Neuroscience of aging

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The neuroscience of aging is the study of the changes in the nervous system that occur with aging. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex, which is considered non-pathological. Aging is also associated with many neurological and neurodegenerative diseases, such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, Parkinson's disease, and Creutzfeldt–Jakob disease. [1]

Contents

Normal structural and neural changes

Neurogenesis occurs very little in adults; it only occurs in the hypothalamus and striatum to a small extent in a process called adult neurogenesis. Environmental enrichment, physical activity and stress (which can stimulate or hinder this process) are key environmental and physiological factors affecting adult neurogenesis [2] . Sensory stimulation, social interactions, and cognitive challenges can describe an enriched environment [3] . Exercising has frequently increased the reproduction of neuronal precursor cells and helped with age-related declines in neurogenesis. The brain volume decreases roughly 5% per decade after forty. It is currently unclear why brain volume decreases with age. However, a few causes may include cell death, decreased cell volume, and changes in synaptic structure. The changes in brain volume are heterogeneous across regions, with the prefrontal cortex receiving the most significant reduction in volume, followed in order by the striatum, the temporal lobe, the cerebellar vermis, the cerebellar hemispheres, and the hippocampus [4] . However, one review found that the amygdala and ventromedial prefrontal cortex remained relatively free of atrophy, consistent with the finding of emotional stability occurring with non-pathological aging. [5] Enlargement of the ventricles, sulci and fissures is common in non-pathological aging. [6]

Changes may also be associated with neuroplasticity, synaptic functionality and voltage-gated calcium channels. [7] Increased hyperpolarization, possibly due to dysfunctional calcium regulation, decreases neuron firing rate and plasticity. This effect is particularly pronounced in the hippocampus of aged animals and may be an important contributor to age-associated memory deficits. The hyperpolarization of a neuron can be divided into three stages: fast, medium, and slow hyperpolarization. In aged neurons, the medium and slow hyperpolarization phases involve the prolonged opening of calcium-dependent potassium channels. The prolonging of this phase has been hypothesized to result from deregulated calcium and hypoactivity of cholinergic, dopaminergic, serotonergic and glutaminergic pathways. [8]

Normal functional changes

Episodic memory (remembering specific events) declines gradually from middle age, while semantic memory (general knowledge and facts) increases into early old age and then declines thereafter [9] . Older adults can exhibit reduced activity in specific brain regions during cognitive tasks, particularly in medial temporal areas related to memory processing. On the other hand, overrecruitment of other brain areas, mainly in the prefrontal cortex, can be engaged in memory-related tasks [10] . Older adults also tend to engage their prefrontal cortex more often during working memory tasks, possibly to compensate for executive functions. Further impairments of cognitive function associated with aging include decreased processing speed and inability to focus. A model proposed to account for altered activation posits that decreased neural efficiency driven by amyloid plaques and decreased dopamine functionality lead to compensatory activation. [11] Decreased processing of negative stimuli, as opposed to positive stimuli, appears in aging and becomes significant enough to detect even with autonomic nervous responses to emotionally charged stimuli. [12] Aging is also associated with decreased plantar reflex and Achilles reflex response. Nerve conductance also decreases during normal aging. [13]

DNA damage

Certain genes of the human frontal cortex display reduced transcriptional expression after age 40, especially after age 70. [14] In particular, genes with central roles in synaptic plasticity display reduced expression with age. The promoters of genes with reduced expression in the cortex of older individuals have a marked increase in DNA damage, likely oxidative DNA damage. [14]

Pathological changes

Roughly 20% of persons greater than 60 years of age have a neurological disorder, with episodic disorders being the most common, followed by extrapyramidal movement disorders and nerve disorders. [15] Diseases commonly associated with old age include

The misfolding of proteins is a common component of the proposed pathophysiology of many aging-related diseases. However, there is insufficient evidence to prove this. For example, the tau hypothesis for Alzheimer's proposes that tau protein accumulation results in the breakdown of neuron cytoskeletons, leading to Alzheimer's. [25] Another proposed mechanism for Alzheimer's is related to the accumulation of amyloid beta [26] in a similar mechanism to the prion propagation of Creutzfeldt-Jakob disease. Until a recent study, tau proteins were believed to be the precedents for Alzheimer's but in a combination of amyloid beta. [27] Similarly, the protein alpha-synuclein is hypothesized to accumulate in Parkinson's and related diseases. [28]

Chemo brain

Treatments with anticancer chemotherapeutic agents often are toxic to the cells of the brain, leading to memory loss and cognitive dysfunction that can persist long after the period of exposure. This condition, termed chemo brain, appears to be due to DNA damages that cause epigenetic changes in the brain that accelerate the brain aging process. [29]

Management

Treatment of an age-related neurological disease varies from disease to disease. Modifiable risk factors for dementia include diabetes, hypertension, smoking, hyperhomocysteinemia, hypercholesterolemia, and obesity (which are usually associated with many other risk factors for dementia). Paradoxically, drinking and smoking confer protection against Parkinson's disease. [30] [31] It also confers protective benefits to age-related neurological disease in the consumption of coffee or caffeine. [32] [33] [34] Consumption of fruits, fish and vegetables confers protection against dementia, as does a Mediterranean diet. [35] In animal experiments, long-term calorie restriction was found to help reduce oxidative DNA damage. [36] Physical exercise significantly lowers the risk of cognitive decline in old age [37] and is an effective treatment for those with dementia [38] [39] and Parkinson's disease. [40] [41] [42] [43]

Related Research Articles

<span class="mw-page-title-main">Dementia</span> Long-term brain disorders causing impaired memory, thinking and behavior

Dementia is a syndrome associated with many neurodegenerative diseases, characterized by a general decline in cognitive abilities that affects a person's ability to perform everyday activities. This typically involves problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms of dementia include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, their caregivers, and their social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than might be caused by the normal aging process.

<span class="mw-page-title-main">Lewy body</span> Spherical inclusion commonly found in damaged neurons

Lewy bodies are the inclusion bodies – abnormal aggregations of protein – that develop inside neurons affected by Parkinson's disease (PD), the Lewy body dementias, and some other disorders. They are also seen in cases of multiple system atrophy, particularly the parkinsonian variant (MSA-P).

<span class="mw-page-title-main">Frontotemporal dementia</span> Types of dementia involving the frontal or temporal lobes

Frontotemporal dementia (FTD), also called frontotemporal degeneration disease or frontotemporal neurocognitive disorder, encompasses several types of dementia involving the progressive degeneration of the brain's frontal and temporal lobes. Men and women appear to be equally affected. FTD generally presents as a behavioral or language disorder with gradual onset. Signs and symptoms tend to appear in late adulthood, typically between the ages of 45 and 65, although it can affect people younger or older than this. Currently, no cure or approved symptomatic treatment for FTD exists, although some off-label drugs and behavioral methods are prescribed.

<span class="mw-page-title-main">Adult neurogenesis</span> Generating of neurons from neural stem cells in adults

Adult neurogenesis is the process in which neurons are generated from neural stem cells in the adult. This process differs from prenatal neurogenesis.

Aging of the brain is a process of transformation of the brain in older age, including changes all individuals experience and those of illness. Usually this refers to humans.

<span class="mw-page-title-main">Locus coeruleus</span> Stress and panic response centre

The locus coeruleus (LC), also spelled locus caeruleus or locus ceruleus, is a nucleus in the pons of the brainstem involved with physiological responses to stress and panic. It is a part of the reticular activating system in the reticular formation.

<span class="mw-page-title-main">Progressive supranuclear palsy</span> Medical condition of the brain

Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. The condition leads to symptoms including loss of balance, slowing of movement, difficulty moving the eyes, and cognitive impairment. PSP may be mistaken for other types of neurodegeneration such as Parkinson's disease, frontotemporal dementia and Alzheimer's disease. The cause of the condition is uncertain, but involves the accumulation of tau protein within the brain. Medications such as levodopa and amantadine may be useful in some cases.

<span class="mw-page-title-main">Tau protein</span> Group of six protein isoforms produced from the MAPT gene

The tau proteins form a group of six highly soluble protein isoforms produced by alternative splicing from the gene MAPT. They have roles primarily in maintaining the stability of microtubules in axons and are abundant in the neurons of the central nervous system (CNS), where the cerebral cortex has the highest abundance. They are less common elsewhere but are also expressed at very low levels in CNS astrocytes and oligodendrocytes.

Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means a decrement in the size of the cell, which can be due to progressive loss of cytoplasmic proteins. In brain tissue, atrophy describes a loss of neurons and the connections between them. Brain atrophy can be classified into two main categories: generalized and focal atrophy. Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location. If the cerebral hemispheres are affected, conscious thought and voluntary processes may be impaired.

<span class="mw-page-title-main">Neurofibrillary tangle</span> Aggregates of tau protein known as a biomarker of Alzheimers disease

Neurofibrillary tangles (NFTs) are intracellular aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.

<span class="mw-page-title-main">Corticobasal degeneration</span> Rare neurodegenerative disease

Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. CBD symptoms typically begin in people from 50 to 70 years of age, and typical survival before death is eight years. It is characterized by marked disorders in movement and cognition, and is classified as one of the Parkinson plus syndromes. Diagnosis is difficult, as symptoms are often similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and dementia with Lewy bodies, and a definitive diagnosis of CBD can only be made upon neuropathologic examination.

<span class="mw-page-title-main">Tauopathy</span> Medical condition

Tauopathies are a class of neurodegenerative diseases characterized by the aggregation of abnormal tau protein. Hyperphosphorylation of tau proteins causes them to dissociate from microtubules and form insoluble aggregates called neurofibrillary tangles. Various neuropathologic phenotypes have been described based on the anatomical regions and cell types involved as well as the unique tau isoforms making up these deposits. The designation 'primary tauopathy' is assigned to disorders where the predominant feature is the deposition of tau protein. Alternatively, diseases exhibiting tau pathologies attributed to different and varied underlying causes are termed 'secondary tauopathies'. Some neuropathologic phenotypes involving tau protein are Alzheimer's disease, frontotemporal dementia, progressive supranuclear palsy, and corticobasal degeneration.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of neurons, in the process known as neurodegeneration. Neuronal damage may also ultimately result in their death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

Cognitive reserve is the mind's and brain's resistance to damage of the brain. The mind's resilience is evaluated behaviorally, whereas the neuropathological damage is evaluated histologically, although damage may be estimated using blood-based markers and imaging methods. There are two models that can be used when exploring the concept of "reserve": brain reserve and cognitive reserve. These terms, albeit often used interchangeably in the literature, provide a useful way of discussing the models. Using a computer analogy, brain reserve can be seen as hardware and cognitive reserve as software. All these factors are currently believed to contribute to global reserve. Cognitive reserve is commonly used to refer to both brain and cognitive reserves in the literature.

<span class="mw-page-title-main">Alzheimer's disease</span> Progressive neurodegenerative disease

Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.

<span class="mw-page-title-main">Environmental enrichment</span> Brain stimulation through physical and social surroundings

Environmental enrichment is the stimulation of the brain by its physical and social surroundings. Brains in richer, more stimulating environments have higher rates of synaptogenesis and more complex dendrite arbors, leading to increased brain activity. This effect takes place primarily during neurodevelopment, but also during adulthood to a lesser degree. With extra synapses there is also increased synapse activity, leading to an increased size and number of glial energy-support cells. Environmental enrichment also enhances capillary vasculation, providing the neurons and glial cells with extra energy. The neuropil expands, thickening the cortex. Research on rodent brains suggests that environmental enrichment may also lead to an increased rate of neurogenesis.

<span class="mw-page-title-main">Type 3 diabetes</span> Medical condition

Type 3 diabetes is a proposed pathological linkage between Alzheimer's disease and certain features of type 1 and type 2 diabetes. Specifically, the term refers to a set of common biochemical and metabolic features seen in the brain in Alzheimer's disease, and in other tissues in diabetes; it may thus be considered a "brain-specific type of diabetes." It was recognized at least as early as 2005 that some features of brain function in Alzheimer's disease mimic those that underlie diabetes. However, the concept of type 3 diabetes is controversial, and as of 2021 it was not a widely or generally recognized diagnosis.

<span class="mw-page-title-main">Neurobiological effects of physical exercise</span> Neural, cognitive, and behavioral effects of physical exercise

The neurobiological effects of physical exercise involve possible interrelated effects on brain structure, brain function, and cognition. Research in humans has demonstrated that consistent aerobic exercise may induce improvements in certain cognitive functions, neuroplasticity and behavioral plasticity; some of these long-term effects may include increased neuron growth, increased neurological activity, improved stress coping, enhanced cognitive control of behavior, improved declarative, spatial, and working memory, and structural and functional improvements in brain structures and pathways associated with cognitive control and memory. The effects of exercise on cognition may affect academic performance in children and college students, improve adult productivity, preserve cognitive function in old age, preventing or treating certain neurological disorders, and improving overall quality of life.

<span class="mw-page-title-main">Cholinergic neuron</span> Type of nerve cell

A cholinergic neuron is a nerve cell which mainly uses the neurotransmitter acetylcholine (ACh) to send its messages. Many neurological systems are cholinergic. Cholinergic neurons provide the primary source of acetylcholine to the cerebral cortex, and promote cortical activation during both wakefulness and rapid eye movement sleep. The cholinergic system of neurons has been a main focus of research in aging and neural degradation, specifically as it relates to Alzheimer's disease. The dysfunction and loss of basal forebrain cholinergic neurons and their cortical projections are among the earliest pathological events in Alzheimer's disease.

<span class="mw-page-title-main">Masud Husain</span> British professor of neuroscience, editor of Brain

Masud Husain FMedSci is a clinical neurologist and neuroscientist working in the UK. He is Professor of Neurology & Cognitive Neuroscience at the Nuffield Department of Clinical Neurosciences and Departmental of Experimental Psychology, University of Oxford, a Professorial Fellow at New College, Oxford, and Editor-in-Chief of the journal Brain. He was born in East Pakistan.

References

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