Benzodiazepines in Alzheimer's disease: beneficial or detrimental effects

被引：27

作者：

Al-Kuraishy, Hayder M. ^{[1
]}

Al-Gareeb, Ali, I ^{[1
]}

Saad, Hebatallah M. ^{[2
]}

Batiha, Gaber El-Saber ^{[3
]}

机构：

[1] Al Mustansiriyah Univ, Coll Med, Med Fac, Dept Pharmacol Toxicol & Med, POB 14132, Baghdad, Iraq

[2] Matrouh Univ, Fac Vet Med, Dept Pathol, Marsa Matruh 51744, Egypt

[3] Damanhour Univ, Fac Vet Med, Dept Pharmacol & Therapeut, Damanhour 22511, Egypt

来源：

INFLAMMOPHARMACOLOGY | 2023年 / 31卷 / 01期

关键词：

Alzheimer's disease; Gamma-aminobutyric acid; Benzodiazepines; Cognitive dysfunction; GABA-A RECEPTORS; INDUCED IMPAIRMENT; AMYLOID-BETA; PLASTICITY; PROTEIN; RISK; DYSFUNCTION; ASSOCIATION; LORAZEPAM; TOXICITY;

D O I：

10.1007/s10787-022-01099-4

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Dementia is considered a clinical syndrome characterized by cognitive dysfunction and memory loss. Alzheimer's disease (AD) is the most common type of dementia. AD is linked with the turbulence of diverse neurotransmitters including gamma-aminobutyric acid (GABA). Notably, GABA in the brain and cerebrospinal fluid was reduced in AD. Thus, allosteric modulation of the GABA effect by benzodiazepines (BDZs) may improve the clinical outcomes of AD patients. Therefore, the objective of the present review was to reveal the possible role of BDZs on the pathogenesis and clinical outcomes in AD patients. Though BDZs may adversely affect cognitive functions mainly in elderly patients, herein it was postulated that BDZs may have beneficial, neutral, or detrimental effects in AD. Taken together, there is strong controversy regarding the use of BDZs and the risk for the development of AD. Therefore, experimental, preclinical and clinical studies are critical to determine the potential protective or detrimental effects of BDZs on AD neuropathology.

引用

页码：221 / 230

页数：10

共 99 条

[11]

Bounds C.G., 2020, BENZODIAZEPINES

[12] Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling [J].

Brady, Megan L. ;

Pilli, Jyotsna ;

Lorenz-Guertin, Joshua M. ;

Das, Sabyasachi ;

Moon, Charles E. ;

Graff, Nicholas ;

Jacob, Tija C. .

NEUROPHARMACOLOGY, 2018, 128 :324-339

[13]

Brigo F., 2020, NEUROPSYCHOPHARMACOT, V2020, P1

[14] Stress as risk factor for Alzheimer's disease [J].

Caruso, Alessandra ;

Nicoletti, Ferdinando ;

Mango, Dalila ;

Saidi, Amira ;

Orlando, Rosamaria ;

Scaccianoce, Sergio .

PHARMACOLOGICAL RESEARCH, 2018, 132 :130-134

[15] First-line management of canine status epilepticus at home and in hospital-opportunities and limitations of the various administration routes of benzodiazepines [J].

Charalambous, Marios ;

Volk, Holger A. ;

Luc Van Ham ;

Bhatti, Sofie F. M. .

BMC VETERINARY RESEARCH, 2021, 17 (01)

[16] Alzheimer Disease Pathogenesis: Insights From Molecular and Cellular Biology Studies of Oligomeric Aβ and Tau Species [J].

Chen, Xu-Qiao ;

Mobley, William C. .

FRONTIERS IN NEUROSCIENCE, 2019, 13

[17] Apolipoprotein E: Structural Insights and Links to Alzheimer Disease Pathogenesis [J].

Chen, Yun ;

Strickland, Michael R. ;

Soranno, Andrea ;

Holtzman, David M. .

NEURON, 2021, 109 (02) :205-221

[18] Dual Functions of Histone-Lysine N-Methyltransferase Setdb1 Protein at Promyelocytic Leukemia-Nuclear Body (PML-NB) MAINTAINING PML-NB STRUCTURE AND REGULATING THE EXPRESSION OF ITS ASSOCIATED GENES [J].

Cho, Sunwha ;

Park, Jung Sun ;

Kang, Yong-Kook .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (47) :41115-41124

[19] New benzodiazepines for sedation [J].

Cornett, Elyse M. ;

Novitch, Matthew B. ;

Brunk, Andrew J. ;

Davidson, Kelly S. ;

Menard, Bethany L. ;

Urman, Richard D. ;

Kaye, Alan D. .

BEST PRACTICE & RESEARCH-CLINICAL ANAESTHESIOLOGY, 2018, 32 (02) :149-164

[20]

Dailly E, 2008, PAK J PHARM SCI, V21, P144

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