Combinatorial Treatment Using Umbilical Cord Perivascular Cells and Aβ Clearance Rescues Vascular Function Following Transient Hypertension in a Rat Model of Alzheimer Disease

Abstract

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Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

“…No genotype differences were observed in PVB + and SST + neurons at 4 months (Additional file 1 : Fig. S5), a pre-pathology stage in TgF344-AD rats [ 42 ], indicating that the interneuron networks developed normally in TgF344-AD rats. The results further support that the compensatory and degenerative changes in these neuronal populations in 9-, 12- and 15-month-old TgF344-AD rats are linked to mounting Aβ and tau pathologies.…”

Stereological Changes in Microvascular Parameters in Hippocampus of a Transgenic Rat Model of Alzheimer’s Disease

“…Here we described previously unreported lower Total L cap in DG of Tg rats, which may be the results of genetic features or possibly angiogenic responses to A␤ deposition. From about 9 months of age these vessel walls begin to lose their elasticity [71] and appear to undergo penetration by A␤ aggregates [18,20,21]. The cytoskeletal proteins desmin and ␣-smooth muscle actin (␣-SMA) in pericytes become upregulated [21], which slows down the active redistribution of local blood flow [72].…”

“…The cytoskeletal proteins desmin and ␣-smooth muscle actin (␣-SMA) in pericytes become upregulated [21], which slows down the active redistribution of local blood flow [72]. Local diffusion changes could promote transient fluctuation of the blood pressure [71] that may induce or exacerbate cerebrovascular damage and progression resulting from A␤ deposition [73,74]. Furthermore, trophic disbalance of the granular cells layer in DG may lead to synaptic disruptions [17,60,75] and weakened effectiveness of synaptic transmission to projections in CA subregions [76].…”

Protective Effect of Patchouli Alcohol Against SH-SY5Y Cell Injury Induced by Aβ25-35 via the Reduction of Oxidative Stress and Apoptosis

“…3 Aβ is composed of 39 to 43 amino acids and generated from amyloid precursor protein (APP) through proteolytic cleavage; Aβ monomers can be polymerized to form water-insoluble Aβ oligomers that can cause neurotoxicity, leading to the occurrence and development of AD. 4,5…”

“…3 Aβ is composed of 39 to 43 amino acids and generated from amyloid precursor protein (APP) through proteolytic cleavage; Aβ monomers can be polymerized to form water-insoluble Aβ oligomers that can cause neurotoxicity, leading to the occurrence and development of AD. 4,5 At present, the main drugs for the clinical treatment of AD are antioxidants, estrogens, lipidemic-modulating agents, brain metabolism improving drugs, nonsteroidal anti-inflammatory drugs, calcium antagonists, and acetylcholinesterase inhibitors, but the treatment effect of these drugs is associated with side effects, high price, and single target, 6,7 so it is of great significance to develop drugs with low toxicity, low price, multiple targets, and good efficacy for the treatment of AD. 8 As one of the main active components of Pogostemon cablin (Blanco) Benth.…”