Reads

1Profile Views

27PubMed Central Citations

Physical exercise induces structural alterations in the hippocampal astrocytes: exploring the role of BDNF-TrkB signaling.

Brain Struct Funct 2017 May 29;222(4):1797-1808. Epub 2016 Sep 29.

VA Palo Alto Health Care System, 3801 Miranda Ave, Palo Alto, CA, 94304, USA.

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http://dx.doi.org/10.1007/s00429-016-1308-8DOI Listing
May 2017
2 Reads
7 Citations
5.620 Impact Factor

GABAergic hyperinnervation of dentate granule cells in the Ts65Dn mouse model of down syndrome: Exploring the role of App.

Hippocampus 2016 12 24;26(12):1641-1654. Epub 2016 Oct 24.

VA Palo Alto Health Care System, Palo Alto, California.

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http://dx.doi.org/10.1002/hipo.22664DOI Listing
December 2016
3 Reads
3 Citations
4.162 Impact Factor

Noradrenergic System in Down Syndrome and Alzheimer's Disease A Target for Therapy.

Curr Alzheimer Res 2016 ;13(1):68-83

Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, VA Palo Alto Health Care System, 3801 Miranda Ave, 151Y, Palo Alto, CA 94304, USA.

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http://dx.doi.org/10.2174/1567205012666150921095924DOI Listing
September 2016
9 Reads
10 Citations
3.890 Impact Factor

Methodology of "Physical and Rehabilitation Medicine practice, Evidence Based Position Papers: the European position" produced by the UEMS-PRM Section.

Eur J Phys Rehabil Med 2016 Feb 17;52(1):134-41. Epub 2015 Dec 17.

Clinical and Experimental Sciences Department, University of Brescia, Brescia, Italy -

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February 2016
22 Reads
1.950 Impact Factor

Increased incidence of intermittent hypoxemia in the Ts65Dn mouse model of Down syndrome.

Neurosci Lett 2015 Sep 1;604:91-6. Epub 2015 Aug 1.

VA Palo Alto Health Care System, Palo Alto, CA 94305, USA; Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, CA 94305, USA. Electronic address:

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http://dx.doi.org/10.1016/j.neulet.2015.07.040DOI Listing
September 2015
4 Reads
2 Citations
2.060 Impact Factor

Increased cortical synaptic activation of TrkB and downstream signaling markers in a mouse model of Down Syndrome.

Neurobiol Dis 2015 May 6;77:173-90. Epub 2015 Mar 6.

Department of Neurosciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

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http://dx.doi.org/10.1016/j.nbd.2015.02.022DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4689307PMC
May 2015
2 Reads
5 Citations
5.080 Impact Factor

EVOLUTION OF MONOAMINERGIC SYSTEM DEGENERATION IN DOWN SYNDROME AND ALZHEIMER'S DISEASE

Bentham Science

A multitude of neuropathological studies has established a robust link between Down Syndrome and Alzheimer's disease. Through massive projections to the entire cortex and hippocampus, the monoaminergic-system exert a powerful modulatory effect on brain regions vitally important for cognition. Nevertheless, substantial evidence demonstrates these systems are inherently vulnerable to neurodegeneration, particularly in Down syndrome and Alzheimer's disease. Accordingly, abnormalities in the structure and function of subcortical monoaminergic systems constitute a common characteristic of both disorders. Underlying these deficits are neuropathological changes in the locus coeruleus, ventral segmental area, substantia nigra and raphe and tuberomamillary nuclei. Fortunately, preclinical and clinical studies suggest that pharmacotherapies targeting of these systems may provide symptomatic relief along with disease modifying effects in Down syndrome and Alzheimer's disease.

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4 Reads