Cerebral atrophy

Last updated November 05, 2024

Cerebral atrophy is a common feature of many of the diseases that affect the brain.^[1] 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.^[2] Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location.^[2] If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.

Some degree of cerebral shrinkage occurs naturally with the dynamic process of aging.^[3] Structural changes continue during adulthood as brain shrinkage commences after the age of 35, at a rate of 0.2% per year.^[4] The rate of decline is accelerated when individuals reach 70 years old.^[5] By the age of 90, the human brain will have experienced a 15% loss of its initial peak weight.^[6] Besides brain atrophy, aging has also been associated with cerebral microbleeds.^[3]

Causes

Cerebral atrophy is not a disease, but rather a sign of one or more disease or biological processes. Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias. Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing and sequencing may also be impaired. Seizures can take different forms, appearing as disorientation, strange repetitive movements, loss of consciousness, or convulsions. Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences. The pattern and rate of progression of cerebral atrophy depends on the disease involved.

Injury

Stroke, loss of brain function due to a sudden interruption of blood supply in the brain
Moderate-to-severe traumatic brain injury ^[7]

Diseases and disorders

Alzheimer's disease; high resolution MRI scans have shown the progression of cerebral atrophy in Alzheimer's disease^[8]
Cerebral palsy, in which lesions (damaged areas) may impair motor coordination
Senile dementia, fronto-temporal dementia, and vascular dementia
Pick's disease, causes progressive destruction of nerve cells in the brain
Huntington's disease, and other genetic disorders that cause build-up of toxic levels of proteins in neurons
Leukodystrophies, such as Krabbe disease, which destroy the myelin sheath that protects axons
Multiple sclerosis, which causes inflammation, myelin damage, and lesions in cerebral tissue
Epilepsy, in which lesions cause abnormal electrochemical discharges that result in seizures
GLUT1 deficiency syndrome ^[9]
Anorexia nervosa, bulimia nervosa, and other eating disorders
Malnutrition, caused by lack or excess of nutrition from foods
Type II diabetes, where the body does not use insulin properly resulting in high blood sugar
Bipolar disorder,^[10] significant loss of brain tissue during manic episodes; however it's not verified whether the episodes cause brain tissue loss or vice versa
Schizophrenia ^[11]
Mitochondrial encephalomyopathies, such as Kearns–Sayre syndrome, which interfere with the basic functions of neurons
Posterior cortical atrophy: in the most posterior area of the brain lies the visual cortex, the area of the brain where visual information is received and processed. When cortical atrophy occurs in this brain area due to neurodegeneration, the first symptom is impairment in vision. A common vision impairment seen in patients with posterior cortical atrophy is simultanagnosia, where a person is unable to see multiple locations at once or to quickly shift attention between these locations. When looking at images of a brain with posterior cortical atrophy, one can see a loss in volume of the dorsal and ventral visual pathways, where visual stimuli is brought to the visual cortex and integrated information is sent back out to other areas of the brain. Because this disorder results in visual impairments, there is often a missed or delayed diagnosis, as the assumption is that there is a problem is in the eyes when the reality is that the problem is all the way in the back of the brain.^[12]
Prion diseases, a group of invariably fatal encephalopathies that cause the progressive death of neurons.

Infections

An infectious agent or the inflammatory reaction to it can destroy neurons and their axons. These include:

Encephalitis, acute inflammation in the brain
Neurosyphilis, an infection in the brain or spinal cord
AIDS, disease of the immune system

Drug-induced

Alcohol (partially reversible):^[13] Standardized MRI evidence suggest chronic alcoholism (alcohol use disorder) is associated with widespread cortical atrophy and major brain changes. In contrast to healthy controls, macrostructural findings indicate alcoholic brains are smaller in mass and volume.^[14] Neuroimaging studies also show that cortical shrinkage in "uncomplicated alcoholism" is most severe in the frontal lobe in comparison to the other divisions of the cerebral cortex.^[15] In addition, neurological diseases that co-occur with excessive alcohol consumption—such as Wernicke–Korsakoff syndrome (WKS)—are characterized by substantial volume deficits of the diencephalon structures.^[15] In comparison to unaffected, non-alcoholic participants, tissue degeneration in WKS patients is found in specific white matter structures including the corpus callosum, the hippocampus, the subcortical basal ganglia (hypothalamus, thalamus, putamen), and the mammillary bodies.^[16]
Antipsychotic
Corticosteroid use (There appears to be correlations between degree of dosing with corticosteroids and cerebral atrophy)^[17]

Diagnosis

Neurofilament light chain

Cerebrospinal fluid (CSF) is a fluid that is found exclusively in the brain and spinal cord that circulates between sections of the brain offering an extra layer of protection. Studies have shown that biomarkers in the CSF and plasma can be tracked for their presence in different parts of the brain—and their presence can tell us about cerebral atrophy. One study took advantage of biomarkers, namely one called neurofilament light chain (NFL), in patients with Alzheimer's disease. Neurofilament light chain is a protein that is important in the growth and branching of neurons—cells found in the brain. In Alzheimer's Disease, neurons will stop working or die in a process called neurodegeneration. By tracking NFL, researchers can see this neurodegeneration, which this study showed was associated with brain atrophy and later cognitive decline in Alzheimer's patients. Other biomarkers like Ng – a protein important in long-term potentiation and memory – have been tracked for their associations with brain atrophy as well, but NFL had the greatest association.^[18]

Measures

CT and MRI are most commonly used to observe the brain for cerebral atrophy. A CT scan takes cross sectional images of the brain using X-rays, while an MRI uses a magnetic field. With both measures, multiple images can be compared to see if there is a loss in brain volume over time.^[20]

Difference from hydrocephalus

Cerebral atrophy can be hard to distinguish from hydrocephalus because both cerebral atrophy and hydrocephalus involve an increase in cerebrospinal fluid (CSF) volume. In cerebral atrophy, this increase in CSF volume comes as a result of the decrease in cortical volume. In hydrocephalus, the increase in volume happens due to the CSF itself.^[20]

Typical imaging findings in normal pressure hydrocephalus versus brain atrophy.^[21]

	Normal pressure hydrocephalus	Brain atrophy
Preferable projection	Coronal plane at the level of the posterior commissure of the brain.
Modality in this example	CT	MRI
CSF spaces over the convexity near the vertex (red ellipse )	Narrowed convexity ("tight convexity") as well as medial cisterns	Widened vertex (red arrow) and medial cisterns (green arrow)
Callosal angle (blue V)	Acute angle	Obtuse angle
Most likely cause of leucoaraiosis (periventricular signal alterations, blue arrows )	Transependymal cerebrospinal fluid diapedesis	Vascular encephalopathy, in this case suggested by unilateral occurrence

Treatment

Prevention of cerebral atrophy depends on preventing the conditions driving it. ^[22] Some steps that can be taken to reduce the risk:

controlling blood pressure
a healthy balanced diet including omega-3's and antioxidants
staying active mentally, physically, and socially.^[23]

Reversibility of cerebral atrophy

While most cerebral atrophy is said to be irreversible, there are recent studies that show this is not always the case. A child who was treated with ACTH originally showed atrophy, but four months after treatment the brain was seemingly normal again.^[24]

As previously mentioned, chronic alcoholism is known to be associated with significant brain damage.^[14] The pronounced shrinkage in the frontal lobes and cerebellum of alcoholics correlates with serious impairments in executive and psychomotor functions. However, longitudinal studies suggest that some of these brain damages are partially reversible with abstinence.^[16] In response to drinking cessation, bodies of gray and white matter including the cerebral cortex, the limbic system (amygdala, hippocampus, thalamus), the cerebellum, and the brainstem all showed a general increase in brain volume.^[15] Similarly, ventricular enlargement—which reflects atrophy of surrounding brain regions—is also reduced in abstinent alcoholics. Following extended sobriety, the volume of the lateral and third ventricles was decreased, and abstainers showed an improvement in working memory and balance.^[16] Finally, evidence for the recovery of brain volume with continued sobriety is supported by the improvement in neuropsychological performance. Compared to the control participants, abstinent alcoholic patients scored significantly better on tests measuring cognitive, sensory, and motor functions including abstract reasoning, memory, visuospatial ability, and gait and balance.^[16] That being said, while short-term abstinence suffices to produce structural and functional recovery, some alcohol-induced brain changes may persist even after long-term sobriety.^[16]

Related Research Articles

White matter refers to areas of the central nervous system (CNS) that are mainly made up of myelinated axons, also called tracts. Long thought to be passive tissue, white matter affects learning and brain functions, modulating the distribution of action potentials, acting as a relay and coordinating communication between different brain regions.

Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and regulation of automatic bodily functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive impairment interferes with normal daily functioning. Together with Parkinson's disease dementia, DLB is one of the two Lewy body dementias. It is a common form of dementia, but the prevalence is not known accurately and many diagnoses are missed. The disease was first described on autopsy by Kenji Kosaka in 1976, and he named the condition several years later.

<span class="mw-page-title-main">Vascular dementia</span> Dementia resulting from stroke

Vascular dementia is dementia caused by a series of strokes. Restricted blood flow due to strokes reduces oxygen and glucose delivery to the brain, causing cell injury and neurological deficits in the affected region. Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia.

<span class="mw-page-title-main">Binswanger's disease</span> Medical condition

Binswanger's disease, also known as subcortical leukoencephalopathy and subcortical arteriosclerotic encephalopathy, is a form of small-vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

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.

Normal pressure hydrocephalus (NPH), also called malresorptive hydrocephalus, is a form of communicating hydrocephalus in which excess cerebrospinal fluid (CSF) builds up in the ventricles, leading to normal or slightly elevated cerebrospinal fluid pressure. The fluid build-up causes the ventricles to enlarge and the pressure inside the head to increase, compressing surrounding brain tissue and leading to neurological complications. Although the cause of idiopathicNPH remains unclear, it has been associated with various co-morbidities including hypertension, diabetes mellitus, Alzheimer's disease, and hyperlipidemia. Causes of secondary NPH include trauma, hemorrhage, or infection. The disease presents in a classic triad of symptoms, which are memory impairment, urinary frequency, and balance problems/gait deviations. The disease was first described by Salomón Hakim and Raymond Adams in 1965.

In neurology, semantic dementia (SD), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain. Semantic dementia is a disorder of semantic memory that causes patients to lose the ability to match words or images to their meanings. However, it is fairly rare for patients with semantic dementia to develop category specific impairments, though there have been documented cases of it occurring. Typically, a more generalized semantic impairment results from dimmed semantic representations in the brain.

Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to medium blood vessels of the central nervous system and meninges. The term congophilic is sometimes used because the presence of the abnormal aggregations of amyloid can be demonstrated by microscopic examination of brain tissue after staining with Congo red. The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis.

<span class="mw-page-title-main">Perivascular space</span> Space surrounding blood vessels

A perivascular space, also known as a Virchow–Robin space, is a fluid-filled space surrounding certain blood vessels in several organs, including the brain, potentially having an immunological function, but more broadly a dispersive role for neural and blood-derived messengers. The brain pia mater is reflected from the surface of the brain onto the surface of blood vessels in the subarachnoid space. In the brain, perivascular cuffs are regions of leukocyte aggregation in the perivascular spaces, usually found in patients with viral encephalitis.

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.

HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory, cognition, behavior, and motor function in HIV-infected individuals during the late stages of the disease, when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.

Psychoorganic syndrome (POS), also known as organic psychosyndrome, is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.

<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.

The inferior temporal gyrus is one of three gyri of the temporal lobe and is located below the middle temporal gyrus, connected behind with the inferior occipital gyrus; it also extends around the infero-lateral border on to the inferior surface of the temporal lobe, where it is limited by the inferior sulcus. This region is one of the higher levels of the ventral stream of visual processing, associated with the representation of objects, places, faces, and colors. It may also be involved in face perception, and in the recognition of numbers and words.

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.

Alcohol-related dementia (ARD) is a form of dementia caused by long-term, excessive consumption of alcohol, resulting in neurological damage and impaired cognitive function.

<span class="mw-page-title-main">Posterior cortical atrophy</span> Medical condition

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a rare form of dementia which is considered a visual variant or an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

Alzheimer's Disease Neuroimaging Initiative (ADNI) is a multisite study that aims to improve clinical trials for the prevention and treatment of Alzheimer's disease (AD). This cooperative study combines expertise and funding from the private and public sector to study subjects with AD, as well as those who may develop AD and controls with no signs of cognitive impairment. Researchers at 63 sites in the US and Canada track the progression of AD in the human brain with neuroimaging, biochemical, and genetic biological markers. This knowledge helps to find better clinical trials for the prevention and treatment of AD. ADNI has made a global impact, firstly by developing a set of standardized protocols to allow the comparison of results from multiple centers, and secondly by its data-sharing policy which makes available all at the data without embargo to qualified researchers worldwide. To date, over 1000 scientific publications have used ADNI data. A number of other initiatives related to AD and other diseases have been designed and implemented using ADNI as a model. ADNI has been running since 2004 and is currently funded until 2021.

Alcohol-related brain damage alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe, limbic system, and cerebellum, with widespread cerebral atrophy, or brain shrinkage caused by neuron degeneration. This damage can be seen on neuroimaging scans.

The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.

References

↑ "Cerebral Atrophy Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Archived from the original on 2016-03-04. Retrieved 2014-03-28.
1 2 Harris TC, de Rooij R, Kuhl E (September 2019). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9): 1941–1959. doi:10.1007/s10439-018-02148-2. PMC 6757025 . PMID 30341741.
1 2 Sungura R, Onyambu C, Mpolya E, Sauli E, Vianney JM (March 2021). "The extended scope of neuroimaging and prospects in brain atrophy mitigation: A systematic review". Interdisciplinary Neurosurgery. 23: 100875. doi: 10.1016/j.inat.2020.100875 . S2CID 224841818.
↑ Siegel JA, Saukko PJ, Houck MM (2013). Encyclopedia of Forensic Sciences. Academic Press. ISBN 978-0-12-382166-9.
↑ Peters R (February 2006). "Ageing and the brain". Postgraduate Medical Journal. 82 (964): 84–88. doi:10.1136/pgmj.2005.036665. PMC 2596698 . PMID 16461469.
↑ Chutinet A, Rost NS (March 2014). "White matter disease as a biomarker for long-term cerebrovascular disease and dementia". Current Treatment Options in Cardiovascular Medicine. 16 (3): 292. doi:10.1007/s11936-013-0292-z. PMC 3964019 . PMID 24496967.
↑ Harris, Taylor C.; de Rooij, Rijk; Kuhl, Ellen (2018-10-17). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9). Springer Science and Business Media LLC: 1941–1959. doi:10.1007/s10439-018-02148-2. ISSN 0090-6964. PMC 6757025 . PMID 30341741.
↑ Fox NC, Schott JM (January 2004). "Imaging cerebral atrophy: normal ageing to Alzheimer's disease". Lancet. 363 (9406): 392–394. doi:10.1016/S0140-6736(04)15441-X. PMID 15074306. S2CID 20494612.
↑ Aktas D, Utine EG, Mrasek K, Weise A, von Eggeling F, Yalaz K; et al. (2010). "Derivative chromosome 1 and GLUT1 deficiency syndrome in a sibling pair". Mol Cytogenet. 3 (1): 10. doi: 10.1186/1755-8166-3-10 . PMC 2887874 . PMID 20509907.{{cite journal}}: CS1 maint: multiple names: authors list (link)
↑ "Study links manic depression with brain tissue loss". EurekAlert!. Retrieved 2017-03-21.
↑ Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC (June 2013). "Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study". The American Journal of Psychiatry. 170 (6): 609–615. doi:10.1176/appi.ajp.2013.12050674. PMC 3835590 . PMID 23558429.
↑ Maia da Silva MN, Millington RS, Bridge H, James-Galton M, Plant GT (2017). "Visual Dysfunction in Posterior Cortical Atrophy". Frontiers in Neurology. 8: 389. doi: 10.3389/fneur.2017.00389 . PMC 5561011 . PMID 28861031.
↑ Pereira JB, Westman E, Hansson O (October 2017). "Association between cerebrospinal fluid and plasma neurodegeneration biomarkers with brain atrophy in Alzheimer's disease". Neurobiology of Aging. 58: 14–29. doi: 10.1016/j.neurobiolaging.2017.06.002 . PMID 28692877. S2CID 46854877.
1 2 Meyer JS, Quenzer LF (2013). Psychopharmacology: Drugs, The Brain, and Behavior (2nd ed.). Sinauer Associates.
1 2 3 Zahr NM, Pfefferbaum A (2017). "Alcohol's Effects on the Brain: Neuroimaging Results in Humans and Animal Models". Alcohol Research. 38 (2): 183–206. PMC 5513685 . PMID 28988573.
1 2 3 4 5 Rosenbloom MJ, Pfefferbaum A (2008). "Magnetic resonance imaging of the living brain: evidence for brain degeneration among alcoholics and recovery with abstinence". Alcohol Research & Health. 31 (4): 362–376. PMC 3860463 . PMID 23584010.
↑ Steroids and Apparent Cerebral Atrophy on Computed Tomograph... : Journal of Computer Assisted Tomography
↑ Pereira JB, Westman E, Hansson O (October 2017). "Association between cerebrospinal fluid and plasma neurodegeneration biomarkers with brain atrophy in Alzheimer's disease". Neurobiology of Aging. 58: 14–29. doi: 10.1016/j.neurobiolaging.2017.06.002 . PMID 28692877. S2CID 46854877.
↑ Velickaite V, Giedraitis V, Ström K, Alafuzoff I, Zetterberg H, Lannfelt L, et al. (September 2017). "Cognitive function in very old men does not correlate to biomarkers of Alzheimer's disease". BMC Geriatrics. 17 (1): 208. doi: 10.1186/s12877-017-0601-6 . PMC 5591537 . PMID 28886705. Creative Commons Attribution 4.0 International License
1 2 "Cerebral Atrophy".
↑ Damasceno BP (2015). "Neuroimaging in normal pressure hydrocephalus". Dementia & Neuropsychologia. 9 (4): 350–355. doi:10.1590/1980-57642015DN94000350. PMC 5619317 . PMID 29213984.
↑ "Supplemental Information 3: Raw data concerning TAGA-LUAD sample aneuploidy scores from literature (PMID: 29622463)". doi: 10.7717/peerj.17545/supp-3 .{{cite web}}: Missing or empty |url= (help)
↑ "Cerebral Atrophy: Causes". Archived from the original on 26 January 2015. Retrieved 26 January 2015.
↑ Gordon N (August 1980). "Apparent cerebral atrophy in patients on treatment with steroids". Developmental Medicine and Child Neurology. 22 (4): 502–506. doi:10.1111/j.1469-8749.1980.tb04355.x. PMID 6250932. S2CID 32099986.

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[1] "Cerebral Atrophy Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Archived from the original on 2016-03-04. Retrieved 2014-03-28.

[Harris_2019-2] 1 2 Harris TC, de Rooij R, Kuhl E (September 2019). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9): 1941–1959. doi:10.1007/s10439-018-02148-2. PMC 6757025 . PMID 30341741.

[Sungura_2021-3] 1 2 Sungura R, Onyambu C, Mpolya E, Sauli E, Vianney JM (March 2021). "The extended scope of neuroimaging and prospects in brain atrophy mitigation: A systematic review". Interdisciplinary Neurosurgery. 23: 100875. doi: 10.1016/j.inat.2020.100875 . S2CID 224841818.

[Siegel_2006-4] Siegel JA, Saukko PJ, Houck MM (2013). Encyclopedia of Forensic Sciences. Academic Press. ISBN 978-0-12-382166-9.

[5] Peters R (February 2006). "Ageing and the brain". Postgraduate Medical Journal. 82 (964): 84–88. doi:10.1136/pgmj.2005.036665. PMC 2596698 . PMID 16461469.

[Chutinet_2014-6] Chutinet A, Rost NS (March 2014). "White matter disease as a biomarker for long-term cerebrovascular disease and dementia". Current Treatment Options in Cardiovascular Medicine. 16 (3): 292. doi:10.1007/s11936-013-0292-z. PMC 3964019 . PMID 24496967.

[Harris_de_Rooij_Kuhl_2019_pp._1941–1959-7] Harris, Taylor C.; de Rooij, Rijk; Kuhl, Ellen (2018-10-17). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9). Springer Science and Business Media LLC: 1941–1959. doi:10.1007/s10439-018-02148-2. ISSN 0090-6964. PMC 6757025 . PMID 30341741.

[8] Fox NC, Schott JM (January 2004). "Imaging cerebral atrophy: normal ageing to Alzheimer's disease". Lancet. 363 (9406): 392–394. doi:10.1016/S0140-6736(04)15441-X. PMID 15074306. S2CID 20494612.

[pmid20509907-9] Aktas D, Utine EG, Mrasek K, Weise A, von Eggeling F, Yalaz K; et al. (2010). "Derivative chromosome 1 and GLUT1 deficiency syndrome in a sibling pair". Mol Cytogenet. 3 (1): 10. doi: 10.1186/1755-8166-3-10 . PMC 2887874 . PMID 20509907.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[10] "Study links manic depression with brain tissue loss". EurekAlert!. Retrieved 2017-03-21.

[11] Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC (June 2013). "Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study". The American Journal of Psychiatry. 170 (6): 609–615. doi:10.1176/appi.ajp.2013.12050674. PMC 3835590 . PMID 23558429.

[12] Maia da Silva MN, Millington RS, Bridge H, James-Galton M, Plant GT (2017). "Visual Dysfunction in Posterior Cortical Atrophy". Frontiers in Neurology. 8: 389. doi: 10.3389/fneur.2017.00389 . PMC 5561011 . PMID 28861031.

[sciencedirect.com.proxy.library.nd.edu-13] Pereira JB, Westman E, Hansson O (October 2017). "Association between cerebrospinal fluid and plasma neurodegeneration biomarkers with brain atrophy in Alzheimer's disease". Neurobiology of Aging. 58: 14–29. doi: 10.1016/j.neurobiolaging.2017.06.002 . PMID 28692877. S2CID 46854877.

[Meyer_2013-14] 1 2 Meyer JS, Quenzer LF (2013). Psychopharmacology: Drugs, The Brain, and Behavior (2nd ed.). Sinauer Associates.

[Zahr_2017-15] 1 2 3 Zahr NM, Pfefferbaum A (2017). "Alcohol's Effects on the Brain: Neuroimaging Results in Humans and Animal Models". Alcohol Research. 38 (2): 183–206. PMC 5513685 . PMID 28988573.

[Rosenbloom_2008-16] 1 2 3 4 5 Rosenbloom MJ, Pfefferbaum A (2008). "Magnetic resonance imaging of the living brain: evidence for brain degeneration among alcoholics and recovery with abstinence". Alcohol Research & Health. 31 (4): 362–376. PMC 3860463 . PMID 23584010.

[17] Steroids and Apparent Cerebral Atrophy on Computed Tomograph... : Journal of Computer Assisted Tomography

[pmid28692877-18] Pereira JB, Westman E, Hansson O (October 2017). "Association between cerebrospinal fluid and plasma neurodegeneration biomarkers with brain atrophy in Alzheimer's disease". Neurobiology of Aging. 58: 14–29. doi: 10.1016/j.neurobiolaging.2017.06.002 . PMID 28692877. S2CID 46854877.

[19] Velickaite V, Giedraitis V, Ström K, Alafuzoff I, Zetterberg H, Lannfelt L, et al. (September 2017). "Cognitive function in very old men does not correlate to biomarkers of Alzheimer's disease". BMC Geriatrics. 17 (1): 208. doi: 10.1186/s12877-017-0601-6 . PMC 5591537 . PMID 28886705. Creative Commons Attribution 4.0 International License

[radiopaedia-20] 1 2 "Cerebral Atrophy".

[Damasceno2015-21] Damasceno BP (2015). "Neuroimaging in normal pressure hydrocephalus". Dementia & Neuropsychologia. 9 (4): 350–355. doi:10.1590/1980-57642015DN94000350. PMC 5619317 . PMID 29213984.

[22] "Supplemental Information 3: Raw data concerning TAGA-LUAD sample aneuploidy scores from literature (PMID: 29622463)". doi: 10.7717/peerj.17545/supp-3 .{{cite web}}: Missing or empty |url= (help)

[23] "Cerebral Atrophy: Causes". Archived from the original on 26 January 2015. Retrieved 26 January 2015.

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