scispace - formally typeset
A

Alasdair M. Barr

Researcher at University of British Columbia

Publications -  231
Citations -  7960

Alasdair M. Barr is an academic researcher from University of British Columbia. The author has contributed to research in topics: Antipsychotic & Clozapine. The author has an hindex of 45, co-authored 211 publications receiving 6915 citations. Previous affiliations of Alasdair M. Barr include UBC Hospital & Scripps Research Institute.

Papers
More filters
Journal Article

The need for speed: an update on methamphetamine addiction.

TL;DR: This work provides a comprehensive description of the factors relating to MA use and the major health-related consequences, with an emphasis on MA-induced psychosis, and hopes that increased knowledge of MA abuse will provide the basis for future treatment strategies.
Journal ArticleDOI

Methamphetamine use: a comprehensive review of molecular, preclinical and clinical findings.

TL;DR: A review of the evidence that chronic MA use is associated with substantial neurotoxicity and cognitive impairment and key findings in the literature spanning from molecular through to clinical effects are summarized.
Journal ArticleDOI

Much of late life cognitive decline is not due to common neurodegenerative pathologies

TL;DR: The hypothesis that these pathologic indices of Alzheimer disease, cerebrovascular disease, and Lewy body disease account for the majority of late life cognitive decline is tested.
Journal ArticleDOI

Estradiol alleviates depressive-like symptoms in a novel animal model of post-partum depression.

TL;DR: The results imply that withdrawal from chronic high levels of pregnancy-associated hormones (estradiol and progesterone) can produce depressed symptomology in rodents, which can be prevented by prolonging exposure to high Levels of estradiol through the post-partum period.
Journal ArticleDOI

Stimulation of the Ventral Subiculum of the Hippocampus Evokes Glutamate Receptor‐mediated Changes in Dopamine Efflux in the Rat Nucleus Accumbens

TL;DR: The results suggest that ventral subiculum/CA1 glutamatergic inputs to the nucleus accumbens may presynaptically modulate dopamine efflux by synaptic activation of both ionotropic and metabotropic glutamate receptors in the nucleus Accumbens.