Normal Aging Induces Changes in the Brain and Neurodegeneration Progress: Review of the Structural, Biochemical, Metabolic, Cellular, and Molecular Changes

Lee, Jiseon; Kim, Hee‐Jin

doi:10.3389/fnagi.2022.931536

Cited by 92 publications

(45 citation statements)

References 115 publications

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“…Due to neurophysiological and neuroanatomical alterations including brain atrophy ( Lee and Kim, 2022 ), cortical thinning ( McGinnis et al, 2011 ; Fjell et al, 2014 ), and neurotransmitter disbalance ( Mora et al, 2007 ), EEG recordings undergo characteristic changes with growing age. Elderly patients under general anesthesia are known to exhibit a decreased power in the EEG due to an amplitude reduction of 2- to 3-fold compared to young adults ( Purdon et al, 2015a ).…”

Section: Discussionmentioning

confidence: 99%

Unveiling age-independent spectral markers of propofol-induced loss of consciousness by decomposing the electroencephalographic spectrum into its periodic and aperiodic components

LeRoy

Major

Bublitz

et al. 2023

Front. Aging Neurosci.

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BackgroundInduction of general anesthesia with propofol induces radical changes in cortical network organization, leading to unconsciousness. While perioperative frontal electroencephalography (EEG) has been widely implemented in the past decades, validated and age-independent EEG markers for the timepoint of loss of consciousness (LOC) are lacking. Especially the appearance of spatially coherent frontal alpha oscillations (8–12 Hz) marks the transition to unconsciousness.Here we explored whether decomposing the EEG spectrum into its periodic and aperiodic components unveiled markers of LOC and investigated their age-dependency. We further characterized the LOC-associated alpha oscillations by parametrizing the adjusted power over the aperiodic component, the center frequency, and the bandwidth of the peak in the alpha range.MethodsIn this prospective observational trial, EEG were recorded in a young (18–30 years) and an elderly age-cohort (≥ 70 years) over the transition to propofol-induced unconsciousness. An event marker was set in the EEG recordings at the timepoint of LOC, defined with the suppression of the lid closure reflex. Spectral analysis was conducted with the multitaper method. Aperiodic and periodic components were parametrized with the FOOOF toolbox. Aperiodic parametrization comprised the exponent and the offset. The periodic parametrization consisted in the characterization of the peak in the alpha range with its adjusted power, center frequency and bandwidth. Three time-segments were defined: preLOC (105 – 75 s before LOC), LOC (15 s before to 15 s after LOC), postLOC (190 – 220 s after LOC). Statistical significance was determined with a repeated-measures ANOVA.ResultsLoss of consciousness was associated with an increase in the aperiodic exponent (young: p = 0.004, elderly: p = 0.007) and offset (young: p = 0.020, elderly: p = 0.004) as well as an increase in the adjusted power (young: p < 0.001, elderly p = 0.011) and center frequency (young: p = 0.008, elderly: p < 0.001) of the periodic alpha peak. We saw age-related differences in the aperiodic exponent and offset after LOC as well as in the power and bandwidth of the periodic alpha peak during LOC.ConclusionDecomposing the EEG spectrum over induction of anesthesia into its periodic and aperiodic components unveiled novel age-independent EEG markers of propofol-induced LOC: the aperiodic exponent and offset as well as the center frequency and adjusted power of the power peak in the alpha range.

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Section: Discussionmentioning

confidence: 99%

Unveiling age-independent spectral markers of propofol-induced loss of consciousness by decomposing the electroencephalographic spectrum into its periodic and aperiodic components

LeRoy

Major

Bublitz

et al. 2023

Front. Aging Neurosci.

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“…Hence, the increase in slope in old group in HFR could be a reflection of age-related changes in these neural processes. In addition, it could be due to age-related alteration of physiological properties in brain tissue (Aalami et al, 2003; Lee and Kim, 2022), cortical thickness (Lillie et al, 2016) and skin conductance (Lim et al, 1996; Venables and Mitchell, 1996), which could determine the amplitude of this high-frequency signal measured from the scalp.…”

Section: Discussionmentioning

confidence: 99%

Slope of the power spectral density flattens at low frequencies (<150 Hz) with healthy aging but also steepens at higher frequency (>200 Hz) in human electroencephalogram

Aggarwal

Ray

2023

Preprint

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Brain signals such as electroencephalogram (EEG) often show oscillations at various frequencies, which are represented as distinct ″bumps″ in the power spectral density (PSD) of these signals. In addition, the PSD also shows a distinct reduction in power with increasing frequency, which pertains to aperiodic activity and is often termed as the ″1/f″ component. While a change in periodic activity in brain signals with healthy aging and mental disorders has been reported, recent studies have shown a reduction in the slope of the aperiodic activity with these factors as well. However, these studies only analysed PSD slopes over a limited frequency range (<100 Hz). To test whether the PSD slope is affected over a wider frequency range with aging and mental disorder, we collected EEG data with high sampling rate (2500 Hz) from a large population of elderly subjects (>49 years) who were healthy (N=217) or had mild cognitive impairment (MCI; N=11) or Alzheimer′s Disease (AD; N=5), and analysed the PSD slope till 800 Hz. Consistent with previous studies, the 1/f slope up to ~150 Hz reduced with healthy aging. Surprisingly, we found the opposite at higher frequencies (>200 Hz): the slope increased with age. This result was observed in all electrodes, for both eyes open and eyes closed conditions, and for different reference schemes. Slopes were not significantly different in MCI/AD subjects compared to age and gender matched healthy controls. Overall, our results constrain the biophysical mechanisms that are reflected in the PSD slopes in healthy and pathological aging.

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“…There are gross and microscopic alterations in the brain structure and metabolism (e.g., volume loss, demyelination, enlargement of ventriculi, dysfunction of the cholinergic system, decreased ligand binding affinity of several receptors, alteration in gene expression, a decrease in synaptic function, lipofuscin accumulation, disturbances of the blood-brain-barrier (BBB) function, an increase in cellular waste, etc.) [ 14 ]. Tissue atrophy, alteration in certain neurotransmitters, and dyshomeostasis of the cellular environment accompany normal aging and ultimately result in cognitive decline [ 14 ].…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

“…[ 14 ]. Tissue atrophy, alteration in certain neurotransmitters, and dyshomeostasis of the cellular environment accompany normal aging and ultimately result in cognitive decline [ 14 ].…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

New Pathways Identify Novel Drug Targets for the Prevention and Treatment of Alzheimer’s Disease

Penke

Szücs

Bogár³

2023

IJMS

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Alzheimer’s disease (AD) is an incurable, progressive neurodegenerative disorder. AD is a complex and multifactorial disease that is responsible for 60–80% of dementia cases. Aging, genetic factors, and epigenetic changes are the main risk factors for AD. Two aggregation-prone proteins play a decisive role in AD pathogenesis: β-amyloid (Aβ) and hyperphosphorylated tau (pTau). Both of them form deposits and diffusible toxic aggregates in the brain. These proteins are the biomarkers of AD. Different hypotheses have tried to explain AD pathogenesis and served as platforms for AD drug research. Experiments demonstrated that both Aβ and pTau might start neurodegenerative processes and are necessary for cognitive decline. The two pathologies act in synergy. Inhibition of the formation of toxic Aβ and pTau aggregates has been an old drug target. Recently, successful Aβ clearance by monoclonal antibodies has raised new hopes for AD treatments if the disease is detected at early stages. More recently, novel targets, e.g., improvements in amyloid clearance from the brain, application of small heat shock proteins (Hsps), modulation of chronic neuroinflammation by different receptor ligands, modulation of microglial phagocytosis, and increase in myelination have been revealed in AD research.

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Normal Aging Induces Changes in the Brain and Neurodegeneration Progress: Review of the Structural, Biochemical, Metabolic, Cellular, and Molecular Changes

Cited by 92 publications

References 115 publications

Unveiling age-independent spectral markers of propofol-induced loss of consciousness by decomposing the electroencephalographic spectrum into its periodic and aperiodic components

Unveiling age-independent spectral markers of propofol-induced loss of consciousness by decomposing the electroencephalographic spectrum into its periodic and aperiodic components

Slope of the power spectral density flattens at low frequencies (<150 Hz) with healthy aging but also steepens at higher frequency (>200 Hz) in human electroencephalogram

New Pathways Identify Novel Drug Targets for the Prevention and Treatment of Alzheimer’s Disease

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