Therapeutics of Alzheimer's disease: Past, present and future

Anand, Ravi; Gill, Kiran Dip; Mahdi, Abbas Ali

doi:10.1016/j.neuropharm.2013.07.004

Cited by 669 publications

(475 citation statements)

References 394 publications

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“…Such changes have led to the cholinergic hypothesis of memory dysfunction (Bartus, 2000;Craig et al, 2011). In fact, enhancing cholinergic function by continued use of cholinesterase inhibitor drugs is the currently accepted treatment against the onset of Alzheimer's disease (Anand et al, 2014). However, several studies indicate that directly activating the a7 and a4b2 subtypes of nAChR can improve both synaptic transmission and cognition (Wallace and Porter, 2011;Kroker et al, 2011;Ondrejcak et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

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Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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Abstract-Brain glucose metabolism is altered in sporadic Alzheimer's disease (sAD), whose pathologies are reproduced in rodents by intracerebroventricular (icv) infusion of streptozotocin (STZ) in subdiabetogenic doses. The icv-STZ model also culminates in central cholinergic dysfunctions, which in turn are known to underlie both the sAD cognitive decline, and synaptic plasticity impairments. Considering the cognitive-enhancing potential of chronic nicotine (Nic), we investigated whether it attenuates icv-STZ-induced impairments in recognition memory and synaptic plasticity in a cognition-relevant substrate: the hippocampal CA1-medial prefrontal cortex (mPFC) pathway. Rats treated with icv-STZ were submitted to a chronic Nic regime, and were evaluated for recognition memory. We then examined long-term potentiation (LTP), paired-pulse facilitation (PPF) under urethane anesthesia, and brains were also evaluated for hippocampus-mPFC cell density. We found that Nic treatment prevents icv-STZ-induced disruptions in recognition memory and LTP. STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Through combining behavioral, neurophysiological, and neuropathological observations into the Nic-STZ interplay, our study reinforces that cholinergic treatments are of clinical importance against earlystage Alzheimer's disease and mild cognitive impairments.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

et al. 2017

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“…Alzheimer's disease is characterized by the deposition of toxic senile plaques of b amyloid protein and intracellular neurofibrillary tangles containing hyperphosphorylated tau [95]. The b amyloid proteins are formed as a result of cleavage of amyloid precursor protein (APP) by the action of b-secretase (BACE) and !-secretase.…”

Section: Er Stress and Alzheimer's Diseasementioning

confidence: 99%

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

2015

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Endoplasmic reticulum (ER) is the site of protein synthesis, protein folding, maintainance of calcium homeostasis, synthesis of lipids and sterols. Genetic or environmental insults can alter its function generating ER stress. ER senses stress mainly by three stress sensor pathways, namely protein kinase R-like endoplasmic reticulum kinase-eukaryotic translation-initiation factor 2a, inositol-requiring enzyme 1a-X-box-binding protein 1 and activating transcription factor 6-CREBH, which induce unfolded protein responses (UPR) after the recognition of stress. Recent studies have demonstrated that ER stress and UPR signaling are involved in cancer, metabolic disorders, inflammatory diseases, osteoporosis and neurodegenerative diseases. However, the precise knowledge regarding involvement of ER stress in different disease processes is still debatable. Here we discuss the possible role of ER stress in various disorders on the basis of existing literature. An attempt has also been made to highlight the present knowledge of this field which may help to elucidate and conjure basic mechanisms and novel insights into disease processes which could assist in devising better future diagnostic and therapeutic strategies.

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“…Antiamyloid strategies consist of pharmaceutical agents with distinct mechanisms that will enable the clearance and/or inhibit the production and/or prevent the aggregation of Aβ [60][61][62][63] . The compounds targeting amyloid pathway with their current status are summarized in Table 2 [ [60][61][62][63][64][65][66][67][68] .…”

Section: New Targets For Treatments: Inhibitors Of Ap Formation and τmentioning

confidence: 99%

Management of Alzheimers Disease: Role of Existing Therapies, Traditional Medicines and New Treatment Targets

Malve¹

2017

ijps

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Therapeutics of Alzheimer's disease: Past, present and future

Cited by 669 publications

References 394 publications

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

Chronic nicotine attenuates behavioral and synaptic plasticity impairments in a streptozotocin model of Alzheimer’s disease

Role of Endoplasmic Reticulum Stress and Unfolded Protein Responses in Health and Diseases

Management of Alzheimers Disease: Role of Existing Therapies, Traditional Medicines and New Treatment Targets

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