Module 4 Flashcards

1
Q

Functions of the Nervous System

A
  • The nervous system is the body’s main communication system, coordinating and controlling body functions.

Key responsibilities:
- Motor responses
- Interpreting sensory info (touch, taste, smell, sound)
- Maintaining internal balance (breathing, heart rate)
- Emotion, learning, memory, and higher thinking (planning, problem-solving, empathy)

  • Neuroscience is a rapidly growing field focused on understanding and treating nervous system disorders.
  • There is a complex connection between nervous system disorders and mental health, involving many underlying mechanisms.
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2
Q

Central Nervous System (CNS)

A

consists of brain and spinal cord

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3
Q

Peripheral Nervous System (PNS)

A
  • The Peripheral Nervous System (PNS) includes all nerve tissue outside the CNS.

Made up of:
- Motor nerves – control muscles (e.g., skeletal muscle movement)
- Sensory nerves – carry info like touch, temperature, and pain to the CNS

  • The CNS and PNS work both independently and together to control many body functions.
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4
Q

Nerve or neuron

A

basic unit of nervous system that communicates with one another in order to transmit important info between the CNS and PNS

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5
Q

Glial cells

A
  • help neurons communicate with each other
  • Regulate environment around the neurons, maintain the position of neurons and help repair the neurons if they become damaged
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6
Q

Cell body

A

contains nucleus, mitochondria and other organelles

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7
Q

Dendrites

A

protrusions of membrane. Act as connections for receiving incoming signals. Some neurons may have dendrites, while some might not have any at all

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8
Q

Axon

A

extension from the cell body transmits outgoing signals away from the cell body

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9
Q

Myelin Sheath

A
  • fatty coating
  • Acts as insulation for neuronal signals, increasing the speed of signal transmission along the axon
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10
Q

Axon terminals

A
  • signals travel down the neuron and eventually reach this terminal.
  • Signal is transmitted to adjacent neurons
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11
Q

Nerve impulses

A
  • signals transmitted through neurons
  • Transmission of these signals is an electrochemical process consisting of both electrical and chemical events.
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12
Q

Four steps of signalling

A

1) reception
2) action potential
3) synapse
4) Transmission

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13
Q

step 2 of signalling: action potential

A

dendritic stimulation generates an electrical signal known as an action potential. Signal propagates from the dendrites through the cell body, down the axon

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13
Q

step 1 of signalling: reception

A
  • signal beginning from outside the neuron is received at its dendrites
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13
Q

step 3 of signalling: synapse

A
  • When an electrical signal reaches the axon terminals, it triggers the release of neurotransmitters.
  • These chemicals travel into the space between neurons.
  • Dendrites of the next neuron receive the signal.
  • The synapse is the space where this happens — includes the axon terminal of one neuron and the dendrites of the next.
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14
Q

step 4 of signalling: Transmission

A

neurotransmitters trigger an action potential in the adjacent cell and this process repeated itself across many neuron cells until the signal reaches its final destination and fulfills its purpose

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14
Q

Neurotransmission in depth

A
  • Neuronal signaling is tightly controlled.
  • At rest, neurotransmitters are stored in vesicles in the axon terminal.
  • When an action potential arrives, neurotransmitters are released into the space between neurons.
  • They bind to receptors on the next neuron, starting a new signal.

After signaling:
- Neurotransmitters unbind
- Vesicles are recycled
- Both neurons reset to resting state, ready for the next signal.

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14
Q

Glial Cells

A

Facilitate function of neurons in various ways

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14
Q

Role of Myelin in Action Potential Transmission

A
  • An action potential is an electrical signal that travels down the axon to the axon terminal.
  • This signal moves at a relatively slow speed without help.
  • The myelin sheath (a fatty layer around the axon) helps the signal travel much faster.
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15
Q

Schwann Cells

A
  • Support and insulate neurons in the Peripheral Nervous System (PNS).
  • Help form and maintain the myelin sheath around axons.
  • Myelin starts forming before birth and speeds up in infancy.
  • Schwann cells wrap around the axon in a spiral, covering its entire length.
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15
Q

Oligodendrocytes

A
  • glial cells that produce and maintain myelin sheaths around axons in the CNS.
  • Each oligodendrocyte typically myelinates multiple adjacent axons
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16
Q

Microglial cells

A
  • act as the resident immune system in the brain
  • Responsible for multiple functions including clearing damaged neurons, pruning synapses in development, and removing cellular debris, to keep the brain health
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17
Q

Astrocytes

A
  • star-like appearance.
  • Cell bodies give rise to multiple processes that come into contact with both neurons and the brain’s blood supply.
  • Perform a variety of functions including growth factors and nutrients to neurons and maintain the cells that make up the blood brain barrier and help tissue repair.
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18
Q

Supporting Cells of the Nervous System

A
  • Glial cell problems (not just neurons) are linked to many nervous system diseases.
  • This shows how important glial cells are for brain health.
  • A 2009 study found the brain has a 1:1 ratio of neurons to glial cells — showing their equal importance.
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19
Mental Health
- Mental health is the state of psychological and emotional well-being. - It's important for overall health and a healthy life. - Poor mental health can lead to both mental and physical illness. Treating mental health issues can be complex and may involve: - Therapy - Wellness strategies - Medications
20
what is the nervous system responsible for?
- Memory, encoding, and recall - Complex emotions - Decision-making - Spatial navigation - Fight-or-flight and rest-and-digest responses
21
Mental Illness
- Mental illness is a diagnosable and treatable condition, like diabetes or heart disease. - Unlike neurodegenerative diseases, it usually does not involve brain structure damage. It involves a long-term reduced ability to function, often due to: - Stress - Changes in thinking, mood, or behavior - Possible causes: isolation, loneliness, sadness Examples include: - Anxiety - Depression - Eating disorders - Schizophrenia
22
Mental Health Supports
- Stress, anxiety, low mood, and depression can affect daily life, including academic performance. - IDIS199 covers these mental health topics. - Although this section focuses on neurodegenerative diseases, many discussed risk factors also affect mental health.
23
Determinants of Mental Health
- ACE Score (Adverse Childhood Experiences) is an emerging tool using a questionnaire to assess negative experiences in the first 18 years of life. - A higher ACE score is linked to a greater risk of physical, mental, and social problems in adulthood. Early adverse exposures can: - Disrupt brain development - Affect social development - Compromise the immune system
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Adverse Childhood Experiences
Adverse Childhood Experiences (ACEs) include traumatic events before age 18 such as: - Neglect - Physical and mental abuse - Unstable home environments - ACEs negatively impact overall health later in life As ACE score increases, so does: - The risk of various diseases - The prevalence of other risk factors
25
How ACE scores are a tool to lead to Resilience
- ACE scores help guide interventions and treatments for individuals and families. If parents have high ACE scores, practitioners can: - Provide support for them - Help break the cycle of intergenerational abuse, neglect, and dysfunction - ACE scores also help identify at-risk children and allow for early intervention to build resilience. The ACE questionnaire gives practitioners key background info to: - Address individual needs - Improve mental health - Support resilience development Resilience factors include: - Developing positive coping strategies - Asking for help - Building healthy, trusting relationships These can reduce or reverse the negative impacts of ACEs and improve long-term health outcomes.
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Strategies to help prevent ACEs and promote resilience
- individual factors - family and relational factors - community factors
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Strategies to help prevent ACEs and promote resilience: Individual factors
- Strong cultural identity - Self-regulation: ability to control actions, behaviours, and emotional responses - Sense of meaning and or purpose - Effective coping skills: ability to react appropriately to adverse experiences - Problem solving skills
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Strategies to help prevent ACEs and promote resilience: family and relational factors
- Stable and supportive relationships - Adequate housing and income - Stimulating home environment - Role modelling - Connection to positive social network
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Strategies to help prevent ACEs and promote resilience: community factors
- Safe and connected communities - Access to service - Mentorship - Positive relationships with peers - Access to extracurricular activities - Positive school environments - Quality child care
30
Alzheimer's Disease
affects the hippocampus and cerebral cortex
31
Parkinsons and Huntingtons Disease
two distinct disorders that both affect the neurons in the basal ganglia
32
Spinocerebellar Ataxias
group of neurological disorders preferentially affecting the spinal cord and/or cerebellum, resulting in impairment of balance and coordination of movement called ‘ataxia’
33
Charcot Marie Tooth:
Umbrella definition for several genetic disorders affect the peripheral nervous system (PNS)
34
Neurodegenerative Diseases and age
- Increasing age is a major risk factor for neurodegenerative diseases. As we age, mitochondrial metabolism becomes defective, leading to: - Increased production of reactive oxygen species (ROS) - Cell injury - Cell death
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Neurodegenerative Diseases and protein Misfolding
Abnormal protein folding and subsequent clumping known as aggregation play a key pathogenic role in many neurodegenerative diseases
36
Neurodegenerative Diseases and synaptic dysfunction
- disturbance in the structure or function of the synapse. (site where neural impulses are transmitted between neighbouring neurons) - Important early event in many neurodegenerative diseases
37
Neurodegenerative Diseases and neuronal cell death
Neurons in the most affects region of the nervous system eventually die, and this is the hallmark of many neurodegenerative disorders
38
Dementia
- Dementia is a general term describing a decline in cognitive function that interferes with daily living. It may involve: - Memory loss - Impaired thinking and reasoning - Decline in complex motor skills - Caused by neurodegeneration in the brain. - Dementia is not a diagnosis itself—it doesn’t specify the cause. Most common causes include: - Alzheimer’s disease (most common) - Lewy body dementia (third most common) - Currently incurable, but some treatments can slow symptom progression.
39
what is the biggest factor for dementia
increasing age
40
health factors for dementia
Genetics, diabetes, high blood pressure, unhealthy cholesterol levels
41
lifestyle/dietary factors for dementia
smoking, physical inactivity, obesity, drug and alcohol abuse, poor access to good diet
42
mental health factors for mental health
PTSD, depression, schizophrenia
43
Burden of Dementia on Indigenous Communities
- Indigenous populations in Canada and globally have been found to experience higher rates of dementia. - Age of onset for dementia in some Indigenous communities can be up to 10 years earlier than in the general population. - Late diagnoses are common, meaning individuals and their families may miss out on early support and care options. In response, health equity initiatives have been started to: - Address social and structural factors contributing to the increased risk - Promote early diagnosis - Provide culturally appropriate care and support services
44
How is dementia perceived in many Indigenous cultures?
Dementia is often viewed as a natural part of aging rather than a disease. Terms like “mind changes” or “second childhood” reflect a gentle, spiritual understanding—seen as becoming “closer to the Creator.”
45
Why is early diagnosis of dementia less common in Indigenous communities?
Cultural perceptions of dementia as normal aging delay recognition and access to health services. There may also be no direct word for "dementia" in some Indigenous languages.
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Why is culturally safe care important for dementia in Indigenous communities?
It respects Indigenous worldviews, helps families recognize serious cognitive decline, and encourages early support and diagnosis.
47
I-CAARE
- The Indigenous Cognition and Aging Awareness Research Exchange - a network of experts from communities, universities, and governments who advocate for issues related to Alzheimer's disease, dementia, and healthy aging in Indigenous Peoples.
48
medicine wheel for dementia: North (spiritual health)
- Attend ceremonies and use medicines for wellness - Use prayer for strength and comfort - Maintain health holistically - Attend ceremony or church - Express gratitude
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medicine wheel for dementia:east (physical health)
- Eat healthy, unprocessed food - Prevent head injuries - Exercise - Don't misuse alc or drugs - Stay away from contaminants when gathering food or medicine - Grow and/or gather your own food
50
medicine wheel for dementia: south (mental health)
- Laugh, sing, dance - Read - Seek therapy and/or advice from elders - Stay connected to community and loved ones - Be responsible and accountable for choices in life - Practice kindness
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medicine wheel for dementia: west (emotional health)
- Speak, learn and listen to original languages - Participate in storytelling and singing - Craft,bead, knit crochet or sew - Learn and remember protocols for ceremony - Carry and share songs, teachings or ceremonies - Do puzzles or crosswords - Be aware of aging and dementia - use the internet
52
Pearls case study
- 73 yo woman in good health - family notices some memory lapses - Struggles to find right name of an object, can't remember people's names - Son books a check up for her at family clinic behaviours noticed: - No longer interested in the news or family updates - Neighbours and friends dont really hear from her - Not taking meds on time or refilling scripts - Forgetting conversations and other basic tasks - Does care about her garden, though she was once a big gardener nurse determines she has dementia and meets criteria for Alzheimers
53
Alzheimer's Disease
- Progressive neurodegenerative disease - Most common cause of dementia (50–70% of cases) - Typical lifespan post-diagnosis: 4–8 years, some live up to 20 years - Named after Dr. Alois Alzheimer (German psychiatrist) --First reported in 1907 with the case of Auguste Deter, a 55-year-old woman -- Died from progressive cognitive and behavioral decline
54
Burden of AD in Canada overall
- Over 747,000 canadians are living with some form of dementia - At least 44 million people are living with the disease making it a global health crisis
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Burden of AD in Canada gen pop
- 1 in 20 Canadians over 65 have AD - 1 in 4 Canadians over 85 have AD - AD cases expected to double by 2030 and triple by 2050 - Increased burden on healthcare system - AD is a public health care priority
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Burden of AD in Canada indigenous pop
- Limited epidemiological research on AD in Indigenous communities in Canada - Most studies focus on First Nations; no studies on Inuit or Métis - No validated cognitive screening tool sensitive to First Nations or Inuit culture - Lack of consideration for broader social determinants of health - Projected 4-fold increase in AD rates in First Nations populations (2006-2031) - Projected 2-fold increase in AD rates in non-First Nations by 2030
57
Risk Factors for AD: genetics
Around 1% of AD cases are caused by inherited mutations affecting amyloid-beta processing Other mutations can increase the risk of developing the more common sporadic form of AD
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Risk Factors for AD: sex
- Incidence of AD in women is up to twice that of men - Hormones and lifestyle factors may play a role in this difference
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Risk Factors for AD: lifestyle
- Diabetes - Obesity - Depression - Smoking - Low educational attainment
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Microscopic Changes Associated with AD: Tau Oligomers and Neurofibrillary Tangles
- Tau binds to microtubules, stabilizing them for cargo transport (e.g., vesicles, mitochondria). - In AD, tau misfolds, weakens microtubule binding → microtubules disassemble → disrupted neurotransmission. - Misfolded tau forms toxic oligomers and neurofibrillary tangles inside neurons. - Misfolded tau can spread between neurons, causing further tau misfolding across the brain.
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Microscopic Changes Associated with AD: Amyloid- β Oligomers and Plaques
- Amyloid Beta (Aβ): Small protein fragment formed from amyloid precursor protein (APP), found in neuron membranes. - In AD, Aβ form that easily aggregates is cleaved from APP. Aβ Aggregation: - Synaptic disruption: Aβ oligomers accumulate at synapses, impairing function. - Outside the neuron, Aβ oligomers aggregate into larger structures (plaques)
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Microscopic Changes Associated with AD: Aβ plaques
- Plaques: Aβ aggregates form plaques that activate microglia. --Microglia release inflammatory mediators, causing neuronal injury. Cerebral Amyloid Angiopathy (CAA): - Aβ can damage blood vessel walls in the brain. - CAA contributes to dementia and increases the risk of stroke.
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Amyloid Cascade Hypothesis
- proposes that accumulation and deposition of misfolded Aß in the brain is the primary cause of AD. - suggests that neurofibrillary tangles (or tau tangles) occur later in this process to further exacerbate the disease. 1. Aβ formed by cleavage of APP in neuron membranes. 2. Aβ oligomers disrupt synapses between neurons. 3. Oligomers → plaques outside neurons → impair function. 4. Plaques activate microglia, causing harmful inflammation. 5. Tau misfolds, forms tangles inside neurons, displacing organelles. 6. Misfolded tau spreads between neurons, worsening degeneration.
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early stage AD
- AD often begins near the hippocampus (medial temporal lobe). - Hippocampus is key for memory encoding, retrieval, and spatial navigation.
65
middle stage AD
- Pathology begins near the hippocampus (memory & navigation). - Over time, larger areas of the cerebral cortex are affected. - Accumulation of amyloid-β plaques & neurofibrillary tangles → progressive neuron death.
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late stage AD
- Progression from mild to severe AD typically takes several years - Worsening symptoms linked to increasing buildup of amyloid-β plaques and tau tangles in the brain
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Decline of Cognitive Function in AD
- Amyloid-β plaques accumulate 10–15 years before diagnosis - Tau tangles build up later, closer to symptom onset - Mild Cognitive Impairment (MCI) = early abnormal cognitive decline - 10–15% with MCI develop dementia each year
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Macroscopic change with AD: Cerebral cortical Atrophy
- Neuronal damage from AD causes the outermost layer of brain cells to atrophy. - This decreases the overall size and weight of the brain.
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Macroscopic change with AD: Enlarged ventricles
- the brain has fluid filled spaces known as ventricles. - Due to increasing degeneration of brain tissue in AD ventricles progressively enlarge’ in a process called ‘ex-vacuo hydrocephalus’
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Macroscopic change with AD: Hippocampal atrophy
- hippocampal region is where early pathological changes of AD are seen. - As disease progresses the hippocampus progressively atrophies (shrinks) as result of neuronal death
71
what is the hippocampus shaped like
seahorse on either side
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what hapopens to size of cerebral cortex when you have AD
shrinks
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Benefits of the Early Diagnosis of AD
- Improves treatment options & quality of life - Enables accurate diagnosis (including other conditions) - Allows active involvement in care planning - Helps with life planning (e.g., retirement, travel) - Supports legal & financial preparations
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Jack's story
- 18 y/o Varsity Soccer Player – Motor Issues - Difficulty walking & frequent tripping - Decreased soccer performance (cutting, shooting) - Pain on lateral calf, lasts >30 min, not exercise-related - No trauma, concussion, or spinal injury reported has CMT ( Charcot-Marie-Tooth Disease)
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Nerve conduction Study
- Tests electrical signal function in nerves - Electrodes placed on skin, deliver small electrical impulses - Weak response → possible issue with nerve signal transmission
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Electromyography test (EMG)
- Thin needle inserted into muscle, connected to a monitor - Measures muscle's electrical activity during flex and relaxation - Detects nerve or muscle dysfunction
77
Charcot-Marie-Tooth Disease
- Most common inherited neurological disorder (~1 in 2500) - Onset in childhood - Leg weakness & atrophy → trouble running - Reduced/absent reflexes, mild sensory loss - Slow progression, normal lifespan - had duplicate of chromosome 17 for PMP22 gene symptoms: - Breathing problems - Sleep apnea - Scoliosis - Hip dysplasia - Some cases; loss of hearing and troubles with sight
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CMT type 1
- Caused by mutation affecting Schwann cells - Demyelination → slower nerve signals - Slowly progressive - Starts with leg weakness/atrophy in childhood - May later affect hands, with loss of sensation in feet/legs
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CMT type 2
- Abnormality in axon → degeneration - Leads to muscle atrophy from lost nerve supply - Similar symptoms to CMT1, but milder - Less sensory loss and disability - Symptoms often appear in childhood/adolescence
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Challenges in Developing Therapies
- Genetic complexity (100+ mutations cause CMT). - Difficult clinical trials (rare disease, global patient spread). - Blood-brain barrier limits drug delivery to neurons.
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Emerging Therapies for neurological diseases
- Gene silencing (CMT1A) to reduce harmful gene duplication. - Gene replacement & repair (CMT type 1). --CMT1B: change in the MPZ gene --CMT1C: change in the SIMPLE gene -- CMT1D: change in the EGR2 gene -- CMT1X: mutations in GJB1 - Small molecules & viral vectors to improve nerve function (CRISPR, ASOs-antisense oligonucleotides) CMT type 2.