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27/100

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Disease mechanisms

Topic: Risk, prevention and care in population studies

Dementia encompasses a group of progressive neurodegenerative disorders marked by cognitive, behavioural, and functional decline, underpinned by complex neurobiological processes. This chapter outlines the anatomical, cellular, and molecular mechanisms that drive disease onset and progression. Structural vulnerability of the hippocampus, cerebral cortex, white matter, and cognitive networks underlies characteristic clinical manifestations. At the microscopic level, neuro-inflammation, mitochondrial dysfunction, oxidative stress, excitotoxicity, impaired protein clearance, and synaptic loss converge to promote neuronal injury. Distinct proteinopathies—including amyloid- plaques and tau tangles in Alzheimer’s disease, -synuclein inclusions in Lewy body dementia, and TDP-43 or tau aggregates in frontotemporal lobar degeneration—define specific dementia subtypes, yet share overlapping cascades of pathology. Vascular contributions, such as ischemia, hypoperfusion, and blood–brain barrier disruption, further compound neuronal vulnerability, highlighting the prevalence of mixed dementias. Collectively, these mechanisms illustrate dementia as a multifactorial disorder of network disintegration and cellular stress. Advancing insights into these processes are driving the development of biomarkers and disease-modifying therapies, paving the way for more precise, personalized approaches to diagnosis and care.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Abyad, A. (2025). Neurobiology of dementia. World Family Medicine Journal/Middle East Journal of Family Medicine. https://doi.org/10.5742/mewfm.2025.805257903

Vancouver

Abyad A. Neurobiology of dementia. World Family Medicine Journal/Middle East Journal of Family Medicine. 2025. doi:10.5742/mewfm.2025.805257903.

BibTeX

@article{abyad2025-86818921,
  author  = {Abyad, Abdulrazak},
  title   = {{Neurobiology of dementia}},
  journal = {World Family Medicine Journal/Middle East Journal of Family Medicine},
  year    = {2025},
  doi     = {10.5742/mewfm.2025.805257903},
  url     = {https://doi.org/10.5742/mewfm.2025.805257903}
}

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Key findings

At the microscopic level, neuro-inflammation, mitochondrial dysfunction, oxidative stress, excitotoxicity, impaired protein clearance, and synaptic loss converge to promote neuronal injury.
Distinct proteinopathies—including amyloid- plaques and tau tangles in Alzheimer’s disease, -synuclein inclusions in Lewy body dementia, and TDP-43 or tau aggregates in frontotemporal lobar degeneration—define specific dementia subtypes, yet share overlapping cascades of pathology.
Vascular contributions, such as ischemia, hypoperfusion, and blood–brain barrier disruption, further compound neuronal vulnerability, highlighting the prevalence of mixed dementias.
Collectively, these mechanisms illustrate dementia as a multifactorial disorder of network disintegration and cellular stress.
Advancing insights into these processes are driving the development of biomarkers and disease-modifying therapies, paving the way for more precise, personalized approaches to diagnosis and care.

Why it matters

This chapter describes dementia as a multifactorial disorder involving neuroinflammation, mitochondrial dysfunction, oxidative stress, impaired protein clearance and synaptic loss, alongside proteinopathies and vascular contributions. It states that these insights are driving development of biomarkers and disease-modifying therapies, but reports no treatment results.

Study details

Evidence strengthLow

How this study scored 27/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on institution's track record, so that was left out: it earned 26 of the 97 points we could judge it on, which is 27 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (World Family Medicine Journal/Middle East Journal of Family Medicine)
Journal's citation record	0 / 4	World Family Medicine Journal/Middle East Journal of Family Medicine: journal h-index 21 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	4 / 5	2025 — within 3 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	0 / 7	Cited 0 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.0 citations a year over 3 year(s) since 2025
Impact for its field and year	0 / 6	Cited 0.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	0 / 4	Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Abdulrazak Abyad: h-index 16 (OpenAlex, whole career)
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multi-centre collaboration	0 / 3	OpenAlex lists 0 institution(s) in 0 countries — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	1 / 2	Not in PubMed, but has a DOI
Free to read	2 / 2	Free to read
Points	26 / 97	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 26 of the 97 points we could judge it on is 27 out of 100.
Total	27 / 100	—

What each of these 20 components measures, and what this score is not →

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