Henry J. Waldvogel

ORCID: 0000-0003-2165-8568
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Genetic Neurodegenerative Diseases
  • Neurological disorders and treatments
  • Mitochondrial Function and Pathology
  • Alzheimer's disease research and treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Receptor Mechanisms and Signaling
  • Nicotinic Acetylcholine Receptors Study
  • Neurotransmitter Receptor Influence on Behavior
  • Neurogenesis and neuroplasticity mechanisms
  • Neurological diseases and metabolism
  • Ion channel regulation and function
  • Memory and Neural Mechanisms
  • Tryptophan and brain disorders
  • Neuropeptides and Animal Physiology
  • Neural dynamics and brain function
  • Muscle metabolism and nutrition
  • Neuroscience of respiration and sleep
  • Amyotrophic Lateral Sclerosis Research
  • RNA Research and Splicing
  • Muscle Physiology and Disorders
  • GABA and Rice Research
  • Amino Acid Enzymes and Metabolism
  • Metabolism and Genetic Disorders

University of Auckland
2015-2024

Brain Research New Zealand
2015-2021

Zero to Three
2009

University of Zurich
1988

University of Waikato
1979

The PARK8 gene responsible for late-onset autosomal dominant Parkinson's disease encodes a large novel protein of unknown biological function termed leucine-rich repeat kinase 2 (LRRK2). studies herein explore the localization LRRK2 in mammalian brain.Polyclonal antibodies generated against amino or carboxy termini were used to examine biochemical, subcellular, and immunohistochemical distribution LRRK2.LRRK2 is detected rat brain as an approximate 280kDa by Western blot analysis....

10.1002/ana.21019 article EN Annals of Neurology 2006-11-01

Papertrinucleotide repeat expansion resulting in an elongated polyglutamine stretch near the N-terminus of huntingtin (HTT) protein [2].HD patients have CAG lengths greater than 36 on one HTT alleles.Although HD affects a number brain regions such as cortex, thalamus, and subthalamic nucleus, www.impactaging.com

10.18632/aging.101005 article EN cc-by Aging 2016-07-27

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease. HD patients present with movement disorders, behavioral and psychiatric symptoms cognitive decline. This review summarizes the contribution of microglia astrocytes to pathophysiology. Neuroinflammation in brain characterized by a reactive morphology these glial cells. Microglia are critical regulating neuronal activity maintaining optimal milieu for function. Previous studies provide evidence that activated...

10.3389/fnmol.2019.00258 article EN cc-by Frontiers in Molecular Neuroscience 2019-10-25

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that currently affects 36 million people worldwide with no effective treatment available. Development of AD follows distinctive pattern in the brain and poorly modelled animals. Therefore, it vital to widen spatial scope study prioritise human brains. Here we show functionally distinct regions display varying region-specific changes protein expression. These provide insights into progression disease, novel AD-related...

10.1038/s42003-018-0254-9 article EN cc-by Communications Biology 2019-02-04

Huntington's disease is an autosomal dominant inherited neurodegenerative with motor symptoms that are variably co-expressed mood and cognitive symptoms, in which variable neuronal degeneration also observed the basal ganglia cerebral cortex. We have recently shown symptomatology correlates compartmental pattern of GABAA receptor cell loss striatum. To determine whether phenotypic variability related to cortex, we undertook a double-blind study using unbiased stereological counting methods...

10.1093/brain/awq047 article EN Brain 2010-04-01

Huntington's disease (HD) is an inherited autosomal dominant neurodegenerative disorder caused by expansion of a CAG trinucleotide repeat in the huntingtin (HTT) gene [Huntington's Disease Collaborative Research Group (1993) A novel containing that expanded and unstable on chromosomes. The Group. Cell, 72, 971–983]. Despite identification 1993, underlying life-long process effective treatments to prevent or delay it remain elusive. In effort fast-track treatment strategies for HD into...

10.1093/hmg/ddq063 article EN Human Molecular Genetics 2010-02-13

Background and purpose: The histamine H 4 receptor is the most recently identified of G protein‐coupled family binds several neuroactive drugs, including amitriptyline clozapine. So far, receptors have been found only on haematopoietic cells, highlighting its importance in inflammatory conditions. Here we investigated possibility that may be expressed both human mouse CNS. Methods: Immunological pharmacological studies were performed using a novel anti‐H antibody brains, electrophysiological...

10.1111/j.1476-5381.2009.00227.x article EN British Journal of Pharmacology 2009-04-08

The trigeminovascular system plays a central role in migraine, condition need of new treatments. neuropeptide, calcitonin gene-related peptide (CGRP), is proposed as causative migraine and the subject intensive drug discovery efforts. This study explores expression functionality two CGRP receptor candidates sensory trigeminal system.Receptor was determined using Taqman G protein-coupled arrays immunohistochemistry ganglia (TG) spinal complex brainstem rat human. Receptor pharmacology...

10.1002/acn3.197 article EN Annals of Clinical and Translational Neurology 2015-04-01

Abstract Vascular degeneration plays a significant role in contributing to neurodegenerative conditions such as A lzheimer's disease. Our understanding of the vascular components P arkinson's disease ( PD ) is however limited. We have examined morphology human brain tissue from both and control cases using immunohistochemical staining image analysis. The degenerative seen included formation endothelial cell “clusters,” which may be contributed by fragmentation capillaries. When compared...

10.1111/j.1750-3639.2012.00628.x article EN Brain Pathology 2012-08-16

Alzheimer's disease (AD) is an age-related neurodegenerative disorder that displays pathological characteristics including senile plaques and neurofibrillary tangles. Metabolic defects are also present in AD-brain: for example, signs of deficient cerebral glucose uptake may occur decades before onset cognitive dysfunction tissue damage. There have been few systematic studies the metabolite content AD human brain, possibly due to scarcity high-quality brain and/or lack reliable experimental...

10.1016/j.bbadis.2016.03.001 article EN cc-by Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 2016-03-06

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG expansion in the gene-encoding Huntingtin (HTT). Transcriptome dysregulation major feature of HD pathogenesis, as revealed large body work on gene expression profiling tissues from human patients and mouse models. These studies were primarily focused transcriptional changes affecting steady-state overall levels using microarray based approaches. A missing component, however, has been study...

10.1093/hmg/ddw187 article EN Human Molecular Genetics 2016-07-04

Widespread brain-copper deficiency in patients with Alzheimer's dementia (red) compared to controls (blue).

10.1039/c7mt00074j article EN cc-by Metallomics 2017-01-01

Significance We present evidence for the presymptomatic dysregulation of urea metabolism in Huntington’s disease (HD). identified increased levels a transporter transcript and other osmotic regulators striatum our prodromal sheep model HD concomitant increase striatal cerebellar urea. Elevated was also detected brain tissue from postmortem cases, including cases with low-level cell loss, implying that is not just product end-stage cachexia. Disruption known to cause neurologic impairment...

10.1073/pnas.1711243115 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2017-12-11
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