Amy Birch
Postdoctoral neuroscientist specialising in neuronal plasticity and behaviour, with particular interest in neurodegenerative diseases.
I have a wide range of skills and experience in:
Behavioural testing
Biochemical analysis of tissue
Editing & copy-editing
Management
Project Supervision
Small to medium group tutoring
Science Communication
Public Engagement
Oral & written communication
I have a wide range of skills and experience in:
Behavioural testing
Biochemical analysis of tissue
Editing & copy-editing
Management
Project Supervision
Small to medium group tutoring
Science Communication
Public Engagement
Oral & written communication
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Papers by Amy Birch
Alzheimer’s disease (AD) because of their neuroprotective properties and effects on neuronal proliferation.
Basic fibroblast growth factor or fibroblast growth factor-2 (FGF2) is an anti-inflammatory,
angiogenic, and neurotrophic factor that is expressed in many cell types, including neurons and glial
cells. Here, we explored whether subcutaneous administration of FGF2 could have therapeutic effects in
the APP 23 transgenic mouse, a model of amyloid pathology. FGF2 treatment attenuated spatial memory
deficits, reduced amyloid-b (Ab) and tau pathologies, decreased inducible nitric oxide synthase
expression, and increased the number of astrocytes in the dentate gyrus in APP 23 mice compared with
the vehicle-treated controls. The decrease in Ab deposition was associated with a reduction in the
expression of BACE1, the main enzyme responsible for Ab generation. These results were confirmed in a
neuroblastoma cell line, which demonstrated that incubation with FGF2 regulates BACE1 transcription. In
addition, and in contrast with what has been previously published, the levels of FGF2 were reduced in
postmortem brains from AD patients compared with controls. These data, therefore, suggest that systemic
administration of FGF2 could have a potential therapeutic application in AD
(AD) field, not only for its potential role in neuronal degeneration but also as a promising therapeutic target.
However, recent research in this field has provided divergent outcomes, largely due to the use of different models
and different stages of the disease when the investigations have been carried out. It is now accepted that
microglia, and possibly astrocytes, change their activation phenotype during ageing and the stage of the disease,
and therefore these are important factors to have in mind to define the function of different inflammatory
components as well as potential therapies. Modulating inflammation using animal models of AD has offered the
possibility to investigate inflammatory components individually and manipulate inflammatory genes in amyloid
precursor protein and tau transgenics independently. This has also offered some hints on the mechanisms by
which these factors may affect AD pathology. In this review we examine the different transgenic approaches and
treatments that have been reported to modulate inflammation using animal models of AD. These studies have
provided evidence that enhancing inflammation is linked with increases in amyloid-beta (Aβ) generation, Aβ aggregation
and tau phosphorylation. However, the alterations on tau phosphorylation can be independent of changes in Aβ levels
by these inflammatory mediators.
may modulate forms of structural and functional plasticity, including neurogenesis. We have shown
previously that six weeks of housing in an enriched environment (EE) that did not include access to
running wheels resulted in improved recognition memory concomitant with increased NGF expression
and neurogenesis in the hippocampus. Here we have attempted to probe a causal link between NGF and
the observed enrichment-induced changes in hippocampal function by assessing the effects of six weeks
continuous intracerebroventricular (i.c.v.) infusion of NGF on recognition memory and cell proliferation.
We report that NGF-infused rats show enhanced recognition memory when compared with vehicletreated
controls. Expression of NGF and its receptor, TrkA, was increased in treated rats, as was
expression of the synaptic vesicle protein, synapsin. Finally, we observed an increase in cell proliferation
in the dentate gyrus of NGF-treated rats. These data indicate that chronic infusion of NGF can stimulate
an improvement in learning and memory that is associated with specific cellular changes in the hippocampus,
including synaptogenesis and cell proliferation.
Alzheimer’s disease (AD) because of their neuroprotective properties and effects on neuronal proliferation.
Basic fibroblast growth factor or fibroblast growth factor-2 (FGF2) is an anti-inflammatory,
angiogenic, and neurotrophic factor that is expressed in many cell types, including neurons and glial
cells. Here, we explored whether subcutaneous administration of FGF2 could have therapeutic effects in
the APP 23 transgenic mouse, a model of amyloid pathology. FGF2 treatment attenuated spatial memory
deficits, reduced amyloid-b (Ab) and tau pathologies, decreased inducible nitric oxide synthase
expression, and increased the number of astrocytes in the dentate gyrus in APP 23 mice compared with
the vehicle-treated controls. The decrease in Ab deposition was associated with a reduction in the
expression of BACE1, the main enzyme responsible for Ab generation. These results were confirmed in a
neuroblastoma cell line, which demonstrated that incubation with FGF2 regulates BACE1 transcription. In
addition, and in contrast with what has been previously published, the levels of FGF2 were reduced in
postmortem brains from AD patients compared with controls. These data, therefore, suggest that systemic
administration of FGF2 could have a potential therapeutic application in AD
(AD) field, not only for its potential role in neuronal degeneration but also as a promising therapeutic target.
However, recent research in this field has provided divergent outcomes, largely due to the use of different models
and different stages of the disease when the investigations have been carried out. It is now accepted that
microglia, and possibly astrocytes, change their activation phenotype during ageing and the stage of the disease,
and therefore these are important factors to have in mind to define the function of different inflammatory
components as well as potential therapies. Modulating inflammation using animal models of AD has offered the
possibility to investigate inflammatory components individually and manipulate inflammatory genes in amyloid
precursor protein and tau transgenics independently. This has also offered some hints on the mechanisms by
which these factors may affect AD pathology. In this review we examine the different transgenic approaches and
treatments that have been reported to modulate inflammation using animal models of AD. These studies have
provided evidence that enhancing inflammation is linked with increases in amyloid-beta (Aβ) generation, Aβ aggregation
and tau phosphorylation. However, the alterations on tau phosphorylation can be independent of changes in Aβ levels
by these inflammatory mediators.
may modulate forms of structural and functional plasticity, including neurogenesis. We have shown
previously that six weeks of housing in an enriched environment (EE) that did not include access to
running wheels resulted in improved recognition memory concomitant with increased NGF expression
and neurogenesis in the hippocampus. Here we have attempted to probe a causal link between NGF and
the observed enrichment-induced changes in hippocampal function by assessing the effects of six weeks
continuous intracerebroventricular (i.c.v.) infusion of NGF on recognition memory and cell proliferation.
We report that NGF-infused rats show enhanced recognition memory when compared with vehicletreated
controls. Expression of NGF and its receptor, TrkA, was increased in treated rats, as was
expression of the synaptic vesicle protein, synapsin. Finally, we observed an increase in cell proliferation
in the dentate gyrus of NGF-treated rats. These data indicate that chronic infusion of NGF can stimulate
an improvement in learning and memory that is associated with specific cellular changes in the hippocampus,
including synaptogenesis and cell proliferation.