P2-352 Alzheimer's disease: potential beneficial effects of estrogen on performance-based battery of physical function skills for older women

2004 ◽  
Vol 25 ◽  
pp. S333
Author(s):  
Angela M. Slattery ◽  
Tracy L. Ohrt ◽  
Carey E. Gleason ◽  
Jennifer R. Helmers ◽  
Brenna Cholerton ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Function ◽  
Older Women ◽  
Beneficial Effects

scholarly journals Repetitive Transcranial Magnetic Stimulation in the Treatment of Alzheimer’s Disease and Other Dementias

Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 949
Author(s):  
Athina-Maria Aloizou ◽  
Georgia Pateraki ◽  
Konstantinos Anargyros ◽  
Vasileios Siokas ◽  
Christos Bakirtzis ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Lewy Body Dementia ◽  
Standard Of Care ◽  
Central Position ◽  
Beneficial Effects ◽  
Dorsolateral Prefrontal

Dementia is a debilitating impairment of cognitive functions that affects millions of people worldwide. There are several diseases belonging to the dementia spectrum, most prominently Alzheimer’s disease (AD), vascular dementia (VD), Lewy body dementia (LBD) and frontotemporal dementia (FTD). Repetitive transcranial magnetic stimulation (rTMS) is a safe, non-invasive form of brain stimulation that utilizes a magnetic coil to generate an electrical field and induce numerous changes in the brain. It is considered efficacious for the treatment of various neuropsychiatric disorders. In this paper, we review the available studies involving rTMS in the treatment of these dementia types. The majority of studies have involved AD and shown beneficial effects, either as a standalone, or as an add-on to standard-of-care pharmacological treatment and cognitive training. The dorsolateral prefrontal cortex seems to hold a central position in the applied protocols, but several parameters still need to be defined. In addition, rTMS has shown potential in mild cognitive impairment as well. Regarding the remaining dementias, research is still at preliminary phases, and large, randomized studies are currently lacking.

scholarly journals Cytokine signaling convergence regulates the microglial state transition in Alzheimer’s disease

2021 ◽  
Author(s):  
Shun-Fat Lau ◽  
Amy K. Y. Fu ◽  
Nancy Y. Ip
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathways ◽  
State Transition ◽  
Cytokine Signaling ◽  
Interleukin 33 ◽  
Beneficial Effects ◽  
Activated State ◽  
Therapeutic Development ◽  
Functional States

AbstractGenetic analyses have revealed the pivotal contribution of microglial dysfunctions to the pathogenesis of Alzheimer’s disease (AD). Along AD progression, the accumulation of danger-associated molecular patterns (DAMPs) including beta-amyloid and hyperphosphorylated tau continuously stimulates microglia, which results in their chronic activation. Chronically activated microglia secrete excessive pro-inflammatory cytokines, which further regulate microglial responses towards DAMPs. This has spurred longstanding interest in targeting cytokine-induced microglial responses for AD therapeutic development. However, the cytokine-induced microglial state transition is not comprehensively understood. Cytokines are assumed to induce microglial state transition from a resting state to an activated state. However, recent evidence indicate that this microglial state transition involves multiple sequential functional states. Moreover, the mechanisms by which different functional states within the cytokine-induced microglial state transition regulate AD pathology remain unclear. In this review, we summarize how different cytokine signaling pathways, including those of IL-33 (interleukin-33), NLRP3 inflammasome–IL-1β, IL-10, and IL-12/IL-23, regulate microglial functions in AD. Furthermore, we discuss how the modulation of these cytokine signaling pathways can result in beneficial outcomes in AD. Finally, we describe a stepwise functional state transition of microglia induced by cytokine signaling that can provide insights into the molecular basis of the beneficial effects of cytokine modulation in AD and potentially aid therapeutic development.

scholarly journals Effects of optogenetic stimulation of basal forebrain parvalbumin neurons on Alzheimer’s disease pathology

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Caroline A. Wilson ◽  
Sarah Fouda ◽  
Shuzo Sakata
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Basal Forebrain ◽  
Gamma Oscillations ◽  
Cortical Region ◽  
Sensory Stimuli ◽  
Beneficial Effects ◽  
Amyloid Load ◽  
5Xfad Mice ◽  
Frontal Cortical Region

Abstract Neuronal activity can modify Alzheimer’s disease pathology. Overexcitation of neurons can facilitate disease progression whereas the induction of cortical gamma oscillations can reduce amyloid load and improve cognitive functions in mouse models. Although previous studies have induced cortical gamma oscillations by either optogenetic activation of cortical parvalbumin-positive (PV+) neurons or sensory stimuli, it is still unclear whether other approaches to induce gamma oscillations can also be beneficial. Here we show that optogenetic activation of PV+ neurons in the basal forebrain (BF) increases amyloid burden, rather than reducing it. We applied 40 Hz optical stimulation in the BF by expressing channelrhodopsin-2 (ChR2) in PV+ neurons of 5xFAD mice. After 1-h induction of cortical gamma oscillations over three days, we observed the increase in the concentration of amyloid-β42 in the frontal cortical region, but not amyloid-β40. Amyloid plaques were accumulated more in the medial prefrontal cortex and the septal nuclei, both of which are targets of BF PV+ neurons. These results suggest that beneficial effects of cortical gamma oscillations on Alzheimer’s disease pathology can depend on the induction mechanisms of cortical gamma oscillations.

scholarly journals Probiotics Fermentation Technology, a Novel Kefir Product, Ameliorates Cognitive Impairment in Streptozotocin-Induced Sporadic Alzheimer’s Disease in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Nesrine S. El Sayed ◽  
Esraa A. Kandil ◽  
Mamdooh H. Ghoneum
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Gut Microbiota ◽  
Neuronal Degeneration ◽  
Amyloid Plaque ◽  
Dependent Manner ◽  
Insulin Degrading Enzyme ◽  
Beneficial Effects ◽  
Fermentation Technology

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by cognitive impairment. Gut microbiota dysfunction (dysbiosis) is implicated in the pathology of AD and is associated with several detrimental consequences, including neurotransmitter depletion, oxidative stress, inflammation, apoptosis, and insulin resistance, which all contribute to the onset of AD. The objective of this study was to assess the effectiveness of Probiotics Fermentation Technology (PFT), a kefir product, in alleviating AD symptoms via regulation of the gut microbiota using a streptozotocin- (STZ-) induced AD mouse model and to compare its activity with simvastatin, which has been proven to effectively treat AD. Mice received one intracerebroventricular injection of STZ (3 mg/kg). PFT (100, 300, 600 mg/kg) and simvastatin (20 mg/kg) were administered orally for 3 weeks. PFT supplementation mitigated STZ-induced neuronal degeneration in the cortex and hippocampus, restored hippocampal acetylcholine levels, and improved cognition in a dose-dependent manner. These effects were accompanied by reductions in oxidative damage, proinflammatory cytokine expression, apoptosis, and tau hyperphosphorylation. Moreover, PFT hindered amyloid plaque accumulation via the enhancement of insulin-degrading enzyme. These beneficial effects were comparable to those produced by simvastatin. The results suggest that PFT can alleviate AD symptoms by regulating the gut microbiota and by inhibiting AD-related pathological events.

scholarly journals Chronic Memantine Treatment Ameliorates Behavioral Deficits, Neuron Loss, and Impaired Neurogenesis in a Model of Alzheimer’s Disease

2020 ◽  
Vol 58 (1) ◽  
pp. 204-216
Author(s):  
Martina Stazi ◽  
Oliver Wirths
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Recognition Task ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Behavioral Deficits ◽  
Neuron Loss ◽  
Beneficial Effects ◽  
Memantine Treatment

AbstractMemantine, a non-competitive NMDA receptor antagonist possessing neuroprotective properties, belongs to the small group of drugs which have been approved for the treatment of Alzheimer’s disease (AD). While several preclinical studies employing different transgenic AD mouse models have described beneficial effects with regard to rescued behavioral deficits or reduced amyloid plaque pathology, it is largely unknown whether memantine might have beneficial effects on neurodegeneration. In the current study, we assessed whether memantine treatment has an impact on hippocampal neuron loss and associated behavioral deficits in the Tg4-42 mouse model of AD. We demonstrate that a chronic oral memantine treatment for 4 months diminishes hippocampal CA1 neuron loss and rescues learning and memory performance in different behavioral paradigms, such as Morris water maze or a novel object recognition task. Cognitive benefits of chronic memantine treatment were accompanied by an amelioration of impaired adult hippocampal neurogenesis. Taken together, our results demonstrate that memantine successfully counteracts pathological alterations in a preclinical mouse model of AD.

scholarly journals Non-Aβ-Dependent Factors Associated with Global Cognitive and Physical Function in Alzheimer’s Disease: A Pilot Multivariate Analysis

2019 ◽  
Vol 8 (2) ◽  
pp. 224 ◽  
Author(s):  
Anna Pedrinolla ◽  
Massimo Venturelli ◽  
Stefano Tamburin ◽  
Cristina Fonte ◽  
Anna Maria Stabile ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Function ◽  
Vascular Function ◽  
Stepwise Regression ◽  
Performance Test ◽  
Physical Decline ◽  
Factors Associated ◽  
Inflammatory Status ◽  
Factor Α

Recent literature highlights the importance of identifying factors associated with mild cognitive impairment (MCI) and Alzheimer’s Disease (AD). Actual validated biomarkers include neuroimaging and cerebrospinal fluid assessments; however, we investigated non-Aβ-dependent factors associated with dementia in 12 MCI and 30 AD patients. Patients were assessed for global cognitive function (Mini-Mental state examination—MMSE), physical function (Physical Performance Test—PPT), exercise capacity (6-min walking test—6MWT), maximal oxygen uptake (VO2max), brain volume, vascular function (flow-mediated dilation—FMD), inflammatory status (tumor necrosis factor—α ,TNF- α, interleukin-6, -10 and -15) and neurotrophin receptors (p75NTR and Tropomyosin receptor kinase A -TrkA). Baseline multifactorial information was submitted to two separate backward stepwise regression analyses to identify the variables associated with cognitive and physical decline in demented patients. A multivariate regression was then applied to verify the stepwise regression. The results indicated that the combination of 6MWT and VO2max was associated with both global cognitive and physical function (MMSE = 11.384 + (0.00599 × 6MWT) − (0.235 × VO2max)); (PPT = 1.848 + (0.0264 × 6MWT) + (19.693 × VO2max)). These results may offer important information that might help to identify specific targets for therapeutic strategies (NIH Clinical trial identification number NCT03034746).

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