Tract tracing, neuronal morphology and ultrastructural studies in human postmortem brain

Author(s):  
Rosalinda C. Roberts ◽  
Michael W. Vogel ◽  
Maarten de Rijk ◽  
Frank J. Peretti ◽  
Robert R. Conley ◽  
...  

Classical and modern neuroanatomical techniques are applied to an analysis of the neuroanatomical basis of schizophrenia using postmortem brain tissue from the Maryland Brain Collection. Techniques for Golgi staining of cell bodies and dendritic arbors, axonal tract tracing with the carbocyanine dye, DiI and ultrastructural analyses will be used to study brain tissue with postmortem times of less than 6 hours. Although these techniques are routinely used in animal models, they are rarely used for studying human brain tissue. These techniques will allow us to characterize neuronal architecture in normal and diseased brains.

2002 ◽  
Vol 16 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Ronald W. H. Verwer ◽  
Wim T. J. M. C. Hermens ◽  
Paul A. Dijkhuizen ◽  
Olivier Ter Brake ◽  
Robert E. Baker ◽  
...  

Author(s):  
Matthew P. Anderson ◽  
Reade Quinton ◽  
Karen Kelly ◽  
Andrew Falzon ◽  
Alycia Halladay ◽  
...  

Context.— Autism spectrum disorder is a neurodevelopmental condition that affects over 1% of the population worldwide. Developing effective preventions and treatments for autism will depend on understanding the neuropathology of the disorder. While evidence from magnetic resonance imaging indicates altered development of the autistic brain, it lacks the resolution needed to identify the cellular and molecular underpinnings of the disorder. Postmortem studies of human brain tissue currently represent the only viable option to pursuing these critical studies. Historically, the availability of autism brain tissue has been extremely limited. Objective.— To overcome this limitation, Autism BrainNet, funded by the Simons Foundation, was formed as a network of brain collection sites that work in a coordinated fashion to develop a library of human postmortem brain tissues for distribution to researchers worldwide. Autism BrainNet has collection sites (or Nodes) in California, Texas, and Massachusetts; affiliated, international Nodes are located in Oxford, England and Montreal, Quebec, Canada. Data Sources.— Pubmed, Autism BrainNet. Conclusions.— Because the death of autistic individuals is often because of an accident, drowning, suicide, or sudden unexpected death in epilepsy, they often are seen in a Medical Examiner's or Coroner's office. Yet, autism is rarely considered when evaluating the cause of death. Advances in our understanding of chronic traumatic encephalopathy have occurred because medical examiners and neuropathologists questioned whether a pathologic change might exist in individuals who played contact sports and later developed severe behavioral problems. This article highlights the potential for equally significant breakthroughs in autism arising from the proactive efforts of medical examiners, pathologists, and coroners in partnership with Autism BrainNet.


2021 ◽  
Vol 13 (595) ◽  
pp. eaba7394
Author(s):  
Ari W. Schaler ◽  
Avery M. Runyan ◽  
Catherine L. Clelland ◽  
Eric J. Sydney ◽  
Stephanie L. Fowler ◽  
...  

Accumulation of pathological tau in synapses has been identified as an early event in Alzheimer’s disease (AD) and correlates with cognitive decline in patients with AD. Tau is a cytosolic axonal protein, but under disease conditions, tau accumulates in postsynaptic compartments and presynaptic terminals, due to missorting within neurons, transsynaptic transfer between neurons, or a failure of clearance pathways. Using subcellular fractionation of brain tissue from rTg4510 tau transgenic mice with tauopathy and human postmortem brain tissue from patients with AD, we found accumulation of seed-competent tau predominantly in postsynaptic compartments. Tau-mediated toxicity in postsynaptic compartments was exacerbated by impaired proteasome activity detected by measuring lysine-48 polyubiquitination of proteins targeted for proteasomal degradation. To combat the accumulation of tau and proteasome impairment in the postsynaptic compartments of rTg4510 mouse brain, we stimulated the pituitary adenylate cyclase–activating polypeptide (PACAP) type 1 receptor (PAC1R) with its ligand PACAP administered intracerebroventricularly to rTg4510 mice. We observed enhanced synaptic proteasome activity and reduced total tau in postsynaptic compartments in mouse brain after PACAP treatment. The clearance of tau from postsynaptic compartments correlated with attenuated tauopathy and improved cognitive performance of rTg4510 transgenic mice on two behavioral tests. These results suggest that activating PAC1R could prevent accumulation of aggregate-prone tau and indicate a potential therapeutic approach for AD and other tauopathies.


2009 ◽  
Vol 110 (5) ◽  
pp. 1400-1408 ◽  
Author(s):  
Edna Grünblatt ◽  
Camelia Maria Monoranu ◽  
Manuela Apfelbacher ◽  
Daniela Keller ◽  
Tanja M. Michel ◽  
...  

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