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Clinical presentation of depression in the elderly
Published in Simon Lovestone, Robert Howard, Depression in Elderly People, 2020
Simon Lovestone, Robert Howard
The neurodegeneration of Alzheimer’s disease and other dementias results in a loss of brain tissue, as well as the characteristic neuritic plaques and neurofibrillary tangles (Figs. 5 and 6). As well as the invariable symptom of loss of memory, depression frequently occurs as a secondary symptom. Often presenting relatively early in the condition, symptoms of depression include lowered mood and tearfulness or a change in behaviour. Depression is thought to be more common in non-Alzheimer disease dementias, although rigorous studies to test this hypothesis have not yet been performed. Depression as part of a dementia syndrome can occur in the early stages, perhaps as a result of retained insight. Even partial knowledge of a deterioration and an indication of a progressive loss of ability is profoundly distressing. We recall a pair of sisters, both with dementia but one more advanced than the other, who were seriously depressed. The least demented of the two realized that her sister was seriously ill and became extremely distraught. The sister with more advanced dementia had little insight but repeated frequently that half of her brain was missing. Both sisters spent much of the day crying and increasingly refused to eat and lost considerable weight.
Estrogens and dementia: a clinical and epidemiological update
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
Pathologically, Alzheimer’s disease is manifest by the accumulation of neurofibrillary tangles within vulnerable neurons of the central nervous system and by the abundance of neuritic plaques in the neuropil between nerve cell bodies. A typical neuritic plaque consists of a central core β-amyloid protein surrounded by distended nerve cell processes (neurites). An inflammatory process is suggested by the colocalization within the plaque of microglia and reactive astrocytes, together with cytokines, complement proteins, and acute phase reactants5,6.
The Nervous System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Alzheimer's disease (AD) is a degenerative dementia resulting in brain atrophy much earlier than usual but with symptoms of anxiety, difficulty with speech, loss of memory, and irrationality as in senile dementia (more commonly called senility). The degeneration is complex, involving an increased amount of the protein amyloid in and around blood vessels, reduced amount of the enzyme protein kinase C, and accumulation of neuritic plaques and tangled neurofilaments, and a loss of cholinergic nerves in parts of the brain. This complexity and the lack of any definitive indicator make diagnosis difficult or impossible in many cases.
The histopathological staging of tau, but not amyloid, corresponds to antemortem cognitive status, dementia stage, functional abilities and neuropsychiatric symptoms
Published in International Journal of Neuroscience, 2021
Charles B. Malpas, Sifat Sharmin, Tomas Kalincik
Neuropathological staging was performed and recorded as per CERAD protocols [14]. Only standard blocks were used to assign histopathological staging as described by Montine and colleagues [17]. The presence of tauopathy was determined using Braak staging for neurofibrillary degeneration (CERAD B score: stage 0–stage VI; [5]). Neuritic plaques were staged according to the density of neocortical plaques with argyrophilic dystrophic neurites (CERAD C score: ‘no neuritic plaques’ to ‘frequent neuritic plaques’). Diffuse plaques were staged according to the density of plaques with non-compact amyloid and no apparent dystrophic features (‘no diffuse plaques’ to frequent diffuse plaques’). We used only the ‘derived’ variables from the NACC database, which ensure consistency over different iterations of the of the neuropathology data set.
The cognitive safety of antimuscarinics in the treatment of overactive bladder
Published in Expert Opinion on Drug Safety, 2020
George Araklitis, Dudley Robinson
Patients with Alzheimer’s disease have been shown to have accumulation of amyloid in cortical neuritic plaques and walls of vessels as well as intraneuronal deposition of neurofibrillary tangles [37]. There is also damage to the microcirculation and the BBB. The deposition of amyloid-beta (Aβ) peptide around cortical vessels causes stenosis, leading to ischemia. The peptide also destroys the myocytes in the vessels leading to disruption in the control of cerebral blood flow. Furthermore, the vessels in the brain, which are innervated by cholinergic neurons of the nucleus basalis of Meynert, are damaged in Alzheimer’s disease. A study on rabbits, found that ablation of the cholinergic neurons of the nucleus basalis of Meynert, caused Aβ peptide deposition around cerebral vessels [37] although this was not the case in sham rabbits. The authors conclude that loss of cholinergic innervation was an important factor in the development of Alzheimer’s disease.
Epigenetic mechanisms underlying the effects of triptolide and tripchlorolide on the expression of neuroligin-1 in the hippocampus of APP/PS1 transgenic mice
Published in Pharmaceutical Biology, 2019
Xiaomei Lu, Baolin Yang, Hao Yu, Xiaoling Hu, Jing Nie, Bin Wan, Ming Zhang, Cheng Lü
The histopathological changes that are typical of Alzheimer’s disease (AD) are neuritic plaques, neurofibrillary tangles, synapse loss and gliosis. The β-amyloid (Aβ) protein is the main component of neuritic plaques. A common hypothesis is that the abnormal metabolism and deposition of Aβ constitute the initial factor and key step inducing the pathogenesis of AD (Reiss et al. 2018). Aβ activates microglia in the brain, which secrete and release various inflammatory mediators (Hansen et al. 2018). Inflammatory mediators inhibit long-term potentiation during synaptic transmission, resulting in structural and functional synaptic impairments (Kelly et al. 2003; Griffin et al. 2006; Jebelli et al. 2014; Liu et al. 2018). However, the specific mechanisms by which inflammatory responses lead to synaptic damage remain unclear. According to Bie et al. (2014), Aβ-induced neuroinflammation increases the binding of histone deacetylase 2 (HDAC2) and methyl-CpG-binding protein 2 (MeCP2) to the neuroligin-1 (NLGN1) promoter and cytosine methylation at the NLGN1 promoter, and inhibits histone H3 acetylation at the latter region. Thus, Aβ-induced neuroinflammation reduces NLGN1 expression by affecting the epigenetic modification of NLGN1, ultimately damaging the structure and function of synapses. NLGN1 is a cell adhesion protein located on the excitatory postsynaptic membrane that plays an important role in synaptic plasticity (Liu et al. 2016). NLGN1 dysfunction is closely related to the pathogenesis of AD (Tristán-Clavijo et al. 2015).