Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats | Zendy

Maibouge Tanko Mahamane Salissou | Zendy; Yacoubou Abdoul Razak Mahaman | Zendy; Feiqi Zhu | Zendy; Fang Huang | Zendy; Yuman Wang | Zendy; Zhendong Xu | Zendy; Dan Ke | Zendy; Qun Wang | Zendy; Rong Liu | Zendy; JianZhi Wang | Zendy; Bin Zhang | Zendy; Xiaochuan Wang | Zendy

Open Access

Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats

Author(s) -

Maibouge Tanko Mahamane Salissou,

Yacoubou Abdoul Razak Mahaman,

Feiqi Zhu,

Fang Huang,

Yuman Wang,

Zhendong Xu,

Dan Ke,

Qun Wang,

Rong Liu,

JianZhi Wang,

Bin Zhang,

Xiaochuan Wang

Publication year - 2018

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.101627

Subject(s) - neuroinflammation , proinflammatory cytokine , neurodegeneration , homocysteine , cognitive decline , oxidative stress , medicine , cognitive deficit , hyperhomocysteinemia , pharmacology , endocrinology , dementia , inflammation , disease , cognitive impairment

Although few drugs are available today for the management of Alzheimer's disease (AD) and many plants and their extracts are extensively employed in animals' studies and AD patients, yet no drug or plant extract is able to reverse AD symptoms adequately. In the present study, Tamarix gallica (TG), a naturally occurring plant known for its strong antioxidative, anti-inflammatory and anti-amyloidogenic properties, was evaluated on homocysteine (Hcy) induced AD-like pathology and cognitive impairments in rats. We found that TG attenuated Hcy-induced oxidative stress and memory deficits. TG also improved neurodegeneration and neuroinflammation by upregulating synaptic proteins such as PSD95 and synapsin 1 and downregulating inflammatory markers including CD68 and GFAP with concomitant decrease in proinflammatory mediators interlukin-1β (IL1β) and tumor necrosis factor α (TNFα). TG attenuated tau hyperphosphorylation at multiple AD-related sites through decreasing some kinases and increasing phosphatase activities. Moreover, TG rescued amyloid-β (Aβ) pathology through downregulating BACE1. Our data for the first time provide evidence that TG attenuates Hcy-induced AD-like pathological changes and cognitive impairments, making TG a promising candidate for the treatment of AD-associated pathological changes.

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