Evidence map›Paper›PMID 31998117›Full record

ReviewFrontiers in aging neuroscience2019

Lifestyle Modifications and Nutritional Interventions in Aging-Associated Cognitive Decline and Alzheimer's Disease.

Gurjit Kaur Bhatti, Arubala P Reddy, P Hemachandra Reddy, Jasvinder Singh Bhatti

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 6 pooled it
10.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 6 syntheses or guidelines pooled it, 142 citations in OpenAlex.

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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Gurjit Kaur BhattiDepartment of Medical Lab Technology, University Institute of Applied Health Sciences, Chandigarh University, Mohali, India.
Arubala P ReddyDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
P Hemachandra ReddyInternal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, United States.
Jasvinder Singh BhattiDepartment of Biotechnology and Microbial Biotechnology, Sri Guru Gobind Singh College, Chandigarh, India.
Chandigarh University · INTexas Tech University · USTexas Tech University Health Sciences Center · US

Funding

Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Voltage-Dependent Anion Channel and Neurodegeneration in Alzheimer's DiseaseR01AG047812 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2014 to 2018
$1.9M
Mitochondrial Fragmentation and Neurodegeneration in Huntington's DiseaseR01NS105473 · NINDS · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2017 to 2021
$1.8M
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812NINDS NIH HHS R01 NS105473
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a type of incurable neurodegenerative disease that is characterized by the accumulation of amyloid-β (Aβ; plaques) and tau hyperphosphorylation as neurofibrillary tangles (NFTs) in the brain followed by neuronal death, cognitive decline, and memory loss. The high prevalence of AD in the developed world has become a major public health challenge associated with social and economic burdens on individuals and society. Due to there being limited options for early diagnosis and determining the exact pathophysiology of AD, finding effective therapeutic strategies has become a great challenge. Several possible risk factors associated with AD pathology have been identified; however, their roles are still inconclusive. Recent clinical trials of the drugs targeting Aβ and tau have failed to find a cure for the AD pathology. Therefore, effective preventive strategies should be followed to reduce the exponential increase in the prevalence of cognitive decline and dementia, especially AD. Although the search for new therapeutic targets is a great challenge for the scientific community, the roles of lifestyle interventions and nutraceuticals in the prevention of many metabolic and neurodegenerative diseases are highly appreciated in the literature. In this article, we summarize the molecular mechanisms involved in AD pathology and the possible ameliorative action of lifestyle and nutritional interventions including diet, exercise, Calorie restriction (CR), and various bioactive compounds on cognitive decline and dementia. This article will provide insights into the role of non-pharmacologic interventions in the modulation of AD pathology, which may offer the benefit of improving quality of life by reducing cognitive decline and incident AD.

Indexed as

Alzheimer’s diseaseantioxidantsdietexerciseinflammationlifestylenutraceuticalsoxidative stress

Identifiers

PMID31998117
PMCPMC6966236
OpenAlexW3000512444

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.