Neurological Disorders

Neurological diseases are disorders of the brain, spinal cord, and nerves throughout the body. These diseases can affect almost any function of the human body, including voluntary control of muscles, perception of sensations, cognition, and autonomic functions such as heartbeat and digestion.

Definition and Overview

A neurological disorder is any disorder of the nervous system. Structural, biochemical, or electrical abnormalities in the brain, spinal cord, or other nerves can result in a range of symptoms. These may include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain, and altered levels of consciousness.

Classification of Neurological Diseases

Neurological diseases can be classified based on the primary location affected, the primary type of dysfunction involved, or the primary cause when known.

By Location

Central Nervous System Diseases: These affect the brain and spinal cord. Examples include stroke, multiple sclerosis, and Parkinson's disease.
Peripheral Nervous System Diseases: These affect the peripheral nerves. Examples include peripheral neuropathy, Guillain-Barré syndrome, and carpal tunnel syndrome.

By Dysfunction

Functional Disorders: Such as epilepsy, where there may be intermittent malfunctioning.
Structural Disorders: Such as brain or spinal cord injury, where there is physical damage.
Degenerative Disorders: Such as Alzheimer's disease and Amyotrophic Lateral Sclerosis (ALS), where there is progressive loss of structure or function.

By Cause

Genetic Diseases: Such as Huntington's disease and Duchenne Muscular Dystrophy.
Infections: Such as meningitis or polio.
Lifestyle or Environmental Factors: Such as the effects of substance abuse or prolonged exposure to toxic substances.

Common Age-Related Neurological Disorders

Neurological disorders that are predominantly age-related typically manifest and progress with advancing age, reflecting changes in neurological function over time. These conditions often result from the cumulative effect of various biological processes such as neuronal loss, protein misfolding, vascular changes, or inflammatory mechanisms.

Alzheimer's Disease: A progressive degenerative disease that primarily affects individuals over 65, impacting memory, thinking, and behavior. Early-onset Alzheimer's can occur in individuals between 30 and 65 years of age, although it is less common.
Parkinson's Disease: This degenerative disorder of the central nervous system predominantly affects middle-aged and elderly people, usually presenting itself after the age of 60. Symptoms such as impaired motor skills and speech progressively worsen over time.
Stroke: The risk of stroke increases significantly with age, particularly after the age of 55. It occurs when there is a loss of blood flow to a part of the brain, resulting in tissue damage and loss of function in the affected area.
Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, ALS leads to the progressive loss of muscle control due to nerve cell damage in the brain and spinal cord and is most common between the ages of 40 and 70, though it can occur at any age.
Vascular Dementia: The second most common form of dementia after Alzheimer's disease, vascular dementia is caused by problems in the supply of blood to the brain, often due to strokes or small vessel disease.
Frontotemporal Dementia: An umbrella term for a range of disorders that primarily affect the frontal and temporal lobes of the brain, which are generally associated with personality, behavior, and language. While it can start as early as 45 years old, it becomes more common in older adults.
Lewy Body Dementia: Characterized by the presence of Lewy bodies (abnormal aggregates of protein) in the brain, it affects cognition, behavior, movement, and sleep. It is typically a disease of older adults, most commonly appearing after the age of 60.
Normal Pressure Hydrocephalus: Although it can occur at any age, it is more prevalent in the elderly population and is caused by the build-up of cerebrospinal fluid in the brain ventricles, leading to walking difficulties, urinary incontinence, and cognitive impairment.
Multiple System Atrophy (MSA): A rare degenerative neurological disorder affecting adults, typically in their 50s. MSA is characterized by a combination of symptoms affecting movement, blood pressure control, and other bodily functions.
Huntington's Disease: This is a hereditary disorder caused by a faulty gene for a protein called huntingtin. Symptoms usually start between 30 and 50 years of age and can include movement disorders, cognitive decline, and psychiatric problems.

Other Common Neurological Disorders

Epilepsy: Characterized by recurrent seizures, which are sudden bursts of electrical activity in the brain that temporarily affect how it works.
Migraine: A type of headache associated with sensory disturbances, often a chronic condition with recurrent episodes.
Multiple Sclerosis (MS): An autoimmune disease where the immune system attacks the protective sheath (myelin) that covers nerve fibers, causing communication problems between the brain and the rest of the body.
Traumatic Brain Injury (TBI): Caused by a blow to the head or a penetrating head injury that disrupts the normal function of the brain.
Spinal Cord Injury: Damage to any part of the spinal cord or nerves at the end of the spinal canal, often causing permanent changes in strength, sensation, and other body functions below the site of the injury.
Peripheral Neuropathy: A result of damage to the peripheral nerves, often causing weakness, numbness, and pain, usually in the hands and feet.
Bell's Palsy: A sudden weakness in the muscles on one half of the face, resulting in a drooping appearance.
Guillain-Barré Syndrome: A rare disorder where the body's immune system attacks the peripheral nerves.
Cerebral Palsy: A group of disorders that affect movement and muscle tone or posture, caused by damage that occurs to the immature brain as it develops, most often before birth.
Huntington's Disease: A genetic disorder causing the progressive breakdown (degeneration) of nerve cells in the brain.
Duchenne Muscular Dystrophy: A genetic disorder characterized by progressive muscle degeneration and weakness due to alterations of a protein called dystrophin that helps keep muscle cells intact.

Supplementation in Neurological Diseases

Supplementation can play a role in the management of neurological diseases, particularly in cases where dietary deficiencies are identified or where evidence supports their use in symptom management or disease progression. It's important to note that while some supplements may help reduce symptoms or support neurological health, they are not a substitute for medical treatment but rather a complementary approach.

Vitamins and Minerals

Vitamin B12 and Folate: Essential for nerve function and the synthesis of DNA and neurotransmitters. Deficiencies can lead to neurological problems and are often checked in the context of neuropathies and cognitive disorders.
Vitamin D: Has been linked to the nervous system's health and immune regulation. Low levels are associated with an increased risk of multiple sclerosis and the severity of neurodegenerative diseases.
Magnesium: Important for nerve transmission and has been studied for its potential in migraine prevention and treatment.
Omega-3 Fatty Acids: Found in fish oil, they are important for maintaining the structure of cell membranes and have anti-inflammatory effects, potentially beneficial in diseases like multiple sclerosis.

Antioxidants

Vitamin E and Selenium: Antioxidants that protect against oxidative stress, which is implicated in stroke, Alzheimer's disease, and Parkinson's disease.
Coenzyme Q10: Acts as an antioxidant and is involved in energy production. It has been studied for potential benefits in neurodegenerative disorders.

Herbal Supplements

Ginkgo Biloba: Widely used for cognitive impairment and dementia, though evidence for its effectiveness is mixed.
Turmeric (Curcumin): Has anti-inflammatory properties and has been researched for its potential neuroprotective benefits in a range of neurological conditions.

Amino Acids and Proteins

Creatine: Shown to have neuroprotective effects in some models of neurological diseases and may support energy metabolism in neurological tissues.
Acetyl-L-Carnitine: Involved in mitochondrial energy metabolism and has been explored for peripheral neuropathy and Alzheimer's disease.

Todo

Include links to senesent cells
2022, The Impact of Supplements on Recovery After Peripheral Nerve Injury: A Review of the Literature ^[1]
2022, SIRT1 activation and its circadian clock control: a promising approach against (frailty in) neurodegenerative disorders ^[2]

References

↑ Abushukur Y & Knackstedt R: The Impact of Supplements on Recovery After Peripheral Nerve Injury: A Review of the Literature. Cureus 2022. (PMID 35733475) [PubMed] [DOI] [Full text] Peripheral nerve injury (PNI) can result from trauma, surgical resection, iatrogenic injury, and/or local anesthetic toxicity. Damage to peripheral nerves may result in debilitating weakness, numbness, paresthesia, pain, and/or autonomic instability. As PNI is associated with inflammation and nerve degeneration, means to mitigate this response could result in improved outcomes. Numerous nutrients have been investigated to prevent the negative sequelae of PNI. Alpha-lipoic acid, cytidine diphosphate-choline (CDP Choline), curcumin, melatonin, vitamin B12, and vitamin E have demonstrated notable success in improving recovery following PNI within animal models. While animal studies show ample evidence that various supplements may improve recovery after PNI, similar evidence in human patients is limited. The goal of this review is to analyze supplements that have been used successfully in animal models of PNI to serve as a reference for future studies on human patients. By analyzing supplements that have shown efficacy in animal studies, healthcare providers will have a resource from which to guide decision-making regarding future human studies investigating the role that supplements could play in PNI recovery. Ultimately, establishing a comprehensive understanding of these supplements in human patients following PNI may significantly improve post-surgical outcomes, quality of life, and peripheral nerve regeneration.
↑ Ribeiro RFN et al.: SIRT1 activation and its circadian clock control: a promising approach against (frailty in) neurodegenerative disorders. Aging Clin Exp Res 2022. (PMID 36306110) [PubMed] [DOI] [Full text] With the increase in life expectancy, the incidence of neurodegenerative disorders and their impact worldwide has been increasing in recent years. Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, have complex and varied mechanisms of pathogenesis. Importantly, they share the common feature of disrupted circadian rhythms. This hallmark is believed to underlie the symptoms of such diseases and even potentially contribute to their onset. In addition, the association of physical frailty with dementia and neurodegenerative disorders has been demonstrated. In fact, frail persons are 8 times more likely to have some form of dementia and population studies report a significant prevalence for frailty in older patients with AD and PD. SIRT1 regulates the acetylation status of clock components and controls circadian amplitude of clock genes. However, the mechanisms responsible for this circadian clock control have been the subject of contradictory findings. Importantly, the activation of SIRT1 has been shown to have very relevant therapeutic potential against neurodegeneration. Nevertheless, few studies have attempted to connect the therapeutic reestablishing of SIRT1 as an approach against circadian disruption in neurodegenerative diseases. In this review, we address: circadian rhythms as an important early biomarker of neurodegenerative disorders; mechanisms for SIRT1 activation and the novel sirtuin-activating compounds (STACs); SIRT1 circadian paradox and subsequent studies in an unprecedented way in the literature; the beneficial role of SIRT1 activation in neurodegeneration; innovative proposals of how circadian-based interventions (e.g., SIRT1 activators) may become an important therapeutic approach against neurodegenerative disorders and how non-pharmacologic interventions (e.g., Mediterranean-style diet) might help in the prevention and/or treatment of these high-burden disorders, while tackling frailty and enhancing robustness.

[pmid35733475-1] Abushukur Y & Knackstedt R: The Impact of Supplements on Recovery After Peripheral Nerve Injury: A Review of the Literature. Cureus 2022. (PMID 35733475) [PubMed] [DOI] [Full text] Peripheral nerve injury (PNI) can result from trauma, surgical resection, iatrogenic injury, and/or local anesthetic toxicity. Damage to peripheral nerves may result in debilitating weakness, numbness, paresthesia, pain, and/or autonomic instability. As PNI is associated with inflammation and nerve degeneration, means to mitigate this response could result in improved outcomes. Numerous nutrients have been investigated to prevent the negative sequelae of PNI. Alpha-lipoic acid, cytidine diphosphate-choline (CDP Choline), curcumin, melatonin, vitamin B12, and vitamin E have demonstrated notable success in improving recovery following PNI within animal models. While animal studies show ample evidence that various supplements may improve recovery after PNI, similar evidence in human patients is limited. The goal of this review is to analyze supplements that have been used successfully in animal models of PNI to serve as a reference for future studies on human patients. By analyzing supplements that have shown efficacy in animal studies, healthcare providers will have a resource from which to guide decision-making regarding future human studies investigating the role that supplements could play in PNI recovery. Ultimately, establishing a comprehensive understanding of these supplements in human patients following PNI may significantly improve post-surgical outcomes, quality of life, and peripheral nerve regeneration.

[pmid36306110-2] Ribeiro RFN et al.: SIRT1 activation and its circadian clock control: a promising approach against (frailty in) neurodegenerative disorders. Aging Clin Exp Res 2022. (PMID 36306110) [PubMed] [DOI] [Full text] With the increase in life expectancy, the incidence of neurodegenerative disorders and their impact worldwide has been increasing in recent years. Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, have complex and varied mechanisms of pathogenesis. Importantly, they share the common feature of disrupted circadian rhythms. This hallmark is believed to underlie the symptoms of such diseases and even potentially contribute to their onset. In addition, the association of physical frailty with dementia and neurodegenerative disorders has been demonstrated. In fact, frail persons are 8 times more likely to have some form of dementia and population studies report a significant prevalence for frailty in older patients with AD and PD. SIRT1 regulates the acetylation status of clock components and controls circadian amplitude of clock genes. However, the mechanisms responsible for this circadian clock control have been the subject of contradictory findings. Importantly, the activation of SIRT1 has been shown to have very relevant therapeutic potential against neurodegeneration. Nevertheless, few studies have attempted to connect the therapeutic reestablishing of SIRT1 as an approach against circadian disruption in neurodegenerative diseases. In this review, we address: circadian rhythms as an important early biomarker of neurodegenerative disorders; mechanisms for SIRT1 activation and the novel sirtuin-activating compounds (STACs); SIRT1 circadian paradox and subsequent studies in an unprecedented way in the literature; the beneficial role of SIRT1 activation in neurodegeneration; innovative proposals of how circadian-based interventions (e.g., SIRT1 activators) may become an important therapeutic approach against neurodegenerative disorders and how non-pharmacologic interventions (e.g., Mediterranean-style diet) might help in the prevention and/or treatment of these high-burden disorders, while tackling frailty and enhancing robustness.

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