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Physiology of Aging - Lecture 6
Terms in this set (95)
Changes in the Nervous System
Early 20th Century view on neurologicla aging: there are progressive structural, biochemical, and functional losses that lead to dementia;
Today's view: it is believed that it is quite possible for humans to age successfully so that compensatory, adaptive, and learning capabilities are maintained at all ages
Three functional categories of the nervous system:
(3) Central Nervous System (CNS)
peripheral nervous system
includes the sensory systems and motor control; how you feel sensations in your skin, abdomen, and limbs
Autonomic Nervous System
controls ital functions like the cardiovascular and respiratory systems. also controls the fight or flight responses, and much of these responses are unconscious.
autonomic nervous system is found primarily in the..
the nervous system has:
plasticity - it can be shaped, formed, or influenced by external and internal stimuli --> brain can recovver from damage; the way our brain is wired is not set, it is constantly being changed
plasticity is achieved by..
sprouting new dendrites, axons, or synapses, or by altering neurotransmitter release or response to neurotransmitter
plasticity and aging
plasticity is decreased in the aging brain, but not entirely lost
Cell types in the Nervous system:
Typical Structure of a neuron
contains a cell body with a nucleus, dendrites that have receptors for neurotransmitters, and axons that have terminals that release neurontransmitters.
receptors for neurotransmitters are stimulated by..
neurotransmitters released by nearby neurons
polarization of neurons
neurons can be either depolarized of hyperpolarized by neurotransmitters.
depolarization can lead to...
an action potential that travels down the axon and causes subsequent neurotransmitter release fro the nerve terminals
some axons are myelinated. this promotes faster transmission of the electrical signal down along the axon.
4 main types of neuroglia
(3) Ependymal cells
neuroglia vs. neurons in CNS
there are more of these than neurons in the central nervous system.
primary role of neurglia
to support neurons; the different types of neuroglia have different supporting roles
type of neuroglial cells that have end-feet that surround and support blood vessels and neurons. they are involved in neuron metabolism and transmission, and stimulate formation of the blood-brain barrier
neuroglial cells that are involved in myelin formation; myelin increases the rate of transmission of depolarization
neuroglial cells that line the cerebral ventricles (compartments of the brain) and spinal cord canal
neuroglial cells that have immune function; this includes phagocytosis and inflammatory responses; the immune cells of the brain!
these are the smallest blood vessels; they are composed of a single layer of endothelial cells
capillaries of the CNS
are found in the brain; they are enveloped by the end-feet of astrocytes
blood brain barrier
formed by the capillaries of the CNS, which have tight junctions between endothelial cells that prevent the diffusion of substances into the brain from the blood, or diffusion of neurotransmitters into the blood.
How is the transportation of small molecules across the blood brain barrier achieved?
by highly regulated transporters in the membranes of endothelial cells. These capillaries that form the barrier are specific to the brain, so only certain types of molecules are allowed to diffuse through it.
Structural Changes that occur in the Brain with Aging:
(1) Brain weight
(2) Neural cell number
(3) Dendritic and Synaptic loss
(4) Neural cell pathological markers
Brain Weight and Aging
Brain size, volume, and metabolism does not differ significantly between the young and old; there can be about a 6-11 percent decrease in brain volume in some healthy individuals, but brain volume
brain weight and alzheimers
some patients with alzheimer's dementia have a significant decrease in brain weight, because it kills neurons
the brain and redundency
we have more neurons that are needed, therefore we can lose about 40 percent before there are profound changes in function.
Neural cell number
there are 10^12 neurons in the adult brain, and 10^13 glial cells
How many connections does each neuron have?
Each neuron has about 10,000 connections to other neurons. This is what creates the complexity of the brain
the total number of connections in the CNS are:
neurons increase connections to compensate for neuron loss
neurons and aging
total neurons see only a little loss in their number of neurons with aging; overall, loss of neurons is typically low in all areas of the CNS compared to the redundancy of neuron function
Neurons in healthy elderly (no functional loss):
neuron loss in healthy older people is limited to descrete areas with considerable vulnerability
Particular areas of the brain where neuron loss can occur:
(1) locus ceruleus
(2) substantia nigra
(3) nucleus basalis of Meynert
consists of catecholaminergic neurons, which release norepinephrine, in the brain stem. This region is involved in reactions to stress and panic --> flight or flight
consists of dopaminergic neurons, which release dopamine; located in the mid-brain; involved in voluntary movement and mood, and therefore this region can see a severe loss in weight/volume with Parkiinson's disease
nucleus basalis of Meynert
made up of cholinergic neurons (release acetylcholine); located in the forebrain with connections to neocortex; involved in memory and learning; there can be a severe loss in volume with alzheimer's disease
made up of cholinergic neurons; located in the temporal lobe of the brain, in the cerebrum (middle area); involved in memory, learning, and emotion (part of the limbic system); can see severe loss of the hippocampus with Alzheimer's disease, and this loss can also be seen in the frontal cortex
the number of glial cells increase with aging in most areas; this process might be a compensatory response to slight neuron loss; it is a normal response to neuron damage experienced at all ages
Dendritic and Synaptic loss with normal aging
dendrite loss is minimal or absent with continued environmental stimulation. There also may be increase in dendrites to compensate for neuron loss. They preserve these with more stimulation
Dendritic and Synaptic loss with dementias
when dementia is present, dendrite loss can be severe and progressive, leading to cell death
axonal sprouting that increases connections of a single neuron with other neurons. This is a normal compensatory response to neuron damage or loss, and therefore occurs with aging.
aging and the complexity of cell processes
with aging, there can be a decrease in the complexity of cell processes and a decrease in plasticity and dynamics of the brain
Other changes that can Contribute to disruption of neural circuitry:
(1) decrease in vascular responsibeness
(2) metabolic alterations
(3) changes in axons
(4) changes in neuron cytoskeleton
(5) accumulation of amyloid protein
(6) impaired cell survival
(7) alterations in cerebral spinal fluid composition and/or volume
decrease in vascular responsiveness
this can lead to inadequate matching of blood supply with neuronal requirements and can be involved in strokes
changes in axons
changes nclude loss of myelin, axon swelling, changes in neurofilaments and neurotubules
example of changes in neuron cytoskeleton
formation of neurofibrillary tangles
accumulation of amyloid proteins
forms neuritic plaques
impaired cell survivval may be due to
a decrease in antiapoptotic proteins
Neural cell pathological markers are
abnormal deposits in the brain
major cell alterations
these can occur with certain diseases and are manifested by:
(1) intracellular accumulation of abnormal inclusion
(2) accumulation of abnormal extracelllar proteins in neuritic plaques and surrounding blood vessels
deposits of some sort (accumulation)
examples of intracellular accumulations of abnormal inclusions:
lipofuscin, melanin, lewy bodies, neurofibrillary and amyloid proteins; these can alter depolarization
gather into blobs outside of neurons
Types of Inclusions:
(1) Lipofuscin and Melanin
(2) Lewy and hirano bodies
(3) Neurofibrillary tangles and neuritic plaques
fluorescent deposits that are composed of protein and oxidized lipid
lipfuscin accumulates in..
the cytoplasm or nucleus in most cells of the CNS with aging.
order of regions of brain in which lipofuscin accumulates:
(1) hippocampus --> cerebellum --> anterior horn of spinal cord --> other areas of the brain
pigment located in the locus ceruleus and substantia nigrea
melanin and aging
melanin increases in cells of the locus ceruleus and substantia nigra until about age 60. After this point it decreases, probably as a result of cell loss
accumulation of lipofuscin and melanin with aging
the accumulation of these two is not greater with dementia; the functional significance of their accumulations is unknown
Lewy and Hirano bodies
are thought to be markers of malfunctioning neurons; they are granular cytoplasmic inclusions due to differential expression of proteins, and they may be responsible for selective neuronal vulnerability
shape of lewy bodies
spheroid in shape
frequency of lewy bodies
lewy bodies are present, but relatively scarce in the elderly (60+) that have no neurological disease
parkinson's disease and lewy bodies
they are numerous in patients with parkinson's and other dementias. In these people lewy bodies can be found in dopaminergic neurons of hte locus ceruleus, substantia nigra, and sometimes at the cerebral cortex
structure of hirano bodies
spindle-shaped and fusiform.
presence of hirano bodies is related to....
aging; they are numerous with Alzheimer's and other forms of dementia; are predominantly found in the hippocampus
intracellular masses of fibrous proteins that are often flame-shaped bundles
neurofibrillary tangles and aging
these are present in the normal aging brain, especially in the hippocampus; wih Alzheimer's and other dementias, they accumulate in the cortex and other areas of the brain; accumulation is correlated to the severity of the dementia
neurofibrillary tangles are composed of:
(1) paired helical filaments (PHF)
(2) precise protein composition is unknown
(3) includes cytoskeletal proteins, like microtubular proteins
(4) hyperphosphorylated tau proteins are implicated in PHF formation
microtubular proteins; these increase with aging
extracellular proteinaceous fibrillar deposits with a central core of amyloid
insoluble and resistant to enzymatic degradation; surrounded by coarse fibers
neuritic plaques and normal aging
these are at low levels in normal aging
neuritic plaques and alzheimer's disease
they are abundant in the frontal, temporal, and occipital cortex, as well as the hippocampus.
glial cells, microglial cells, and neuritic plaques
glial and microglial cells accumulate around the plaques
theories on the formation of neuritic plaques:
(1) abnormal neural proceses lead to the deposition of amyloid, which stimulates glial proliferation
(2) amyloid leaks from brain capillaries (protein in the blood) and then diffuse into brain tissues. accumulation leads to neuron destruction then glial cell proliferation, causing plaque formation
abnormal protein accumulattion actiates:
"ubiquitin-dependent degradation system"
ubiquitin and normal aging
ubiquitin is low in normal aging
ubiquitin and dementia
ubiquitin accumulates in Alzheimer's and Parkinson's.
the global deterioration of intellectual and cognitive function, characterized by defects in all 5 major mental functions, though there is persistence of clear consciousness
5 major mental functions:
(3) intellect (the ability to rationalize things)
(5) Affect (the experience of feeling, emotion; personality)
Can dementia be reversed?
dementia can be reversible or irreversible, it varies/depends
Underlying causes of dementia:
(2) Emotional disorders
(3) Metabolic or endocrine disorders
(4) Eye and ear dysfunctions
(5) Nutritional deficiencies
(6) tumor or trauma
(8) Atherosclerosis (myocardial infaction, stroke, heart failure)
Causes/Types of Dementia in Elderly and their frequency:
50 - 60% Alzheimer's Disease; 20 - 30% Multiple Infact Dementia; 10 - 20% Reversible Dementias; 1 - 5% Other forms of dementia
Quantitative differences between normal and pathological aging
neurofibirillary tangles and neuritic plaques are present but in low numbers in normal, healthy elderly. These two are wide-spread and abundant in Alzheimer's, however.
Diagnosing Alzheimer's disease
Alzheimer's can only be definitively diagnosed at autopsy. Because of this, other cognitive impairments and dementias must first be ruled out before a diagnosis is made.
Brain characteristics of Alzheimer's disease:
(1) brain atrophy
(2) loss of cholinergic neurons in the nucleus of Meynert, hippocampus, and association cortex
(3) loss of adrenergic neurons in the locus ceruleus
(4) abnormal neural actiity, which may include hperactivity in some regions of the brain
(5) denudation of neurons, stripping of dendrites, damage to axons
(6) increased microglia
(7) the accumulation of lipofuscin, hirano and lewy bodies, altered tau protein (it becomes hyperphosphorylated), and an increase in ubiquitin
(8) an accumulation of neurofibrillary tangles and neuritic plaques with amyloid-beta
(9) perivascular amyloid is found throughout the brain, especially in the frontal and prefrontal lobes, hippocampus, and association cortices, decreasing the blood brain barrier
(10) more neuron damage, due to increased levels of oxidative stress
involves the profound shrinking of the brain, due to loss of brain mass and neurons
is a type of immune response; an increased number of microglial cells leads to immune cells from other parts of the body getting past the blood brain barrier, which exacerbates the disease
What causes Alzheimer's disease?
(1) neuron dysfunction --> immune response inceases oxidative stress, which decreases the blood brain barrier, causing neuron death.
(2) decreased blood brain barrier leads to neuron dysfunction, which causes an immune response, ultimately bringing about neuron death; this is a viable model in APOE4
Pathogenesis of Alzheimer's
this is currently unknown. But there are many known factors associated with it
factors associated with alzheimer's:
(1) free-radical accumulation
(2) prions (viral particles) --> induce the formation of amyloid plaque, which leads to the loss of cholinergic nerves
(3) the immune response may aggravate neural damage by causing inflammation
(4) decreased oxidative metabolism and slower enzyme activity
(5) impaired homeostasis of toxic metals like iron, zinc, and aluminum
(6) insulin resistance in the brain
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