Alzheimer's Disease
Marc E. Agronin in Alzheimer's Disease and Other Dementias, 2014
Research suggests that either intracellular hyperphosphorylated tau spreads cell-to-cell to induce pathology in the next cell or pathology in one cell induces pathology in neighboring cells without movement of tau from one to the next. In a transgenic mouse model followed over 22 months, abnormal tau spread along a linked anatomic pathway (Liu et al., 2012). On a larger level, close inspection of the brain tissue indicates that the following key brain regions are affected successively during the course of AD: the entorhinal cortex, the hippocampus, and the basal forebrain, and, eventually, general cortical regions. Both the entorhinal cortex and the hippocampus, which are located adjacent to one another in the temporal lobes, are critical to memory formation. Functional scanning has found that deterioration in these structures is an early indicator of AD.
Advanced Glycation Endproducts and Neurological Diseases
Sara C. Zapico in Mechanisms Linking Aging, Diseases and Biological Age Estimation, 2017
AD is the most common age-related degenerative disease of the nervous system characterized by severe diffuse cerebral atrophy evolving over a few years, which leads to progressive dementia due to neuronal death. Neuronal degeneration is mostly localized in the entorhinal cortex, hippocampus, and medial temporal lobe areas. Histologically, AD is characterized by three microscopic changes: (1) Intracellular deposits of thick fibers in the form of coils, loops or tangles of insoluble phosphorylated tau protein called neurofibrillary tangles (Braak and Braak 1988); (2) Deposits of amorphous material dispersed throughout the cerebral cortex composed of the protein, amyloid, which is surrounded by degenerating nerve terminals: amyloid plaques. The β-amyloid, a 39–43 amino acid peptide, the principal component in the amyloid plaques, is formed by intracellular proteolytic degradation of the transmembrane β-amyloid precursor protein (Tienari et al. 1997); (3) Neuronal degeneration, which is more evident in the hippocampus and is thought to reflect, in part, a defect in the phagocytosis of degraded proteins.
Bacteriophage Involvement in Neurodegenerative Diseases
David Perlmutter in The Microbiome and the Brain, 2019
There are a variety of neurodegenerative diseases characterized by a progressive cognitive decline accompanied by memory loss, and Alzheimer’s disease is the most common among them.1 These cognitive symptoms and neurodegeneration are primarily related to neuronal death caused by deposits of misfolded proteins in the brain—β-amyloid and tau proteins in Alzheimer’s, α-synuclein in Parkinson’s disease, and SOD1 and TDP-43 in amyotrophic lateral sclerosis (ALS).2,3 The appearance of these extracellular protein aggregates results in neuronal death and synapse loss. This degradation in turn contributes to neural atrophy that, at least in the initial stages of Alzheimer’s disease, is localized within the hippocampus and the entorhinal cortex.4,5
Time Reproduction Deficits at Young Adult Follow-Up in Childhood ADHD: The Role of Persistence of Disorder and Executive Functioning
Published in Developmental Neuropsychology, 2019
Russell A. Barkley, Mariellen Fischer
Reproduction errors are inversely related to estimation errors (Wittmann & Paulus, 2007). Individuals who overestimate a sample time duration usually under-reproduce that time interval when requested to do so. This relationship reflects the subjective sense that time durations are progressing more slowly than is actually the case, perhaps due to errors in an internal clock or time keeping mechanism (Gilden & Marusich, 2009; Wittmann & Paulus, 2007). That mechanism is likely located in the lateral entorhinal cortex adjacent to the hippocampus and near the temporal poles (Tsao et al., 2018). Impaired sense of time and the internal clock contributing to it also may be linked to impaired dopamine dynamics in the brain (Gilden & Marusich, 2009). Dopaminergic problems are routinely associated with ADHD and underlie the rationale for and utility of psychostimulant medications in its management. In short, ADHD is related to a reliably inaccurate and highly variable perception of time, and especially its reproduction (Coghill et al., 2018; Norieka et al., 2013), that may reflect impairment in a central time keeping mechanism and may be related to disturbed dopamine dynamics associated with ADHD.
Examining the relationship between perinatal depression and neurodevelopment in infants and children through structural and functional neuroimaging research
Published in International Review of Psychiatry, 2019
Christy Duan, Megan M. Hare, Morganne Staring, Kristina M. Deligiannidis
Expanding upon their previous work using structural MRI (Qiu et al., 2013), a functional MRI study of 24 mother-infant dyads assessed maternal depression using the EPDS at 26 weeks gestation and 3 months after delivery (Qiu et al., 2015). Infants underwent resting state fMRI at 6 months. In infants exposed to higher antenatal maternal depressive symptoms, there was increased connectivity between the amygdala and areas in three brain networks. In the emotional regulation network, there was increased connectivity to the left insula and bilateral medial prefrontal cortex (anterior cingulate, medial orbitofrontal, ventromedial prefrontal cortices). In the sensory and perceptual network, there was increased connectivity to the left superior, middle, and temporal cortices. Finally, in the emotional memory network, there was increased connectivity to the left entorhinal cortex.
Alpha adrenergic receptors have role in the inhibitory effect of electrical low frequency stimulation on epileptiform activity in rats
Published in International Journal of Neuroscience, 2023
Mahmoud Rezaei, Nooshin Ahmadirad, Zahra Ghasemi, Amir Shojaei, Mohammad Reza Raoufy, Victoria Barkley, Yaghoub Fathollahi, Javad Mirnajafi-Zadeh
All experimental procedures, including brain slice preparation and whole cell recording, are described elsewhere [11]. Briefly, subjects were anesthetized by CO2 inhalation and sacrificed. Each subject’s brain was rapidly extracted, then immersed in ice-cold, cutting artificial cerebrospinal fluid (aCSF).The cutting solution contained (in mM): 238 sucrose, 0.5 CaCl2, 2.5 KCl, 2 MgSO4, 26.2 NaHCO3, 1 NaH2PO4 and 11 D-glucose. Four hundred μm transverse slices were prepared by a vibroslicer (Leica VT1200, USA). Each slice contained both the hippocampus and entorhinal cortex from the right hemisphere. We kept the entorhinal cortex, because of its critical role in seizure generation and epileptiform activity (EA).
Related Knowledge Centers
- Allocortex
- Memory
- Memory Consolidation
- Neocortex
- Nictitating Membrane
- Sleep
- Spatial Memory
- Temporal Lobe
- Hippocampus
- Ec-Hippocampus System