To submit a comment for a journal article, please use the space above and note the following: We use cookies to help provide and enhance our service and tailor content and ads. Genes Brain Behav. Front Aging Neurosci. Title:Acetylome Regulation by Sirtuins in the Brain: From Normal Physiology to Aging and Pathology VOLUME: 19 ISSUE: 38 Author(s):Shaday Michan Affiliation:Instituto Nacional de Geriatría, Institutos Nacionales de Salud.Mexico D. F. 10200. By continuing you agree to the,, A Disease or Not a Disease? Epub 2015 May 9. Several senile changes in the central nervous system in cadavers were examined. severe early-onset COPD patients.In this review, after introducing the main concepts of lung ageing and COPD pathology, we focus on the role of (abnormal) … Microcebus murinus: a useful primate model for human cerebral aging and Alzheimer's disease? Normal and Successful Aging Normal aging has been conceptualized as the typical changes in behavior that occur with age (Schroots and Birren 1993). Front Psychiatry. Here again, the core issue is what is considered normal versus pathological. Respondents classified each symptom as normal aging or disease. Thus, rather than necessarily reflecting early signs of disease, these changes may be part of normal aging, and may inform on why the aging brain is so much more susceptible to AD than is the younger brain. In this study, CSF Aβ42/40 is classified as normal (A-) or abnormal (A+), p-tau as normal (T-) or abnormal (T+), and t-tau as normal (N-) or abnormal (N+) based on the cutoff values above. Longitudinal episodic memory decline in…, Figure 1. However, improvement can only be marginal, unless the system is altered such that a different set of deleterious changes can accumulate in a way that leads to longevity. Synchronization of deleterious changes cannot be perfect, because they are the consequence of the imperfect genome and are influenced throughout the lifespan by environment, and by random events. Selected studies on amyloid and…, Figure 15. Upper panel shows regions of high vs. lower cortical expansion from macaque monkeys to humans (maps re-computed from (Hill et al., 2010)). Three major dimensions of human brain cortical ageing in relation to cognitive decline across the eighth decade of life. Overall, behavioral deficits in animals with normal aging occur at older ages than the earliest deficits in Alzheimer disease mice. The left two panels show the 3D reconstruction of the complete morphology of each spine of an apical dendritic segment at 100 μm distance from the soma, and the estimation of the spine volumes shown in color codes (0–1.345 μm, Upper panel: CSF biomarkers of Aβ and p-Tau, indexing brain levels of amyloid and tangle load, respectively, correlate with temporal atrophy in stable MCI patients from ADNI (n = 213). CSF biomarkers and regional atrophy…, Figure 14. The recognition of aging as a combination of diseases (together with other deleterious changes) should expose the fundamental role of aging in chronic diseases; and to target aging, it may also invite various strategies normally aimed at treating such diseases. Entropy explains aging, genetic determinism explains longevity, and undefined terminology explains misunderstanding both. Author information: (1)Department of Neurology, Gunma University School of Medicine. Left panel: By using a random-effects pattern-mixture model, Josefsson and colleagues (2012), found individual differences both in initial memory scores (offset at time 0) and change over time in their large sample (n > 1500) of initially healthy participants, with some maintaining their functional level (18%), some showing age-average decline (68%), while some declined (13%). Functional studies have supported that there is an only partially coin- ... pathology can be diverse for L1 and L2 depending upon dif - Many fear the futility of fighting chronic diseases without striving to wholly understand their ultimate cause, thinking that conditions of success (to perfectly synchronize the collapse of an organism) are less than what we could achieve with a different investment. We recommend that commenters identify themselves with full names and affiliations. Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO. Although this initial dysfunction differs among individuals within a population, an ever increasing number of other dysfunctional cells, pathologies, and diseases always follows closely behind. While normal aging affects both a fronto-striatal network important for cognitive control and executive function (green structures), AD has additional effects on a temporo-parietal network important for episodic memory function (purple structures). With the slow progression of age-related dementias such as Alzheimer's disease (AD), it is difficult to distinguish age-related changes from effects of undetected disease. Thus, rather than necessarily reflecting early signs of disease, these changes may be part of normal aging, and may inform on why the aging brain is so much more susceptible to … doi: 10.3233/JAD-179903. A speculative model of Aβ-atrophy…, Figure 16. Brain Res. Mormino EC(1), Papp KV(2). PDF | On Aug 9, 2017, Emilie T. Reas published Amyloid and Tau Pathology in Normal Cognitive Aging | Find, read and cite all the research you need on ResearchGate The right panel shows percentage annual change in cortical thickness estimated cross-sectionally in the same sample of participants. Tim Watt | January 10, 2014 Print Email. Would you like email updates of new search results? Lower panel shows the same data, but the values have been re-scaled to yield a mean of zero and a standard deviation of one, to allow better visualization of regional distribution of change. The results are displayed on the white matter surface of the brain. Longitudinal cortical volumetric reductions in aging, Upper panel shows annual percent volume reduction…, Correlations between age and cortical thickness in a healthy multi-site adult…, Figure 4. Misattribution of normal aging signs as disease may prompt physicians to overmedicate and overtreat patients, resulting in adverse clinical outcomes. We conclude that it will be difficult to understand AD without understanding why it preferably affects older brains, and that we need a model that accounts for age-related changes in AD-vulnerable regions independently of AD-pathology. Discourse samples were analyzed according to aspects of coherence using a methodology based on frame analysis (Goffman, 1974). Mecocci P, Baroni M, Senin U, Boccardi V. J Alzheimers Dis. Cross-sectional estimates of annual rate of cortical thinning in the entorhinal cortex across the adult life indicate a marked increase in atrophy from 50 years. Also, estimated change is smaller in the cross-sectional compared to the longitudinal results. Second, TDP-43 pathology in this brain region is not associated with brain aging and/or normal cognition but is instead strongly associated with cognitive impairment. CSF biomarkers and regional atrophy in aging and MCI, Figure 15. Supported by grants from the National Institute on Aging (to V.N.G.). ), and whether it leads to a decrement in quality of life. 2020 Dec 4;12:553461. doi: 10.3389/fnagi.2020.553461. For some, the colors of the effects were changed to aid discriminability between the different studies. Different structural features of the cerebral cortex have different genetic architecture and are reflecting different neurobiological events. Representative studies of the relationship between amyloid levels (PiB PET or CSF Aβ) and cortical thickness (baseline) or cortical atrophy (longitudinal) in healthy elderly (Storandt et al., 2009, Fjell et al., 2010a, Tosun et al., 2010a, Becker et al., 2011, Arenaza-Urquijo et al., 2013b). Selected studies on amyloid and cortical structure in non-demented older adults, Figure 16. (2012). pdf files. Volume is expressed in units of standard deviations. Title:Acetylome Regulation by Sirtuins in the Brain: From Normal Physiology to Aging and Pathology VOLUME: 19 ISSUE: 38 Author(s):Shaday Michan Affiliation:Instituto Nacional de Geriatría, Institutos Nacionales de Salud.Mexico D. F. 10200. The A/T/N classifications were also mapped to the corresponding existing National Institute on Aging-Alzheimer’s Association (NIA-AA) criteria as it had been previously done [ 23 ]. The right panel shows annual volumetric decline in regions of high (z ≥ 0.5 SD), medium (−0.5 < z < 0.5) and low (z ≤ −0.5) evolutionary expansion. In contrast, lesions in other parts of the cortex are less directly related to memory problems and may also be easier to compensate for, thus reducing the likelihood of an MCI/AD diagnosis. Bons N, Rieger F, Prudhomme D, Fisher A, Krause KH. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. [Neuropathological aspects of normal and abnormal aging]. [Article in Japanese] Okamoto K(1). Instead, it combines all age-related diseases and their preclinical forms, in addition to other pathological changes. Across groups, we see common patterns of standardized change in the lateral and medial temporal lobe (including the hippocampus, not shown), and a distinct pattern characterizing only healthy elderly in the prefrontal cortex, especially the orbitofrontal part. Neuropathological basis of magnetic resonance images in aging and dementia. Data from (Fjell et al., 2013a). COVID-19 is an emerging, rapidly evolving situation. Corresponding Author. The worldwide epidemiology of prostate cancer: perspectives from autopsy studies. The present study compared discourse ability across three groups: patients with mild Alzheimer's disease (AD), healthy old-elderly individuals (OE, >80 years), and normal control subjects (NC). We review recent research on changes of the cerebral cortex and the hippocampus in aging and the borders between normal aging and AD. Some consider that aging, similar to disease, can be treated and ultimately stopped: The aging-disease false dichotomy: understanding senescence as pathology. Cox SR, Harris MA, Ritchie SJ, Buchanan CR, Valdés Hernández MC, Corley J, Taylor AM, Madole JW, Harris SE, Whalley HC, McIntosh AM, Russ TC, Bastin ME, Wardlaw JM, Deary IJ, Tucker-Drob EM. Epub 2013 Mar 16. Annual percentage change in brain volume for six selected areas of the default mode network (DMN) in 132 healthy elderly (based on data from Figure 2). Data from the Alzheimer’s Disease Neuroimaging Initiative. 2021 Jan 4. doi: 10.1038/s41380-020-00975-1. Sci Rep. 2020 Dec 11;10(1):21803. doi: 10.1038/s41598-020-78471-3. 2008 Jan;63(1):72-80. doi: 10.1002/ana.21296. Differential Brain Activity in Regions Linked to Visuospatial Processing During Landmark-Based Navigation in Young and Healthy Older Adults. K01 AG029218/AG/NIA NIH HHS/United States, R01 AG031224/AG/NIA NIH HHS/United States, U01 AG024904/AG/NIA NIH HHS/United States, NIA K01AG029218/AG/NIA NIH HHS/United States. A speculative model of Aβ-atrophy relationships in normal aging and MCI, NLM In a study of preclinical AD, Olichney et al. What can be expected in normal aging, and where does normal aging stop and pathological neurodegeneration begin? Respondents classified each symptom as normal aging or disease. As can be seen, the apparent thickening of the anterior cingulate cortex in the cross-sectional analyses is not confirmed by the longitudinal results, indicating that this likely arises from issues with selective sampling. Please enter a term before submitting your search. Copyright © 2014 Elsevier Ltd. All rights reserved. Data from (Fjell et al., 2012). Dendritic spine morphology in aging, Benavides-Piccione et al (2013) 3D reconstructed 8900 individual…, Figure 14. By continuing you agree to the use of cookies. Such abnormal behaviors are easy to characterize, but it is much more difficult to delineate behavioral changes that occur in the absence of obvious disease, such as those associated with aging. However, there is often no right or wrong answer, as the answer is shaped by societal attitudes, political forces, religious issues, and business interests, and not just medicine, Digging deeper into the biochemical roots of the ‘aging versus disease’ debate, we see that living is associated with the accumulation of deleterious changes at all levels of biological organization of an organism, and furthermore, that these changes may be affected by genetic, environmental, and stochastic processes [. Ramanoël S, Durteste M, Bécu M, Habas C, Arleo A. Age-related acceleration of decline in elderly has been confirmed with longitudinal data. NIH However, aging is as natural as age-related diseases, which both essentially comprise pathological changes. This site needs JavaScript to work properly. Different effects of age on cortical surface area, thickness and gyrification, Figure 8. Fronto-striatal vs. temporo-parietal networks, While normal aging affects both a fronto-striatal network important…, Figure 9. Telling the Difference Between Normal and Abnormal Aging. Alzheimer's Disease Neuroimaging Initiative, See this image and copyright information in PMC. (2013) used their incidental verbal learning paradigm to compare the P600 and N400 ERPs of cognitively normal elderly individuals with preclinical AD (i.e., they showed subsequent cognitive decline and/or AD pathology at autopsy) and normal elderly individuals who remained cognitively normal. Front Hum Neurosci. Upper panel shows annual percent volume reduction of the cerebral cortex in a longitudinal sample of 132 healthy elderly (55–91 years at baseline) from ADNI (Alzheimer’s Disease Neuroimaging Initiative). Cortical surface area, thickness and gyrification are all negatively related to age, but to a different degree and with somewhat different regional distribution of effects. Pathological definition is - of or relating to pathology. For instance, some degree of glucose intolerance is thought to be a part of normal aging, but diabetes, though very common, is considered a disease. Get the latest public health information from CDC:, Get the latest research information from NIH:, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: Debates. This lesson looks into the differentiation between what is considered normal, or primary, aging and what is considered abnormal, or secondary, aging. The not-so-close relationship between biological aging and age-associated pathologies in humans. Many of those who oppose the disease label, view aging as a normal, natural, inevitable process that, although predisposing individuals to disease risk, is separate from the pathology of a given disease [. Copyright © 2020 Elsevier Inc. except certain content provided by third parties. Aging and Alzheimer’s disease pathology Renpei Sengoku ... abnormal protein accumulation cannot explain all clinical symptoms of AD. Glio-vascular changes during ageing in wild-type and Alzheimer's disease-like APP/PS1 mice. In contrast, the correlations between atrophy and Aβ in amyloid positive healthy elderly (Aβ. As the divide fostering this dichotomy gets lost in abstraction, our mortal coils must forego semantics: we should decide on designations for age-related diseases that not only encompass the origin and history of the designations, but also their utility in the future. Lysozyme in abnormal dermal elastic fibers of cutaneous aging, solar elastosis and pseudoxanthoma elasticum S. Albrecht Department of Pathology, Women's College Hospital, University of Toronto, Canada Both the medial and the lateral DMN changed significantly more than the whole brain rate of 0.44% (mean atrophy in the medial DMN: 0.70%, t [131] = 4.75, p < 10. In real life, the Holmes’ celebrated centenarian one-hoss shay is as impossible to achieve as healthy aging, because there is absolutely nothing healthy about aging. Please note that the scale is different between MCI/healthy and AD/healthy to allow appreciation of the regional patterns of effects across groups. The debate on the relationship between aging and disease is centered on whether aging is a normal/natural/physiological process or it represents a pathology. The consequences and dangers of miscategorisation. Considering this relationship from medical, molecular, social, and historical perspectives, we argue that aging is neither a disease, nor a non-disease. Interventions to slow aging in humans: are we ready?. It is important to ... observed even in the normal aging brain. Lower panel shows regions of high vs. lower volumetric reduction in aging (based on the data from Figure 2). The effects of aging and Alzheimer's disease on cerebral cortical anatomy: specificity and differential relationships with cognition. By contrast, researchers of the ‘aging as a disease’ camp note the many similarities between the two, and advocate officially designating aging as a disease (therefore suggesting treatment a possibility). Importantly, these regions show high levels of amyloid deposition in AD, and are both structurally and functionally vulnerable early in the disease. MB), Help with In it, you'll learn about the stages of aging, normal vs. abnormal aging, implications of aging on overall wellness, and strategies, tips and local resources for positive aging. DOI: Overall, this study shows that normal aging enlarges the ventricular system, but never causes abnormal ventricular enlargement. There is an ambiguity between clinical symptoms and neuropathological findings. Blue-cyan colors represent areas that are reduced more in one year than the rest of the cortex, while red-yellow colors represent areas of less than average reduction. Gyrification index is defined as the ratio between the buried cortex and the visible, outer surface cortex. The often-observed fronto-temporal pattern of relative increased atrophy is evident, with medial parietal cortex/posterior cingulate as additional regions with high rates of atrophy in aging. Left panel shows percentage annual change in cortical thickness measured longitudinally in a sample of healthy elderly (n = 207, 60–93 years). Ann Neurol. Should we treat aging as a disease? One speculative explanation for the discrepant Aβ-atrophy relationships in healthy aging vs. MCI (see Figure 12) would be to assume that lesions related to amyloid levels can occur in several places in the cortex in aging. Aging in its broadest sense is the gradual progressive impairment or deterioration of normal tissue function and tissue homeostasis. Figures modified from Josefsson et al. In a recent study published in The Journal of Neuroscience, Marks et al. Cellular correlates of cortical thinning throughout the lifespan.  |  In mild cognitive impairment (MCI), rates of cortical volumetric reductions are more than double that seen in healthy aging across large areas of the cerebral cortex, and rates more than three times larger are seen in AD. Brain-Age Prediction Using Shallow Machine Learning: Predictive Analytics Competition 2019. Until the end, it was as good as new, but then suddenly, it ‘went to pieces all at once – all at once, and nothing first – just as bubbles do when they burst.’, The idea of the wear-free and break-free centenarian carriage is analogous to the concept of healthy human aging; a proclaimed target for antiaging research. Bakkour A, Morris JC, Wolk DA, Dickerson BC. In other respects, the results are more similar. Keywords: Evans’ index; Gerotarget; aging; brain; enlargement; ventricular system. Deciding whether to categorize aging as a disease is further complicated by the ambiguity of defining terms such as aging, disease, or pathology. The functional consequences of these brain changes are related to their severity and extent, and can range from almost none via mild cognitive decline to dementia. Atrophy maps are standardized within each group by Z-transformation, yielding maps showing areas of more (blue-cyan) vs. less (red-yellow) atrophy for each group in terms of standard deviations. Evolutionary expansion and volume decline in aging, Figure 10. The question ‘is aging a disease?’ must also be considered in terms of its relation to medicalization: a social process through which a formerly normal condition becomes a medical problem (e.g., shyness vs. avoidant personality disorder, or children's playful behavior vs. attention deficit hyperactivity disorder). 2015 Sep 16;1620:153-68. doi: 10.1016/j.brainres.2015.04.056. Profant O, Škoch A, Tintěra J, Svobodová V, Kuchárová D, Svobodová Burianová J, Syka J. This would cause the observed discrepancy in regional distribution of amyloid-atrophy relationships between clinically normal older adults and MCI patients. Atrophy across the cortex in the healthy elderly and the AD patients correlated .81, showing substantial overlap in regional vulnerability. Data from (Hogstrom et al., 2012). Author information: (1)Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA, USA. Specifically, they evaluated the relationship between aging-related memory deficits and structural and functional alterations in the medial temporal lobe, and they assessed whether the observed neural … 2006 Mar;5(2):120-30. doi: 10.1111/j.1601-183X.2005.00149.x. The core issue here is to weigh in viewing disease as a condition that affects a subset of the population (and can thus be ‘treated’) with the fact that aging affects everybody, and that there is no evidence (at least in human populations) that it can be avoided. Cross-sectional vs. longitudinal results, Left panel shows percentage annual change in cortical thickness…, Figure 7. Alzheimer's disease (AD); Amyloid; Cerebral cortex; Default mode network (DMN); Hippocampus; Normal aging. The bulk of this evidence indicates that cerebral …. As mentioned above, this should be interpreted in light of age-related pathology also occurring much later than Alzheimer changes. One criterion to decide whether aging is a disease is to determine if, as a condition, it is indeed treatable. Normal, Aging, and Pathologic. The aging versus disease debate is simply false, because aging is a combination of all age-related diseases (in both clinical and preclinical forms) together with other deleterious changes. 2020 Dec 2;11:604478. doi: 10.3389/fpsyt.2020.604478. Likewise, chronic diseases and their preclinical forms (combined with a myriad of deleterious changes not yet pathologized) are nothing but aging. On average, residents classified 73.4% of symptoms correctly. The average duration from year 2 to the time of death was 4.1 m 1.6 years for the normal aging cases and 3.3---1.4 years for the pathological aging cases, which makes it unlikely that the greater degree of pathology in the latter subgroup was related to a longer time from testing to autopsy.  |  People over the age of 70 years have multiple chronic diseases; for instance, based on autopsy records, the prevalence of prostate tumors in old men is nearly universal [. However, progression through our lifespan and old age, devoid of pathology or dysfunction, just as a sudden, perfectly synchronized collapse of the one-hoss shay, is not only not observed, but nearly impossible to imagine. 2020 Oct 29;14:552111. doi: 10.3389/fnhum.2020.552111. eCollection 2020. We suggest that regions characterized by a high degree of life-long plasticity are vulnerable to detrimental effects of normal aging, and that this age-vulnerability renders them more susceptible to additional, pathological AD-related changes. Comparison of the standardized pattern of atrophy in a group of APOE ε4 negative elderly with normal levels of CSF Aβ, mild cognitive impairment (MCI) and AD. We extracted the effect sites from the published figures, and projected them onto the same standard brain to allow visual comparison of the results. In medicine, whether a condition is a disease is often determined by how abnormal it is (e.g., how many standard deviations is it from the population norm? The common conception has been that subtle declines in cognition occur as part of the normal aging process. We would like to thank J.P. de Magalhaes, A. Bernstein, and T. Kimura for stimulating discussions on this topic. Thus, some individual cells may become dysfunctional first, and some diseases may appear before others. In fact, we have a guide all about positive aging for seniors. APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging John C. Morris MD. 2013 Aug 1;76:332-44. doi: 10.1016/j.neuroimage.2013.02.059. Lesions targeting the temporal lobe will tend to yield memory problems that are difficult to compensate for, increasing the likelihood of an MCI diagnosis. Amyloid Accumulation and Cognitive Decline in Clinically Normal Older Individuals: Implications for Aging and Early Alzheimer's Disease. Correlations between age and cortical thickness in a healthy multi-site adult life-span sample (n = 1100, age 18–94). 2018;64(s1):S397-S404. Figure from (Fjell et al., 2013a). Life-span trajectories of volumetric reductions, Cross-sectional estimates of adult life-span trajectories of total…, Figure 6. Evans' index values > 0.30 should reflect an underlying neurological condition in every individual. Ignoring the underlying biochemical mechanisms, as well as denying molecular and/or cellular damage and other deleterious processes roles in pathology, can only hinder our ability to produce truly beneficial therapies to fight age-related diseases. Science & Society Series: Current Trends in Aging and Age-Related Diseases, We use cookies to help provide and enhance our service and tailor content and ads. Longitudinal cortical volumetric reductions in…, Figure 2. Normal aging is due to physiological processes over a person’s lifetime, in which the biological clock controls development and survival of nerve cells. In the 19th century, Harvard medical professor and writer Oliver Wendell Holmes wrote a poem about a ‘one-hoss shay’: a carriage that was built to last precisely 100 years. The cut point value was included in the … Correlations exceed −.40 in large regions, approaching −.70 in the prefrontal and lateral temporal cortex. A better understanding of the main differences and similarities between normal lung ageing and the pathology of COPD may improve our understanding of the mechanisms driving COPD pathology, in particular in those patients that develop the most severe form of COPD at a relatively young age, i.e. Common for these studies was the use of anatomically unbiased surface-based cortical analyses using FreeSurfer ( 110, 151 The modern advances in technology, health care and nutrition, led to significant increase in the life expectancy of humans and animals. The researchers were able to identify environmental and genetic factors predicting group membership. With regard to aging, drawing a line to determine if an effect, though intertwined, is definitively excluded as a part of the pathology of a disease, lies at the core of this debate, and revolves around what we consider to be natural. Differences in cortical atrophy rates between healthy elderly and Mild Cognitive Impairment/Alzheimer’s Disease, Figure 12. How to use pathological in a sentence. Evolutionary expansion and volume decline…, Figure 9. On average, residents classified 73.4% of symptoms correctly. Aging of the default mode network, Annual percentage change in brain volume for…, Figure 11. Vidal-Pineiro D, Parker N, Shin J, French L, Grydeland H, Jackowski AP, Mowinckel AM, Patel Y, Pausova Z, Salum G, Sørensen Ø, Walhovd KB, Paus T, Fjell AM; Alzheimer’s Disease Neuroimaging Initiative and the Australian Imaging Biomarkers and Lifestyle flagship study of ageing. This normalcy-pathology homology is critical to understand, since aging itself is the major risk factor for sporadic AD. Benavides-Piccione et al (2013) 3D reconstructed 8900 individual dendritic spines from layer III pyramidal neurons in the cingulate cortex from two male humans of age 40 and 85 years, using intracellular injections of Lucifer Yellow in fixed tissue. University of Massachusetts, Amherst, MA 01002, USA, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. normal and abnormal aging may be anticipated. eCollection 2020. As can be seen, annual decline in aging is related to degree of expansion during evolution (for all comparisons, p < .05, corrected). The following are the supplementary information to this article: © 2016 Elsevier Ltd. All rights reserved. Figure 1. Brain Aging and Late-Onset Alzheimer's Disease: A Matter of Increased Amyloid or Reduced Energy? Longitudinal episodic memory decline in aging, Left panel: By using a random-effects pattern-mixture…, Figure 2. This forum is intended for constructive dialog. Data from (Fjell et al., 2012). Neuroimage. Degeneration of the disc is associated with several clinical conditions, including herniation of the nucleus pulposus, mechanical back pain, spinal stenosis, and other spinal deformities such as scoliosis. Differences in cortical atrophy rates…, Figure 11. Aging: progressive decline in fitness due to the rising deleteriome adjusted by genetic, environmental, and stochastic processes. Deciding whether to categorize aging as a disease is further complicated by the ambiguity of defining terms such as aging, disease, or pathology.  |  Comparison of aging and Mild Cognitive Impairment/Alzheimer’s Disease, Figure 13. A growing amount of data using light and electron microscopy, immunocytochemistry, uptake of brain markers and metabolic studies suggest that the pathogenesis of Alzheimer's disease may be due to impaired vascular delivery of nutrients to the brain.

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