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Printable Handouts
Navigable Slide Index
- Introduction
- The curse of neurological disease
- Neuroglial nature of brain defence
- Disease as a homeostatic failure
- The importance of glial pathology
- Section 1: General astrogliopathology
- Astrogliopathology
- Section 2: Reactive astrogliosis
- Reactive astrogliosis (1)
- Reactive astrogliosis (2)
- Signalling profile of reactive astrocytes
- Reactive astrocyte morphology
- Section 3: Pathological remodelling of astrocytes
- Alexander disease
- Hepatic encephalopathy: A primary astrogliopathy
- Section 4: The new concept: Astroglial atrophy in neurological diseases
- Astrocytopathy in psychiatric diseases
- Chronic stress, anhedonia and astrocytes: Experimental design
- Chronic stress and GFAP+ astroglia density
- Gliotoxin triggers depressive-like behaviour
- Cytoskeletal atrophy in major depression
- Atrophic astrocytes in schizophrenia
- Astroglial atrophy in cocaine addictive rats
- Astroglial atrophy in epileptic rats
- Astroglial atrophy in Parkinson’s disease
- Section 5: Astrocytes in the ageing brain
- Age and cognitive decline
- Ageing of astrocytes: GFAP
- Ageing of astrocytes: s100β
- Ageing of astrocytes: Glutamine synthetase
- Morphological analysis of murine astrocytes
- Age-dependent decrease in the volume of peripheral astrocytic processes
- Section 6: Astrocyte atrophy in Alzheimer’s disease
- History of Alzheimer’s disease
- Dramatic rise in cases of dementia over around 150 years (1)
- Dramatic rise in cases of dementia over around 150 years (2)
- Neurodegeneration: Neuron-centric view
- Alois Alzheimer's drawing of reactive glia associated with damaged neurones
- Alois Alzheimer's drawing of senile plaque containing reactive glia
- Animal models of AD
- Translation of animal models of AD
- Hippocampus in AD: Astroglial atrophy complements astrogliosis
- Astroglial atrophy in neuropathology
- Section 7: Atrophic AD astrocytes fail to support BBB integrity
- AD astrocytes and the BBB
- Section 8: Atrophic astrocytes fail to mount reactive astrogliotic response in AD-susceptible brain regions
- Astrogliosis in AD
- Progression of astrogliodegeneration in AD
- Astrogliotic defence and neuronal damage
- Neuroglial hypothesis of neurodegeneration
- Section 9: Astroglial atrophy in human pathology
- The glial mythology: The numbers
- The glial mythology
- Mammalian astrocytes
- Primate-specific glial cells
- Severe atrophy of interlaminar astrocytes in AD
- Astrocyte reactivity peaks at Braak stages III - IV
- Astrocytic atrophy in familial AD
- Failed astrogliosis in severe AD
- Human astrocytes derived from stem cells
- Atrophic human astrocytes in AD
- Section 10: Life style changes: Diet - caloric restriction
- Caloric restriction increases astrocytic leaflets
- Caloric restriction and hippocampal synapses
- Section 10: Life style changes: Environmental stimulation
- Environmental stimulation rescues astrocyte atrophy
- Enriched environment stimulates neurogenesis
- Conclusions
- Mental decline is not inevitable in old age
- Thank you
Topics Covered
- General astrogliopathology
- Astrocytes are the main homeostatic cells of the brain
- Astrocytes are involved in all brain pathologies
- Glial cells and reactive astrogliosis
- Pathological remodelling of astrocytes
- Astroglial atrophy in neurological diseases
- Astrocyte atrophy and loss of capabilities in Alzheimer’s disease
- Astroglial atrophy is associated with psychiatric diseases and neurodegeneration
- Atrophic AD astrocytes fail to support BBB integrity
- Atrophic AD astrocytes fail to mount reactive astrogliotic response
- Lifestyle changes and astrocyte rescue
Links
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Talk Citation
Verkhratsky, A. (2022, March 31). Principles of astrogliopathology: from reactivity to atrophy and degeneration [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 12, 2024, from https://doi.org/10.69645/GSHI7851.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Alexei Verkhratsky has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Neurology
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Alexei Verkhratsky.
I'm a Professor of Neurophysiology
at Manchester University in the UK.
I do mostly physiology and
pathophysiology of neural glial cells.
My lecture today is dedicated to the
principles of astrogliopathology,
which will cover all
the different phases
of pathological changes in
astrocytes and astroglia
from reactivity to
degeneration and atrophy.
0:29
Unfortunately, I
have to start with
a rather unpleasant statement.
There are about 600 neurological
diseases in this world.
Despite the incredible progress of medicine
that has been achieved in the last century,
we now can change joints
and livers and hearts.
Where we are in terms of
neurological diseases,
this remains still at the level of the late
19th and beginning of the 20th century.
We can alleviate
certain symptoms,
but we cannot cure a single
neurological disease,
particularly when it comes to
chronic diseases of the brain,
such as psychiatric diseases
or neurodegenerative diseases.
Of course, the clear reason for that is that
the brain is an incredibly complex organ,
and we don't even know what happens
in the human brain and physiology
nor say what is going to happen
in pathological conditions.
But also there is
one important thing,
over the last century,
the major target of our therapeutic
strategies were neurons.
At the same time, glial cells,
which are going to be the
focus of these lectures,
have been rather neglected,
despite the fact that they participate
in all neurological diseases.
1:38
Evolution has made a
specialization between the cells.
There is diversification
of functions.
Of course, neurons are perfected for information
processing and sending action potentials.
Neuroglial cells are perfected
for keeping homeostasis.
However, when pathology comes
and a lesion appears
and injures the brain,
the response of those cells to the
lesion are fundamentally different.
Neurons become stressed,
they cannot protect themselves,
and they cannot protect
the brain as an organ.
Glial cells, in contrast,
are changing dramatically
as they undergo
substantial morphological
and functional changes,
which allow them to
protect the brain
and to protect the
nervous tissue.
As long as this
protection is there,
the disease cannot
develop at the moment.
If the protection of
glial cells fail,
then neurological
disease begins evolving.
If we define a disease
as a homeostatic failure
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