Applications of positron emission tomography in animal models of neurological and neuropsychiatric disorders

2012 ◽  
Vol 36 (4) ◽  
pp. 1188-1216 ◽  
Author(s):  
Kanwar Virdee ◽  
Paul Cumming ◽  
Daniele Caprioli ◽  
Bianca Jupp ◽  
Axel Rominger ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Animal Models ◽  
Neuropsychiatric Disorders ◽  
Emission Tomography ◽  
Positron Emission

scholarly journals Positron Emission Tomography in Animal Models of Alzheimer’s Disease Amyloidosis

2021 ◽  
Author(s):  
Ruiqing Ni
Keyword(s):  
Positron Emission Tomography ◽  
Animal Models ◽  
Amyloid Beta ◽  
Emission Tomography ◽  
Imaging Biomarkers ◽  
Preclinical Research ◽  
Non Invasive ◽  
Positron Emission ◽  
Cerebral Amyloid ◽  
On Chip

Animal models of Alzheimer’s disease amyloidosis that recapitulate cerebral amyloid-beta pathology have been widely used in preclinical research, and have greatly enabled the mechanistic understanding of Alzheimer’s disease and the development of therapeutics. Comprehensive deep phenotyping of the pathophysiological and biochemical features in these animal models are essential. Recent advances in positron emission tomography have allowed the non-invasive visualization of the alterations in the brain of animal models as well as in patients with Alzheimer’s disease, These tools have facilitated our understanding of disease mechanisms, and provided longitudinal monitoring of treatment effect in animal models of Alzheimer’s disease amyloidosis. In this review, we focus on recent positron emission tomography studies of cerebral amyloid-beta accumulation, hypoglucose metabolism, synaptic and neurotransmitter receptor deficits (cholinergic and glutamatergic system), blood-brain barrier impairment and neuroinflammation (microgliosis and astrocytosis) in animal models of Alzheimer’s disease amyloidosis. We further propose the emerging targets and tracers for reflecting the pathophysiological changes, and discuss outstanding challenges in disease animal models and future outlook in on-chip characterization of imaging biomarkers towards clinical translation.

scholarly journals Are Animal Studies of Antipsychotics Appropriately Dosed?: Lessons from the Bedside to the Bench

2000 ◽  
Vol 45 (3) ◽  
pp. 241-246 ◽  
Author(s):  
Shitij Kapur ◽  
Marie-Louise Wadenberg ◽  
Gary Remington
Keyword(s):  
Positron Emission Tomography ◽  
Side Effects ◽  
Animal Models ◽  
Mechanism Of Action ◽  
Half Life ◽  
Animal Studies ◽  
Emission Tomography ◽  
Low Doses ◽  
Extrapyramidal Side Effects ◽  
Positron Emission

Animal models are crucial for understanding the mechanism of action of antipsychotics. However, the dose of an antipsychotic in animal studies is often arbitrarily chosen, with haloperidol 1 mg/kg being a rather common standard. Recent clinical positron emission tomography (PET) studies in patients show all antipsychotics to block dopamine D2 receptors, and most are effective at doses that lead to 60% to 80% D2 occupancy. When occupancy exceeds 80%, the incidence of side effects rises sharply. To use this “bedside” information to inform the “bench,” we measured D2 occupancy in rats using a method similar in principle to the [11 C]-raclopride PET method in humans. We found that: 1) as in humans, haloperidol is effective in animal models of antipsychotic action when D2 occupancy > 70% and leads to effects in models of extrapyramidal side effects when D2 occupancy is > 80%; 2) very low doses, 0.06 mg/kg/sc, cause acute D2 occupancy of 75%; 3) and even doses that acutely saturate D2 receptors give little D2 occupancy after 24 hours due to the very short half-life of haloperidol in rats (2.5 hours versus 24 hours in humans). We conclude that most previous animal studies of antipsychotics have used doses giving rise to inappropriately high acute D2 occupancy and inappropriately low D2 occupancy between doses. We exemplify how this dosing confounder could lead to inappropriate conclusions. Data from the bedside translated to the bench—using D2 occupancy as a mediating variable—will lead to more valid animal models.

scholarly journals Positron Emission Tomography in Animal Models of Alzheimer’s Disease Amyloidosis: Translational Implications

2021 ◽  
Vol 14 (11) ◽  
pp. 1179
Author(s):  
Ruiqing Ni
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Positron Emission Tomography ◽  
Animal Models ◽  
Amyloid Beta ◽  
Emission Tomography ◽  
Imaging Biomarkers ◽  
Preclinical Research ◽  
Positron Emission ◽  
Cerebral Amyloid

Animal models of Alzheimer’s disease amyloidosis that recapitulate cerebral amyloid-beta pathology have been widely used in preclinical research and have greatly enabled the mechanistic understanding of Alzheimer’s disease and the development of therapeutics. Comprehensive deep phenotyping of the pathophysiological and biochemical features in these animal models is essential. Recent advances in positron emission tomography have allowed the non-invasive visualization of the alterations in the brain of animal models and in patients with Alzheimer’s disease. These tools have facilitated our understanding of disease mechanisms and provided longitudinal monitoring of treatment effects in animal models of Alzheimer’s disease amyloidosis. In this review, we focus on recent positron emission tomography studies of cerebral amyloid-beta accumulation, hypoglucose metabolism, synaptic and neurotransmitter receptor deficits (cholinergic and glutamatergic system), blood–brain barrier impairment, and neuroinflammation (microgliosis and astrocytosis) in animal models of Alzheimer’s disease amyloidosis. We further propose the emerging targets and tracers for reflecting the pathophysiological changes and discuss outstanding challenges in disease animal models and future outlook in the on-chip characterization of imaging biomarkers towards clinical translation.

Positron Emission Tomography of Cocaine Binding Sites on the Dopamine Transporter

1994 ◽  
Author(s):  
Bertha K. Madras ◽  
◽  
David R. Elmaleh ◽  
Peter C. Meltzer ◽  
Anna Y. Liung ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Dopamine Transporter ◽  
Binding Sites ◽  
Emission Tomography ◽  
Positron Emission
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