E D I T O R I A L
From Alzheimer's disease to vascular dementia: Different roads
leading to cognitive decline
As life expectancy is projected to increase in the coming years, along
with an anticipated increase in the prevalence of cognitive impairment
and dementia, there is a significant emphasis on preserving and pro-
moting brain health as a primary public objective (Fuster et al., 2023).
Preserving cognitive function is a crucial aspect of successful ageing,
while its decline can profoundly impact quality of life, functional inde-
pendence, and the risk of requiring institutional care. Alzheimer's dis-
ease (AD) and vascular dementia (VaD) are the most prevalent types
of dementia in the elderly. However, it is remarkable that conditions
such as ‘pure AD’ or ‘pure VaD’ are relatively uncommon, since most
patients present with mixed pathology. Indeed, the coexistence in
many cases of typical AD neurodegenerative hallmarks (such as amy-
loid plaques and neurofibrillary tangles) and vascular pathology (such
as cerebral microbleeds, micro-infarcts, arteriolosclerosis, etc.) opens
the door for researchers to speculate that vascular and degenerative
pathways may potentially interact with one another, possibly resulting
in a synergistic impact (Iadecola et al., 2019). Vascular pathology is
present in 75% of individuals over 65 years of age and has an impor-
tant additive role when combined with AD pathology (van der Flier
et al., 2018). However, whether vascular pathology may promote or
be a downstream consequence of AD development is unknown and
this chicken-or-egg question probably does not have a straight unique
answer for all patients. Currently, anti-amyloid strategies are showing
promising effects of slowing cognitive decline in mildly symptomatic
individuals, however they have not been demonstrated to effectively
stop the progression of AD, and the occurrence of side effects related
to vascular events has been reported (Sims et al., 2023; van Dyck
et al., 2023). Thus, there is strong need for comprehensive treatments
that address both AD and vascular pathology to avert the increasing
global burden of neurodegenerative diseases and dementia (Figure 1).
The vascular system has a vital impact on brain function through-
out life span, both in health and disease. Within this context, cardio-
vascular disease (CVD) is well recognized as a key contributor to VaD
and a full range of cognitive syndromes, globally defined as vascular
cognitive impairment (VCI). Indeed, cardiovascular risk factors (CVRFs)
can chronically sustain common multiple cellular and molecular
mechanisms leading to vascular pathological damages (i.e., endothelial
dysfunction, arterial stiffness, vasoreactivity alterations and hypoper-
fusion) that, at the brain level, are likely to be implicated in
neurodegenerative conditions (Iadecola et al., 2019). Remarkably, sev-
eral studies have also underscored the role of CVD and CVRFs as an
adjuvant for the expression of other types of dementia, including AD
(Cortes-Canteli & Iadecola, 2020). Curiously, Alois Alzheimer in his
first report already evidenced vascular dysfunction in the AD brain
(Alzheimer et al., 1995). On the one hand, people affected by condi-
tions such as midlife hypertension, obesity, smoking, physical inactiv-
ity, atherosclerosis, and diabetes have a higher risk to develop both
VaD and AD (Iadecola et al., 2019). Notably, some of these conditions
are part of the modifiable risk factors identified by the ‘2020 Lancet
Commission on dementia prevention, intervention, and care’ to be
responsible for 40% of the dementia cases (Livingston et al., 2020).
On the other hand, several vascular alterations including pathology of
the brain microcirculation, neurovascular unit dysfunction, a pro-
coagulant state and hypertensive vascular remodelling have been
described in AD patients (Cortes-Canteli & Iadecola, 2020). Addition-
ally, cerebral blood flow and glucose metabolism are reduced and the
brain vascular resistance is increased in human AD and in mice over-
expressing amyloid precursor protein to mimic AD, as well as in
humans and mice expressing the e4 allele of Apolipoprotein E, which
predisposes to an increased risk of AD (Korte et al., 2020).
CVD and CVRFs are also associated with a sustained chronic
inflammatory status (Furman et al., 2019; Goldfine & Shoelson, 2017),
and lead to immune system activation, including phenomena like
immunothrombosis as well as derangement of bone marrow haemato-
poiesis (Rohde et al., 2022). Over the past decades, emerging evi-
dence has implicated immune system activation as a key player in
neurodegeneration (Endres et al., 2022; Kinney et al., 2018). Conse-
quently, both microglia and elements of the peripheral immune sys-
tem, which may potentially infiltrate the brain, are increasingly
recognized as possible novel targets to enhance the effectiveness of
current therapeutic approaches (Cummings et al., 2022).
This Themed Issue discusses some of these intricate intercon-
nected pathways, and stems from the Round Table ‘From Alzheimer's
disease to vascular dementia: different roads leading to cognitive
decline’ organized with the support of the British Journal of Pharma-
cology and the British Pharmacological Society during the 19th Meet-
ing of the Spanish Society of Neuroscience organized in Lleida (Spain)
on 3–5 November 2021.
Readers of this Themed Issue will find a review by Toribio-
Fernandez, Ceron, Cortes-Canteli and coworkers describing in detail the
vascular dysfunction and pro-coagulant state contributing to AD onset
and progression, with particular emphasis on their effect on the
Abbreviations: AD, Alzheimer's disease; CVD, cardiovascular disease; CVRFs, cardiovascular
risk factors; VaD, vascular dementia; VCI, vascular cognitive impairment.
DOI: 10.1111/bph.16292
Br J Pharmacol. 2024;1–5. wileyonlinelibrary.com/journal/bph © 2024 British Pharmacological Society. 1
deposition/clearance of amyloid-β peptide, one of the pathological hall-
marks of AD (Toribio-Fernandez et al., 2023). With the idea that normal-
izing this abnormal thrombosis could be a plausible AD therapeutic
approach, they provide a comprehensive review of clinical studies in
atrial fibrillation patients using long-term anticoagulation—from the clas-
sic vitamin K antagonists (e.g., warfarin and acenocoumarol) to the
direct oral anticoagulants (e.g., factor Xa inhibitors such as apixaban,
rivaroxaban or edoxaban; and thrombin inhibitors such as dabigatran)—
with a specific focus on dementia development. They finally discuss
which would be the best strategy in a hypothetical clinical trial targeting
the procoagulant state observed in AD. Moreover, this Themed Issue
goes one step further and provides the first comprehensive review link-
ing the vascular component of AD with tau accumulation, the other
pathological hallmark of AD: Kim, Santa-Maria and collaborators sum-
marize how tau proteostasis dysregulation contributes to vascular dys-
function and conversely, they examine the factors and pathways leading
to tau pathological alterations triggered by cerebrovascular dysfunction,
highlighting the role that epigenetic and epitranscriptomic factors play in
regulating the integrity of the cerebrovascular system and the progres-
sion of tauopathy, including a few remarks on potential therapeutic
interventions (Kim et al., 2023).
In line with the contribution of CVRFs such as diabetes, obesity and
other metabolic disorders to dementia development, Bettinetti-Luque
et al. dig into the cross-talk between adipose tissue and the brain. These
authors specifically focus on the effect of a range of endogenous biolog-
ically active factors released by adipose tissue, known as adipokines
(e.g., such as leptin and adiponectin), on inflammation, brain function,
blood–brain barrier permeability and development of neurodegenerative
diseases, including AD, to finally provide an overview of the potential
therapeutic applications related to the actions of these adipokines on
the brain's performance (Bettinetti-Luque et al., 2023).
The involvement of the immune system is increasingly
acknowledged as a common theme in the pathophysiology of the
development and progression of both VaD and AD. In this context,
García-Culebras et al. address the contribution of both central and
peripheral innate immune response to cognitive impairment,
F IGURE 1 Multiple shared risk factors and pathogenetic mechanisms contribute to degeneration and cognitive impairment in Alzheimer's
disease and vascular dementia. Partially created with BioRender.com.
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specifically dissecting the role of cells of the myeloid lineage, mainly
represented by neutrophils and monocytes, as well as resident brain
microglia and border-associated macrophages (García-Culebras et al.,
2023). The interactions of neutrophils with platelets, and the associated
thrombo-inflammation, are highlighted as potentially relevant mecha-
nisms in post-stroke cognitive impairment and AD. Of note, the signifi-
cant role of border-associated macrophages, including their influence on
neuroimmune interfaces, is pinpointed as a focal aspect for understand-
ing how CVRFs may converge to affect the integrity of perivascular
spaces and meningeal homeostasis, with ultimate impact on neurological
dysfunction. Finally, novel pharmacological targets are proposed for
prevention of cognitive disorders, aimed at the peripheral inhibition of
neutrophil extracellular traps (NETs) formation (for instance, with
Cl-amidine, an inhibitor of PAD4), and of myeloid TLR4 receptors.
Within the immune system, adaptive immunity is also involved, as
addressed by Ruiz-Fernández et al. Specifically, the role of T cells and
their interplay with other immune and CNS parenchymal cells in health
and disease are discussed, with an emphasis on the scenarios, mainly
related to neurodegeneration and ageing (AD, Parkinson's disease, multi-
ple sclerosis, ischemic stroke, etc.), in which disruption of these connec-
tions may lead to cognitive impairment (Ruiz-Fernández et al., 2023).
The potential for the pharmacological modulation of T cells is reviewed,
starting from molecules that prevent lymphocyte infiltration in the CNS
(monoclonal antibodies against integrins, like natalizumab, or against
CD49d; S1P1 receptor agonists such as fingolimod), with major clinical
utility in multiple sclerosis, moving to modulators of the intestinal micro-
biota like sodium butyrate and valproic acid, with potential application
in ischemic stroke, and the granulocyte-macrophage colony-stimulating
factor sargramostim for AD.
In part by interacting with the immune system, increasing evi-
dence suggests that commensal microbiota have a major role both in
homeostasis and in pathological contexts including cerebrovascular
diseases. In this vein, Cuartero et al. (2023) underscore the intricate
interplay between microbiota and metabolism, immunity, brain devel-
opment and function. Specifically, the possible participation of
microbiota-derived products in post-stroke cognitive impairment
and dementia is discussed, including potential therapeutic opportuni-
ties ranging from probiotics and prebiotics, antibiotics, and faecal
microbiota transplantation. Strategies aiming at the treatment of
gut dysbiosis are proposed, with special emphasis on the aryl
hydrocarbon receptor. This transcription factor is activated by various
environmental and microbial metabolites and is widely expressed
in both the gut and the CNS, making it a pivotal component in the
brain-gut axis.
Additional roads leading to cognitive decline include other actors.
As an example, in an original article of this issue, Fan et al. (2023)
report that astrocytic lactoferrin, a secreted glycoprotein, may
improve cognitive capacity in AD animal models by increasing the
dephosphorylation of APP, opening new lines in the search for thera-
peutic targets in dementia. With this Themed Issue, we intend to
attract additional interest and effort to the development of a holistic
approach to dementia, acknowledging the multiple brain
co-pathologies associated with ageing, and highlighting the complex
relationships between vascular health, immune responses, and neuro-
degenerative diseases. We stress the importance of this multifaceted
perspective, as it opens up new avenues for lifestyle adjustments and
therapeutic interventions, and is essential in addressing the mounting
challenges posed by our ageing society and the increasing burden of
cognitive decline and dementia.
NOMENCLATURE OF TARGETS AND LIGANDS
Key protein targets and ligands in this article are hyperlinked to corre-
sponding entries in http://www.guidetopharmacology.org, and are
permanently archived in the Concise Guide to PHARMACOLOGY
2021/22 (Alexander, Christopoulos et al., 2021; Alexander, Fabbro,
Kelly, Mathie, Peters, Veale, Armstrong, Faccenda, Harding,
Pawson, Southan, Davies, Beuve et al., 2021a; Alexander, Fabbro,
Kelly, Mathie, Peters, Veale, Armstrong, Faccenda, Harding,
Pawson, Southan, Davies, Boison et al., 2021b; Alexander, Kelly
et al., 2021).
AUTHOR CONTRIBUTIONS
Aurora Semerano: Writing—original draft (equal); writing—review and
editing (equal). Javier Fernandez-Ruiz: Writing—review and editing
(supporting). Marta Cortés-Canteli: Conceptualization (equal);
writing—original draft (lead); writing—review and editing (lead).
Maria Angeles Moro: Conceptualization (equal); writing—original draft
(lead); writing—review and editing (lead).
ACKNOWLEDGEMENTS
A. Semerano is supported by a la Caixa Foundation Predoctoral Fellow-
ship (ID 100010434 and LCF/BQ/DI22/11940002) and M. Cortes-
Canteli is the recipient of a Miguel Servet type II research contract
(CPII21/00007) from Instituto de Salud Carlos III (ISCIII) co-funded by
the European Union (Fondo Social Europeo Plus). The CNIC is sup-
ported by the ISCIII, the Spanish Ministry for Science and Innovation
and the Pro-CNIC Foundation and is a Severo Ochoa Center of Excel-
lence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/
501100011033).
FUNDING INFORMATION
la Caixa Foundation Predoctoral Fellowship, Grant/Award Numbers:
ID 100010434, LCF/BQ/DI22/11940002; Instituto de Salud Carlos
III, Grant/Award Number: CPII21/00007; European Regional Devel-
opment Fund; Spanish Ministry for Science, Innovation and Universi-
ties, Grant/Award Numbers: PID2022-140616OB-I00, MCIN/AEI/
10.13039/501100011033; Pro-CNIC Foundation; Severo Ochoa
Center of Excellence, Grant/Award Number: CEX2020-001041-S;
Leducq Foundation for Cardiovascular Research, Grant/Award Num-
ber: TNE-19CVD01andTNE-21CVD04; European Union (Fondo
Social Europeo) Plus)
CONFLICT OF INTEREST STATEMENT
None.
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DATA AVAILABILITY STATEMENT
N/A-Editorial-Themed Issue.
Aurora Semerano1
Javier Fernández-Ruiz2
Marta Cortes-Canteli1,3
María A. Moro1,4
1Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC),
Madrid, Spain
2Instituto Universitario de Investigaci
on en Neuroquímica (IUIN), CIBER
de Enfermedades Neurodegenerativas (CIBERNED) and Instituto Ram
on y
Cajal de Investigaci
on Sanitaris (IRYCIS), Departamento de Bioquímica y
Biología Molecular, Facultad de Medicina, Universidad Complutense,
Madrid, Spain
3Instituto de Investigaci
on Sanitaria Fundaci
on Jiménez Díaz (IIS-FJD),
Madrid, Spain
4Unidad de Investigaci
on Neurovascular, Departamento de Farmacología
y Terapéutica, Facultad de Medicina, Universidad Complutense de
Madrid and Instituto de Investigaci
on Hospital, Madrid, Spain
Correspondence
María A. Moro and Marta Cortes-Canteli, Centro Nacional de
Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Email: mariaangeles.moro@cnic.es and marta.cortesc@quironsalud.es
ORCID
Javier Fernández-Ruiz https://orcid.org/0000-0002-4490-0604
Marta Cortes-Canteli https://orcid.org/0000-0001-8802-4338
María A. Moro https://orcid.org/0000-0003-1010-8237
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