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Michela Gallagher

Researcher at Johns Hopkins University

Publications -  297
Citations -  33385

Michela Gallagher is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Hippocampal formation & Hippocampus. The author has an hindex of 95, co-authored 293 publications receiving 31710 citations. Previous affiliations of Michela Gallagher include University of Vermont & Texas A&M University.

Papers
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Book ChapterDOI

Insulin-like Growth Factor I: Regulation and Interactions During Aging-Induced Cognitive Decline and Impairment Within the Hippocampus

TL;DR: A considerable body of evidence indicates that hippocampal circuitry is especially vulnerable to the neurodegeneration associated with normal and pathological aging, however, aged hippocampus appears to retain some of its capacity to regenerate in response to this damage.
Patent

Extended release pharmaceutical compositions of levetiracetam

TL;DR: In this paper, extended release pharmaceutical compositions of levetiracetam and preparations and characterizations thereof were presented for the treatment of cognitive impairment associated with central nervous system (CNS) disorders in a subject in need or at risk thereof.
Posted ContentDOI

Heterogeneity of age-related neural hyperactivity along the CA3 transverse axis

TL;DR: It is suggested that, in combination with altered inputs from the entorhinal cortex and dentate gyrus, the proximal CA3 region of aged rats may switch from its normal function that reflects the pattern separation output of the DG and instead performs a computation that reflects an abnormal bias toward pattern completion.
Patent

Cible destinee a la therapie d'un trouble cognitif

TL;DR: In this paper, a procedure d'identification de genes impliques dans un trouble cognitif and des compositions permettant de traiter un tel trouble is described.
Posted ContentDOI

The lateral habenula mediates the association of a conditioned stimulus with the absence of an appetitive unconditioned stimulus

TL;DR: Neurotoxic LHb lesions and chemogenetic LHb inhibition throughout unpaired training attenuated the inhibitory light strength and accelerated the decline in CR induced by repeated light-alone presentations following light-food pairings.